Page last updated: 2024-11-08

estramustine

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Description

Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID259331
CHEMBL ID1575
CHEBI ID4868
SCHEMBL ID4252
MeSH IDM0007783

Synonyms (82)

Synonym
nsc-89201
estra-1,5(10)-triene-3,17-diol (17.beta.)-, 3-[bis(2-chloroethyl)carbamate]
estradiol, 3-[bis(2-chloroethyl)carbamate]
estra-1,5(10)-triene-3,17-diol, 3-[bis(2-chloroethyl)carbamate], (17.beta.)-
estradiol 3-[bis(2-chloroethyl)carbamate]
17.beta.-estradiol 3-[bis(2-chloroethyl)carbamate]
BIDD:GT0482
bis-(2-chloro-ethyl)-carbamic acid 17-hydroxy-13-methyl-7,8,9,11,12,13,14,15,16,17-decahydro-6h-cyclopenta[a]phenanthren-3-yl ester
ro-22-2296-000
bdbm50333646
estramustin
NCI60_041982
LMST02010038
estra-1,3,5(10)-triene-3,17beta-diol, 3-[bis(2-chloroethyl)carbamate]
carbamic acid, bis(2-chloroethyl)-, 17beta-hydroxyestra-1,3,5(10)-trien-3-yl ester
estra-1,3,5(10)-triene-3,17-diol (17beta)-, 3-(bis(2-chloroethyl)carbamate)
estramustina [inn-spanish]
estramustinum [inn-latin]
estradiol, 3-(bis(2-chloroethyl)carbamate)
einecs 221-076-3
estramustine [usan:inn:ban]
estra-1,3,5(10)-triene-3,17-diol, 3-(bis(2-chloroethyl)carbamate), (17beta)-
estradiol 3-(bis(2-chloroethyl)carbamate)
nsc 89201
ro 21-8837
nsc89201
estramustine (usan/inn)
D04066
estramustina
(17beta)-17-hydroxyestra-1(10),2,4-trien-3-yl bis(2-chloroethyl)carbamate
estramustinum
CHEBI:4868 ,
2998-57-4
estramustine
17beta-estradiol 3-(bis(2-chloroethyl)carbamate)
DB01196
estradiol 3-(n,n-bis(2-chloroethyl)carbamate)
NCGC00164581-01
ro-222296000
ro-22-2296000
ro 22-2296/000
CHEMBL1575 ,
[(8r,9s,13s,14s,17s)-17-hydroxy-13-methyl-6,7,8,9,11,12,14,15,16,17-decahydrocyclopenta[a]phenanthren-3-yl] n,n-bis(2-chloroethyl)carbamate
35lt29625a ,
unii-35lt29625a
dtxcid6026458
tox21_112207
cas-2998-57-4
dtxsid8046458 ,
estramustin sodium phosphate
estra-1,3,5(10)-triene-3,17-diol, 3-(bis(2-chloroethyl)carbamate), (17b)-
estramustine [vandf]
estramustine [inn]
estramustine [who-dd]
estramustine [mi]
ro-22-2296/000
estramustine [usan]
CCG-221220
SCHEMBL4252
tox21_112207_1
NCGC00164581-02
FRPJXPJMRWBBIH-RBRWEJTLSA-N
W-106963
gtpl9076
AKOS025402444
estradiol 3-bis(2-chloroethyl)carbamate
AC-9163
HY-103711
HMS3715D22
(8r,9s,13s,14s,17s)-17-hydroxy-13-methyl-7,8,9,11,12,13,14,15,16,17-decahydro-6h-cyclopenta[a]phenanthren-3-yl bis(2-chloroethyl)carbamate
Q412939
AS-12259
A876334
disodium (1s,10r,11s,14s,15s)-5-{[bis(2-chloroethyl)carbamoyl]oxy}-15-methyltetracyclo[8.7.0.0^{2,7}.0^{11,15}]heptadeca-2(7),3,5-trien-14-yl phosphate
EN300-19767105
(1s,3as,3br,9bs,11as)-1-hydroxy-11a-methyl-1h,2h,3h,3ah,3bh,4h,5h,9bh,10h,11h,11ah-cyclopenta[a]phenanthren-7-yl n,n-bis(2-chloroethyl)carbamate
CS-0035073
estramustina (inn-spanish)
estramustinum (inn-latin)
estra-1,3,5(10)triene-317beta-diol 3-(n,n-bis-(2-chloroethyl)carbamate)
17beta-(estra-1,3,5(10)-triene-3,17-diol 3-(bis(2-chloroethyl)carbamate))
l01xx11

Research Excerpts

Overview

Estramustine phosphate is a nitrogen mustard derivative of estradiol-17β-phosphate and has anti-tumour properties. It is an anti-mitotic cytostatic drug that also enhances the effect of radiotherapy.

ExcerptReferenceRelevance
"Estramustine is an stable estradiol and nitrogenated mustard conjugatewith antymicotic properties. "( Long responders to estramustine monophosphate. Report of two cases and literature review.
Castillero, A; Iborra, I; Ramírez-Backhaus, M; Ricós, J; Rubio-Briones, J; Sobrón-Bustamante, M, 2019
)
2.29
"Estramustine is a nitrogen mustard moiety linked to estradiol."( [Primary breast diffuse large B-cell lymphoma developing subsequent to estramustine therapy for prostate cancer].
Goto, M; Higashi, T; Katsuragi, T; Kitamura, N; Morimoto, H; Shimajiri, S; Tanaka, A; Tsukada, J,
)
1.09
"•  Estramustine phosphate is a nitrogen mustard derivative of estradiol-17β-phosphate and has anti-tumour properties. "( The use of estramustine phosphate in the modern management of advanced prostate cancer.
Culine, S; Drouet, L; Eymard, JC; Fizazi, K; Gravis, G; Hennequin, C; Oudard, S; Ravery, V; Zerbib, M, 2011
)
1.38
"Estramustine is an anti-mitotic cytostatic drug that also enhances the effect of radiotherapy. "( Radiation sensitizing effect of estramustine is not dependent on apoptosis.
Dunkel, L; Erkkilä, K; Kairemo, K; Pentikäinen, V; Rannikko, S; Sorvari, P; Ståhlberg, K; Taari, K,
)
1.86
"Estramustine phosphate is a mustard-oestradiol conjugate, and has hormonal and non-hormonal effects. "( Addition of estramustine to chemotherapy and survival of patients with castration-refractory prostate cancer: a meta-analysis of individual patient data.
Berry, WR; Eymard, JC; Fizazi, K; Hudes, G; Kelly, WK; Le Maitre, A; Logothetis, CJ; Michiels, S; Pignon, JP, 2007
)
2.16
"Estramustine is a conjugate of 17 beta-estradiol and the carbamate of nitrogen mustard."( Estramustine phosphate sodium.
Hauser, AR; Merryman, R, 1984
)
2.43
"Estramustine phosphate is a unique antimitotic agent that binds to tubulin and microtubule-associated proteins. "( Phase I study of paclitaxel and estramustine: preliminary activity in hormone-refractory prostate cancer.
Chapman, A; Gallo, J; Greenberg, R; Hudes, GR; McAleer, C; Obasaju, C, 1995
)
2.02
"Estramustine is an estradiol-based agent that accumulates in cells containing estramustine binding protein. "( Selective antimitotic effects of estramustine correlate with its antimicrotubule properties on glioblastoma and astrocytes.
Cornell-Bell, A; Piepmeier, JM; Yoshida, D, 1994
)
2.01
"Estramustine is an estradiol-based antimicrotubule agent that accumulates in malignant glioma cells, resulting in a concentration-dependent inhibition of proliferation. "( Estramustine sensitizes human glioblastoma cells to irradiation.
Piepmeier, J; Weinstein, M; Yoshida, D, 1994
)
3.17
"Estramustine is an estradiol-based agent that has been shown to accumulate in human glioma cells, resulting in a concentration-dependent alteration in cell size and shape within minutes and an inhibition of proliferation over 3 to 6 days. "( Estramustine and estrone analogs rapidly and reversibly inhibit deoxyribonucleic acid synthesis and alter morphology in cultured human glioblastoma cells.
Chen, Z; Keefe, DL; Lin, TT; Naftolin, F; Piepmeier, JM; Weinstein, MA; Yoshida, D; Zielinski, J, 1993
)
3.17
"Estramustine (EaM) is a conjugate of nor-nitrogen mustard (NNM) and 17 beta-estradiol (E2) that has cytotoxic and radiosensitizing effects on experimental malignant glioma. "( Tumor blood flow and the cytotoxic effects of estramustine and its constituents in a rat glioma model.
Bergenheim, AT; Henriksson, R; Johansson, M; Koskinen, LO; Vallbo, C; Widmark, A, 1997
)
2
"Estramustine (EM) is an antimicrotubule drug used in the treatment of hormone refractory advanced prostate cancer. "( Association of estramustine resistance in human prostatic carcinoma cells with modified patterns of tubulin expression.
Calvo, F; Denoulet, P; Fellous, A; Laing, NM; Millot, G; Sangrajrang, S; Tatoud, R; Tew, KD, 1998
)
2.1
"Estramustine (EM) is an antineoplastic drug used in the therapy of human prostatic carcinoma. "( Induction of aneuploidy by the antineoplastic drug estramustine in human lymphocytes.
Cocchi, L; Migliore, L; Sbrana, I; Scarpato, R, 1998
)
1.99
"Estramustine (EM) is an anti-microtubule drug used in the treatment of hormone-refractory advanced prostate cancer. "( Estramustine resistance correlates with tau over-expression in human prostatic carcinoma cells.
Calvo, F; Denoulet, P; Fellous, A; Millot, G; Podgorniak, MP; Sangrajrang, S; Tatoud, R; Tew, KD, 1998
)
3.19
"Estramustine is a combination of estradiol and nitrogen mustard, and alone has shown objective responses in advanced prostatic cancer."( Combined therapy of advanced prostatic carcinoma with estramustine and prednimustine.
Catane, R; Kaufman, J; Mittelman, A; Murphy, GP, 1977
)
1.23
"Estramustine phosphate is a nitrogen mustard derivative of estradiol that has been advocated for the treatment of prostatic cancer. "( Estramustine phosphate: a specific chemotherapeutic agent?.
Muggia, FM; Rozencweig, M; Slavik, M; Von Hoff, DD, 1977
)
3.14
"Estramustine is a novel anti-microtubule drug shown to bind MAP-1 and MAP-2 (microtubule-associated proteins) in vitro. "( Evidence that estramustine binds MAP-1A to inhibit type IV collagenase secretion.
Sousa, O; Stearns, ME; Wang, M, 1991
)
2.08
"Estramustine phosphate is a reversible inhibitor, as the nonionic detergent Triton X-100 was found to counteract the inhibition in a concentration-dependent manner."( Effect of estramustine phosphate on the assembly of trypsin-treated microtubules and microtubules reconstituted from purified tubulin with either tau, MAP2, or the tubulin-binding fragment of MAP2.
Deinum, J; Fridén, B; Luduena, R; Prasad, V; Wallin, M, 1987
)
1.4
"Estramustine (EM) is a conjugate of estradiol and nor-nitrogen mustard (nor-HN2), which is effective in the treatment of prostate cancer. "( Antiinvasive activity of estramustine on malignant MO4 mouse cells and on DU-145 human prostate carcinoma cells in vitro.
De Bruyne, GK; Dragonetti, CH; Hartley-Asp, B; Mareel, MM; Rabaey, ML; Segers, JL; Storme, GA, 1988
)
2.02
"Estramustine is a cytotoxic metabolite of estramustine phosphate (Estracyt), which is used in the treatment of prostatic carcinoma. "( Estramustine binding site in human breast cancer biopsy samples. Its relation to estrogen and progesterone receptor levels, age and menopausal status.
Borg, A; Fernö, M; Idvall, I, 1987
)
3.16

Effects

Estramustine phosphate has been used frequently alone or in combination with other drugs for the treatment of hormone-refractory prostate cancer. It has potent in vitro activity against human glioblastoma cells and can enhance the cytotoxic effects of ionizing radiation.

ExcerptReferenceRelevance
"Estramustine has been shown to potentiate the antimicrotubule effects of vinblastine."( Vinblastine and estramustine phosphate in metastatic renal cell carcinoma: a phase II trial of the Fox Chase Network.
Fox, S; Giantonio, BJ; Greenberg, R; Haas, NB; Halbherr, T; Hudes, GR; Litwin, S; Minniti, CJ; Nahum, K; Reilly, R; Yeslow, G, 2003
)
1.39
"Estramustine phosphate has been administered at a dose of 600 mg/m2 orally daily in three divided doses."( Cooperative clinical trials of the National Prostatic Cancer Project: Protocol 900.
Schmidt, JD, 1984
)
0.99
"Estramustine previously has been shown to interact with P-glycoprotein and to restore intracellular accumulation of vinblastine and paclitaxel in cells overexpressing this drug transporter. "( Modulation of P-glycoprotein activity by estramustine is limited by binding to plasma proteins.
Hudes, GR; Smith, CD; Tew, KD; Zhang, X; Zilfou, JT, 1995
)
2
"Estramustine has been shown to enhance the cytotoxic effects of irradiation in relatively radioresistant glioma cells both in cell culture and in a rat glioma model."( Estramustine in malignant glioma.
Bergenheim, AT; Henriksson, R; Piepmeier, JM; Yoshida, D, 1996
)
2.46
"Estramustine has potent in vitro activity against human glioblastoma cells and can enhance the cytotoxic effects of ionizing radiation. "( Targeting microtubule-associated proteins in glioblastoma: a new strategy for selective therapy.
Greer, C; Pedersen, PE; Piepmeier, JM; Yoshida, D, 1996
)
1.74
"Estramustine and etoposide have been shown to inhibit the growth of prostate cancer cells in experimental models. "( Oral estramustine and oral etoposide for hormone-refractory prostate cancer.
Alivizatos, G; Aravantinos, G; Bamia, C; Constantinidis, C; Deliveliotis, C; Dimopoulos, C; Dimopoulos, MA; Kastriotis, I; Kostakopoulos, A; Panopoulos, C; Pantazopoulos, D; Zervas, A, 1997
)
2.25
"Estramustine has been shown to increase tumour blood flow and potentiate the effect of radiotherapy in experimental glioma."( Effects of radiotherapy and estramustine on the microvasculature in malignant glioma.
Bergenheim, AT; Henriksson, R; Johansson, M; Widmark, A, 1999
)
1.32
"Estramustine phosphate has been used frequently alone or in combination with other drugs for the treatment of hormone-refractory prostate cancer. "( Synergistic effect of estramustine and [3'-keto-Bmtl]-[Val2]-cyclosporine (PSC 833) on the inhibition of androgen receptor phosphorylation in LNCaP cells.
Budman, DR; Kreis, W; Liu, XM; Wang, LG, 1999
)
2.06
"Estramustine has been associated with side effects such as nausea, vomiting, edema, and serious vascular events."( Phase I/II studies of docetaxel (Taxotere) combined with estramustine in men with hormone-refractory prostate cancer.
Bagiella, E; Benson, M; England-Owen, C; Hetjan, D; Judge, T; Macarthur, R; Newhouse, J; O'Connor, J; Olsson, C; Petrylak, DP; Pfaff, C; Sawczuk, I; Shelton, G; Weitzman, A; Zuech, N, 1999
)
1.27
"Estramustine has been shown previously to be an effective drug in the treatment of metastatic prostatic cancer, demonstrating significant objective and subjective responses in long-term non-randomized trials and in other randomized trials. "( The use of estramustine and prednimustine versus prednimustine alone in advanced metastatic prostatic cancer patients who have received prior irradiation.
Chu, TM; Gaeta, JF; Gibbons, RP; Johnson, DE; Loening, SA; Murphy, GP; Prout, GR; Saroff, J; Schmidt, JD; Scott, WW; Slack, N; Soloway, MS; Wajsman, Z, 1979
)
2.09
"Estramustine has been shown previously to be an effective drug in the treatment of metastatic prostatic cancer, demonstrating significant objective and subjective responses in long-term non-randomized trials and in other randomized trials. "( The use of estramustine and prednimustine versus prednimustine alone in advanced metastatic prostatic cancer patients who have received prior irradiation.
Chu, TM; Gaeta, JF; Gibbons, RP; Johnson, DE; Loening, SA; Murphy, GP; Prout, GR; Saroff, J; Schmidt, JD; Scott, WW; Slack, N; Soloway, MS; Wajsman, Z, 1978
)
2.09
"Estramustine phosphate has been used as primary treatment in 38 patients with advanced prostatic carcinoma. "( Primary treatment of prostatic carcinoma with estramustine phosphate: preliminary report.
Jonsson, G; Nilsson, T, 1976
)
1.96
"Estramustine phosphate has been useful in the treatment of advanced carcinoma of the prostate. "( Treatment of advanced carcinoma of the prostate with estramustine phosphate.
Fosså, SD; Miller, A, 1976
)
1.95

Actions

ExcerptReferenceRelevance
"Estramustine did not increase the activity of docetaxel in these models."( High efficacy of docetaxel with and without androgen deprivation and estramustine in preclinical models of advanced prostate cancer.
Fizazi, K; Kim, J; Logothetis, CJ; Martinez, LA; Navone, NM; Olive, MC; Sikes, CR; Yang, J,
)
1.09

Treatment

All estramustine-treated patients lost their libido, whereas only 20 per cent of the patients treated with flutamide did so. Cell treatment was carried out using radioactive nucleotide and leucine additions.

ExcerptReferenceRelevance
"All estramustine-treated patients lost their libido, whereas only 20 per cent of the patients treated with flutamide did so."( Clinical evaluation of flutamide and estramustine as initial treatment of metastatic carcinoma of prostate.
Andersson, SO; Beckman, KW; Johansson, JE; Lingårdh, G; Zador, G, 1987
)
1.03
"Cell treatment with estramustine, nor-nitrogen mustard and tauromustine, followed by radioactive nucleotide and leucine incorporations, as a measure of RNA, DNA and protein labelling, were carried out."( The effect of estramustine, nor-nitrogen mustard and tauromustine on macromolecular labelling in the human prostatic tumour cell line 1013L.
Hartley-Asp, B; Kruse, E, 1989
)
0.95

Toxicity

weekly DTX combined with estramustine has similar efficacy to standard-dose DTX but with fewer adverse events. The CTCAE data were used to identify severe adverse event clusters.

ExcerptReferenceRelevance
" and, especially, the presence of previous cardiovascular disease represented adverse factors in the development of cardiovascular toxicity."( Cardiovascular side effects of diethylstilbestrol, cyproterone acetate, medroxyprogesterone acetate and estramustine phosphate used for the treatment of advanced prostatic cancer: results from European Organization for Research on Treatment of Cancer tria
de Pauw, M; de Voogt, HJ; Pavone-Macaluso, M; Smith, PH; Suciu, S, 1986
)
0.49
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" No serious adverse events were reported during the study and there were no toxicity-related deaths."( Safety and effectiveness of neoadjuvant luteinizing hormone-releasing hormone agonist plus low-dose estramustine phosphate in high-risk prostate cancer: a prospective single-arm study.
Hashimoto, Y; Hatakeyama, S; Kamimura, N; Koie, T; Ohyama, C; Yamamoto, H; Yoneyama, T, 2012
)
0.6
"Six months of LHRH+EMP neoadjuvant therapy followed by RP is safe and oncological outcomes are acceptable."( Safety and effectiveness of neoadjuvant luteinizing hormone-releasing hormone agonist plus low-dose estramustine phosphate in high-risk prostate cancer: a prospective single-arm study.
Hashimoto, Y; Hatakeyama, S; Kamimura, N; Koie, T; Ohyama, C; Yamamoto, H; Yoneyama, T, 2012
)
0.6
"For Japanese CRPC patients, weekly low-dose DTX combined with estramustine has similar efficacy to standard-dose DTX but with fewer adverse events."( Weekly, low-dose docetaxel combined with estramustine for Japanese castration-resistant prostate cancer: its efficacy and safety profile compared with tri-weekly standard-dose treatment.
Nakai, Y; Nakayama, M; Nishimura, K; Nonomura, N; Takayama, H; Tsujimura, A; Uemura, M, 2014
)
0.91
" The results of our phase II study suggest that low-dose EMP is a safe treatment option with the same efficacy in patients with castration-resistant prostate cancer."( Effective and Safe Administration of Low-Dose Estramustine Phosphate for Castration-Resistant Prostate Cancer.
Akamatsu, S; Inoue, T; Kamba, T; Kamoto, T; Kawakita, M; Matsui, Y; Ogawa, O; Ogura, K; Segawa, T; Sugino, Y; Tanaka, S; Tsukino, H; Yamasaki, T, 2016
)
0.69
"Low-dose EMP seems to be a safe treatment option with some efficacy in patients with CRPC."( Effective and Safe Administration of Low-Dose Estramustine Phosphate for Castration-Resistant Prostate Cancer.
Akamatsu, S; Inoue, T; Kamba, T; Kamoto, T; Kawakita, M; Matsui, Y; Ogawa, O; Ogura, K; Segawa, T; Sugino, Y; Tanaka, S; Tsukino, H; Yamasaki, T, 2016
)
0.69
"Exploring the relationships among adverse events is important because those that arise from a common mechanism are amenable to a common intervention, which can improve symptom management, quality of life, and treatment adherence."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
"The CTCAE data from a randomized clinical trial conducted by SWOG that compared docetaxel plus estramustine versus mitoxantrone plus predinsone in patients with advanced prostate cancer were used to identify severe adverse event clusters."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.65
"A total of 109 adverse event types were captured using the CTCAE."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
"Several severe adverse event clusters were identified in patients with advanced prostate cancer."( Identifying Severe Adverse Event Clusters Using the National Cancer Institute's Common Terminology Criteria for Adverse Events.
Hershman, DL; Lee, SM; Lim, EA; Moinpour, CM; Unger, J; Zhong, X, 2016
)
0.43
" We analyzed the main outcomes, including the overall survival (OS), progression-free survival (PFS), prostate-specific antigen (PSA) response, tumor response and severe adverse events (AEs)."( The efficacy and safety comparison of docetaxel, cabazitaxel, estramustine, and mitoxantrone for castration-resistant prostate cancer: A network meta-analysis.
Huang, C; Song, P; Wang, Y, 2018
)
0.72

Pharmacokinetics

ExcerptReferenceRelevance
" The terminal half-life of estromustine was 10-20 h, which suggests that EMP might be given once or twice a day."( Pharmacokinetics of estramustine phosphate (Estracyt) in prostatic cancer patients.
Andersson, SB; Gunnarsson, PO; Johansson, SA; Nilsson, T; Plym-Forshell, G, 1984
)
0.59
" This review summarises the present relatively limited knowledge concerning the pharmacokinetic and pharmacodynamic aspects of estramustine phosphate and its metabolites."( Pharmacokinetics and pharmacodynamics of estramustine phosphate.
Bergenheim, AT; Henriksson, R, 1998
)
0.77

Compound-Compound Interactions

The results of the current study demonstrated that gefitinib combined with estramustine and docetaxel had acceptable and predictable tolerability.

ExcerptReferenceRelevance
" Although the incidence of modest (grade 2) late GI and GU toxicities seem to be increased compared with 3D-CRT alone or in combination with androgen ablation therapy, no severe toxicities were encountered with this regimen."( Results of a phase II study using estramustine phosphate and vinblastine in combination with high-dose three-dimensional conformal radiotherapy for patients with locally advanced prostate cancer.
Fuks, Z; Kelly, WK; Lee, H; Leibel, SA; Metz, E; Scher, HI; Schwartz, L; Smart, T; Zelefsky, MJ, 2000
)
0.59
" Our studies examine the ability of gemcitabine, both alone and in combination with other chemotherapeutic agents, to inhibit the in vitro and in vivo growth of several prostate cancer cell lines."( The study of gemcitabine in combination with other chemotherapeutic agents as an effective treatment for prostate cancer.
Brumfield, SK; Lehr, JE; Mahoney, M; Muenchen, HJ; Pienta, KJ; Pilat, MJ; Quigley, MM,
)
0.13
" EMP in combination with paclitaxel and carboplatin can be safely administered with hepatic toxicity being transient and reversible."( Dose escalation study of intravenous estramustine phosphate in combination with Paclitaxel and Carboplatin in patients with advanced prostate cancer.
Curley, T; Fallon, M; Hartley-Asp, B; Kelly, WK; Larson, S; Pellizzoni, C; Rocchetti, M; Scher, H; Schwartz, L; Slovin, S; Tong, W; Zhu, AX, 2003
)
0.59
" We examined the cytotoxic effects of imatinib in combination with other anticancer agents in the human prostate cancer cell lines LNCaP, PC-3, and DU 145."( In vitro cytotoxic effects of imatinib in combination with anticancer drugs in human prostate cancer cell lines.
Battistel, C; Hartung, R; Kübler, HR; Lehmer, A; Paul, R; Treiber, U; van Randenborgh, H; Wagenpfeil, S; Wutzler, S, 2005
)
0.33
" In combination with etoposide imatinib produced additive effects in two of three cell lines."( In vitro cytotoxic effects of imatinib in combination with anticancer drugs in human prostate cancer cell lines.
Battistel, C; Hartung, R; Kübler, HR; Lehmer, A; Paul, R; Treiber, U; van Randenborgh, H; Wagenpfeil, S; Wutzler, S, 2005
)
0.33
" When given with prednisone, docetaxel was also shown to reduce pain and serum prostate specific antigen levels and improve quality of life compared with mitoxantrone/prednisone."( Which drug combination for hormone-refractory prostate cancer?
Doggrell, SA, 2005
)
0.33
" Based on these results we investigated Ro 28-2653 in combination with estramustine on the G subline of the Dunning tumor."( Matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine: tumor-reducing effects on hormone-sensitive prostate cancer in rats.
Abramjuk, C; Juchem, R; Jung, K; Krell, HW; Lein, M; Loening, SA; Peters, R; Schnorr, J; Staack, A; Stephan, C; Taymoorian, K, 2005
)
0.8
" In this pilot Phase I trial, the authors evaluated the tolerability, efficacy, and pharmacokinetics of gefitinib combined with estramustine and docetaxel in patients with HRPC."( Results from a pilot Phase I trial of gefitinib combined with docetaxel and estramustine in patients with hormone-refractory prostate cancer.
Das-Gupta, A; Small, E; Soulie, P; Trump, D; Wilding, G, 2006
)
0.77
"The results of the current study demonstrated that gefitinib combined with estramustine and docetaxel had acceptable and predictable tolerability."( Results from a pilot Phase I trial of gefitinib combined with docetaxel and estramustine in patients with hormone-refractory prostate cancer.
Das-Gupta, A; Small, E; Soulie, P; Trump, D; Wilding, G, 2006
)
0.79
"The primary objective of the current study was to identify the tolerable dose level of oral vinorelbine when given in combination with estramustine to men with hormone-refractory prostate cancer (HRPC)."( Dose escalation of oral vinorelbine in combination with estramustine in hormone-refractory adenocarcinoma of the prostate.
Cooney, KA; Dunn, RL; Fardig, J; Hellerstedt, B; Mackler, NJ; Olson, K; Pienta, KJ; Smith, DC, 2006
)
0.78
"Oral vinorelbine at doses of 70 mg/m2 may be safely combined with estramustine."( Dose escalation of oral vinorelbine in combination with estramustine in hormone-refractory adenocarcinoma of the prostate.
Cooney, KA; Dunn, RL; Fardig, J; Hellerstedt, B; Mackler, NJ; Olson, K; Pienta, KJ; Smith, DC, 2006
)
0.82
" We hypothesized that the inhibitor effect of Ro 28-2653 on the tumor growth could be improved by combination with chemotherapeutic drugs and examined therefore the effect of Ro 28-2653 alone and in combination with etoposide or estramustine in the MatLyLu Dunning R-3327 rat tumor model characteristic for the androgen-independent prostate cancer (PCa)."( Enhanced inhibitory effect of the matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine and etoposide on the prostate carcinoma in the rat Dunning orthotopic tumor model.
Abramjuk, C; Jung, K; Krell, HW; Lein, M; Loening, SA; Rothaug, W, 2007
)
0.74
"The proliferation rate was only inhibited by etoposide while that effect was increased in combination with Ro 28-2653 and estramustine."( Enhanced inhibitory effect of the matrix metalloproteinase inhibitor Ro 28-2653 in combination with estramustine and etoposide on the prostate carcinoma in the rat Dunning orthotopic tumor model.
Abramjuk, C; Jung, K; Krell, HW; Lein, M; Loening, SA; Rothaug, W, 2007
)
0.76
" Overall, the chemotherapy combined with Sr-89 was well tolerated."( Bone-targeted therapy: phase II study of strontium-89 in combination with alternating weekly chemohormonal therapies for patients with advanced androgen-independent prostate cancer.
Amato, RJ; Henary, H; Hernandez-McClain, J, 2008
)
0.35
"The objective of this study is to assess the safety and efficacy of a treatment regimen comprising neoadjuvant conventional androgen deprivation therapy (ADT) plus estramustine phosphate (EMP) combined with three-dimensional conformal radiotherapy (3D-CRT) for patients with intermediate- to high-risk prostate cancer."( Neoadjuvant LHRH analog plus estramustine phosphate combined with three-dimensional conformal radiotherapy for intermediate- to high-risk prostate cancer: a randomized study.
Hirano, D; Ichinose, T; Maebayashi, T; Mochida, J; Nagane, Y; Saitoh, T; Satoh, K; Sugimoto, S; Takahashi, S, 2010
)
0.85
"The present results indicate that the combination of neoadjuvant ADT plus EMP combined with 3D-CRT sustains freedom from PSA relapse in patients with intermediate- to high-risk prostate cancer."( Neoadjuvant LHRH analog plus estramustine phosphate combined with three-dimensional conformal radiotherapy for intermediate- to high-risk prostate cancer: a randomized study.
Hirano, D; Ichinose, T; Maebayashi, T; Mochida, J; Nagane, Y; Saitoh, T; Satoh, K; Sugimoto, S; Takahashi, S, 2010
)
0.65
"To evaluate the efficacy and safety profile of vinorelbine and estramustine in combination with three-dimensional conformational radiotherapy (3D-CRT) in patients with localized high-risk prostate cancer."( Phase II study of vinorelbine and estramustine in combination with conformational radiotherapy for patients with high-risk prostate cancer.
Carles, J; Domenech, M; Fabregat, X; Ferrer, F; Foro, P; Gallardo, E; García, D; Gayo, J; Gelabert-Mas, A; Nogue, M; Sole, JM; Suarez, M, 2010
)
0.88
"Fifty patients received estramustine, 600 mg/m(2) daily, and vinorelbine, 25 mg/m(2), on days 1 and 8 of a 21-day cycle for three cycles in combination with 8 weeks of 3D-CRT (total dose of 70."( Phase II study of vinorelbine and estramustine in combination with conformational radiotherapy for patients with high-risk prostate cancer.
Carles, J; Domenech, M; Fabregat, X; Ferrer, F; Foro, P; Gallardo, E; García, D; Gayo, J; Gelabert-Mas, A; Nogue, M; Sole, JM; Suarez, M, 2010
)
0.95
"Vinorelbine and estramustine in combination with 3D-CRT is a safe and effective regimen for patients with localized high-risk prostate cancer."( Phase II study of vinorelbine and estramustine in combination with conformational radiotherapy for patients with high-risk prostate cancer.
Carles, J; Domenech, M; Fabregat, X; Ferrer, F; Foro, P; Gallardo, E; García, D; Gayo, J; Gelabert-Mas, A; Nogue, M; Sole, JM; Suarez, M, 2010
)
0.99
"To assess the efficacy of a multiagent taxane-based chemotherapy combined with hormonal therapy in men with metastatic androgen-dependent prostate cancer in a multicenter, cooperative group, single-arm trial."( Phase II evaluation of early oral estramustine, oral etoposide, and intravenous paclitaxel combined with hormonal therapy in patients with high-risk metastatic prostate adenocarcinoma: Southwest Oncology Group S0032.
Golshayan, A; Harrer, GW; Hussain, MH; Mills, GM; Smith, DC; Tangen, CM; Thompson, IM; Van Veldhuizen, PJ; Vogelzang, NJ, 2011
)
0.65
"For Japanese CRPC patients, weekly low-dose DTX combined with estramustine has similar efficacy to standard-dose DTX but with fewer adverse events."( Weekly, low-dose docetaxel combined with estramustine for Japanese castration-resistant prostate cancer: its efficacy and safety profile compared with tri-weekly standard-dose treatment.
Nakai, Y; Nakayama, M; Nishimura, K; Nonomura, N; Takayama, H; Tsujimura, A; Uemura, M, 2014
)
0.91

Bioavailability

The solubility in water of the cytotoxic drug estramustine is less than 1 mg/L. polymorphism can have an impact on the bioavailability of orally administered drug. The interaction of clodronate (800 mg orally four times daily) and estamustine phosphate (280 mg orally twice daily) was studied in twelve patients with prostate carcinoma and bone metastases.

ExcerptReferenceRelevance
"As the solubility in water of the cytotoxic drug estramustine is less than 1 mg/L, polymorphism can have an impact on the bioavailability of orally administered drug."( Polymorphism of estramustine.
Lindberg, NO; Wadsten, T, 1989
)
0.88
" The relative bioavailability of estromustine after administration of EMP-capsules was 44%, which reflects incomplete absorption of EMP rather than first-pass metabolism of estromustine."( Pharmacokinetics of estramustine phosphate (Estracyt) in prostatic cancer patients.
Andersson, SB; Gunnarsson, PO; Johansson, SA; Nilsson, T; Plym-Forshell, G, 1984
)
0.59
" Therefore, the interaction of clodronate (800 mg orally four times daily) and estramustine phosphate (280 mg orally twice daily) on their bioavailability was studied in twelve patients with prostate carcinoma and bone metastases."( Effect of concomitant administration of clodronate and estramustine phosphate on their bioavailability in patients with metastasized prostate cancer.
Castrén-Kortekangas, P; Kylmälä, T; Seppänen, J; Tammela, TL; Ylitalo, P, 1996
)
0.77
" Second, EMP is able to produce a complex with calcium when dairy products are taken concomitantly with EMP, resulting in a decrease in the absorption rate of EMP from the gut."( Necessity of re-evaluation of estramustine phosphate sodium (EMP) as a treatment option for first-line monotherapy in advanced prostate cancer.
Kitamura, T, 2001
)
0.6
" As low bioavailability limits their anticancer properties, we investigated whether conjugation with PAMAM dendrimer (D) could enhance the activity of D-EM and D-PODO by altering their release pattern."( Comparative study of microtubule inhibitors--estramustine and natural podophyllotoxin conjugated PAMAM dendrimer on glioma cell proliferation.
Dixit, D; Sen, E; Sk, UH, 2013
)
0.65
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019
)
0.51

Dosage Studied

Eleven patients with hormone-refractory prostate cancer were treated with escalating weekly doses of docetaxel. Estramustine was administered at a dosage of 600 mg/m2 daily, and paclitaxel was dose-escalated in cohorts from 125 to 250 mg/ m2.

ExcerptRelevanceReference
" This combination appears to be safe, provided the field of radiation is not so large that is may add significantly to the myelosuppressive effect of chemotherapy and the dosage of concomitantly administered radiopotentiating agent(s) is reduced."( Feasibility of integration of modalities in melanomas and sarcomas.
Berger, JL; Friedman, M; Holyoke, ED; Karakousis, CP; Lopez, R; Takita, H, 1979
)
0.26
" Dosage modifications or an anti-emetic may help."( The present role of estramustine phosphate in advanced prostate cancer.
Baert, L; Van Poppel, H, 1991
)
0.6
" As a result the use of Cytonal at least in the dosage hitherto used is no longer worth being advocated."( [Cellular immunity in prostatic cancer modified by Cytonal, Estrazyt and Turisteron].
Fiedler, R; Klebingat, KJ; Lorenz, G; Panzig, E; Steinhauser, I, 1987
)
0.27
" The data also showed that close attention should be given to plasma LH in identifying patients who are unreliable, since intermittent hormone dosage caused an exaggerated rise even when plasma testosterone remained at castrate levels."( Plasma hormone levels in patients with prostatic carcinoma treated with diethylstilboestrol and estramustine.
Bishop, MC; Selby, C; Taylor, M, 1985
)
0.49
" It has become evident that DES at a dosage of 3 mg/day carries a significantly higher risk of overall cardiovascular toxicity than does cyproterone acetate, but severe cardiovascular complications did not differ between treatment groups."( Treatment of prostatic cancer: the EORTC experience--preliminary results of prostatic carcinoma trials.
Schroeder, FH, 1984
)
0.27
" Dosage was 15 mg/kg/day for 2 months, followed by 5 mg/kg/day until progression."( Estramustine phosphate (Estracyt) treatment of T3-T4 prostatic carcinoma.
Artuso, G; Cosciani-Cunico, S; Frustaci, S; Galligioni, E; Grigoletto, E; Merlo, A; Tirelli, U; Trovó, G; Tumolo, S; Veronesi, A; Zattoni, F, 1982
)
1.71
" Long-term ECT completely blocked the rise in luteinizing hormone and testosterone level, but ECT at this dosage was likely to cause complications."( Estramustine phosphate for preventing flare-up in luteinizing hormone-releasing hormone analogue depot therapy.
Jinbo, H; Satoh, J; Shibata, Y; Shimizu, TS; Yamanaka, H, 1995
)
1.73
" To determine the optimal dosage and the toxicities of these two agents for future trials."( Phase I trial of the combination of daily estramustine phosphate and intermittent docetaxel in patients with metastatic hormone refractory prostate carcinoma.
Barile, B; Budman, DR; Fetten, J; Gonzales, AL; Kreis, W; Vinciguerra, V, 1999
)
0.57
" Grades 1 or 2 hypocalcemia and hypophosphatemia were seen at all dosage levels."( Phase I trial of the combination of daily estramustine phosphate and intermittent docetaxel in patients with metastatic hormone refractory prostate carcinoma.
Barile, B; Budman, DR; Fetten, J; Gonzales, AL; Kreis, W; Vinciguerra, V, 1999
)
0.57
" Estramustine phosphate was given on a daily oral dosing schedule of 14 mg/kg; docetaxel was administered intravenously over 1 hour every 3 weeks."( Daily oral estramustine and intermittent intravenous docetaxel (Taxotere) as chemotherapeutic treatment for metastatic, hormone-refractory prostate cancer.
Budman, D; Kreis, W, 1999
)
1.6
" For the following decades, it was used mainly in hormone-refractory cases, with a conventional dosage of 4-9 capsules/day, which showed a 30-35% objective response rate."( Necessity of re-evaluation of estramustine phosphate sodium (EMP) as a treatment option for first-line monotherapy in advanced prostate cancer.
Kitamura, T, 2001
)
0.6
"The major toxicities were gastrointestinal and thromboembolic complications related to daily oral dosing of EM."( Phase I trial of weekly paclitaxel plus oral estramustine phosphate in patients with hormone-refractory prostate cancer.
Babb, J; Entmacher, M; Flinker, D; Garay, C; Gillon, T; Haas, N; Hudes, G; Minnitti, C; Rogatko, A; Roth, B; Weinstein, A; Yeslow, G, 2001
)
0.57
"This phase I study was conducted to identify the maximum tolerated dosage of paclitaxel administered as a 3-hr infusion combined with a stable dosage of estramustine capsules daily in men with hormone refractory prostate cancer."( Phase I trial of oral estramustine and 3-hr infusional paclitaxel for the treatment of hormone refractory prostate cancer.
Hsieh, YC; Kies, MS; Kuzel, TM; Rademaker, AW; Wu, N, 2002
)
0.83
" Estramustine was administered at a dosage of 600 mg/m2 daily, and paclitaxel was dose-escalated in cohorts from 125 to 250 mg/m2 administered as an infusion over 3 hr every 21 days."( Phase I trial of oral estramustine and 3-hr infusional paclitaxel for the treatment of hormone refractory prostate cancer.
Hsieh, YC; Kies, MS; Kuzel, TM; Rademaker, AW; Wu, N, 2002
)
1.54
"The maximum tolerated dose of paclitaxel on this schedule was 225 mg/m2 based on unacceptable dose-limiting fatigue observed at the next higher dosage level."( Phase I trial of oral estramustine and 3-hr infusional paclitaxel for the treatment of hormone refractory prostate cancer.
Hsieh, YC; Kies, MS; Kuzel, TM; Rademaker, AW; Wu, N, 2002
)
0.63
" In an attempt to reduce the incidence of myelosuppression, paclitaxel dosing was changed to weekly dosing."( Phase II study of paclitaxel and estramustine in patients with recurrent and refractory non-Hodgkin lymphoma.
Alden, M; Borghaei, H; Millenson, M; Padavic-Shaller, K; Rogatko, A; Schilder, R; Smith, MR; Wang, H, 2004
)
0.6
" However, further examination is needed about dosage and dosing regimen of Estramustine and Docetaxel."( [Combination therapy with estramustine and docetaxel for hormone refractory prostate cancer].
Kanno, T; Shibasaki, N; Takeuchi, H; Taki, Y; Tsuji, Y, 2004
)
0.85
"Eleven patients with hormone-refractory prostate cancer were treated with escalating weekly doses of docetaxel (level I, 3 patients, 30 mg/m2; level II, 3 patients, 35 mg/m2, level III, 3 patients, 40 mg/mz; level IV, 2 patients, 45 mg/m2) associated with fixed dosage of estramustine (840 mg/day)."( Dose-finding study of weekly docetaxel plus estramustine in patients with hormone-refractory metastatic prostate cancer.
Ardito, R; Coccaro, M; Di Renzo, N; Romano, G; Tartarone, A,
)
0.57
"The effects of 'metronomic' or extended chemotherapy dosing schedules (ECS) are mediated through poorly understood anti-angiogenic mechanisms."( Metronomic chemotherapy dosing-schedules with estramustine and temozolomide act synergistically with anti-VEGFR-2 antibody to cause inhibition of human umbilical venous endothelial cell growth.
Greenman, J; Hetherington, JW; Lam, T; Little, S; Maraveyas, A, 2007
)
0.6
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (3)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
alkylating agentHighly reactive chemical that introduces alkyl radicals into biologically active molecules and thereby prevents their proper functioning. It could be used as an antineoplastic agent, but it might be very toxic, with carcinogenic, mutagenic, teratogenic, and immunosuppressant actions. It could also be used as a component of poison gases.
radiation protective agentAny compound that is able to protect normal cells from the damage caused by radiation therapy.
[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 (3)

ClassDescription
carbamate esterAny ester of carbamic acid or its N-substituted derivatives.
17beta-hydroxy steroidA 17-hydroxy steroid in which the hydroxy group at position 17 has a beta-configuration.
organochlorine compoundAn organochlorine compound is a compound containing at least one carbon-chlorine bond.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (33)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, TYROSYL-DNA PHOSPHODIESTERASEHomo sapiens (human)Potency7.25030.004023.8416100.0000AID489007
Chain A, ATP-DEPENDENT DNA HELICASE Q1Homo sapiens (human)Potency8.13490.125919.1169125.8920AID2708
LuciferasePhotinus pyralis (common eastern firefly)Potency40.53340.007215.758889.3584AID624030
acetylcholinesteraseHomo sapiens (human)Potency6.16550.002541.796015,848.9004AID1347398
hypoxia-inducible factor 1 alpha subunitHomo sapiens (human)Potency30.10653.189029.884159.4836AID1224846
RAR-related orphan receptor gammaMus musculus (house mouse)Potency29.84930.006038.004119,952.5996AID1159521
USP1 protein, partialHomo sapiens (human)Potency50.11870.031637.5844354.8130AID504865
GLS proteinHomo sapiens (human)Potency31.62280.35487.935539.8107AID624170
TDP1 proteinHomo sapiens (human)Potency23.71500.000811.382244.6684AID686978
AR proteinHomo sapiens (human)Potency11.29310.000221.22318,912.5098AID743035; AID743040; AID743063
estrogen receptor 2 (ER beta)Homo sapiens (human)Potency1.94330.000657.913322,387.1992AID1259377; AID1259378; AID1259394
progesterone receptorHomo sapiens (human)Potency13.33320.000417.946075.1148AID1346795
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency38.90180.01237.983543.2770AID1645841
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency10.59090.001530.607315,848.9004AID1224841
farnesoid X nuclear receptorHomo sapiens (human)Potency21.13000.375827.485161.6524AID743217
estrogen nuclear receptor alphaHomo sapiens (human)Potency0.07060.000229.305416,493.5996AID1259383; AID743069; AID743075; AID743077; AID743078; AID743079
GVesicular stomatitis virusPotency38.90180.01238.964839.8107AID1645842
vitamin D (1,25- dihydroxyvitamin D3) receptorHomo sapiens (human)Potency29.84700.023723.228263.5986AID743222
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency2.81840.035520.977089.1251AID504332
activating transcription factor 6Homo sapiens (human)Potency26.08200.143427.612159.8106AID1159516; AID1159519
v-jun sarcoma virus 17 oncogene homolog (avian)Homo sapiens (human)Potency23.32260.057821.109761.2679AID1159526; AID1159528
nuclear receptor subfamily 1, group I, member 2Rattus norvegicus (Norway rat)Potency39.81070.10009.191631.6228AID1346983
Bloom syndrome protein isoform 1Homo sapiens (human)Potency22.26100.540617.639296.1227AID2528; AID2585
vitamin D3 receptor isoform VDRAHomo sapiens (human)Potency50.11870.354828.065989.1251AID504847
gemininHomo sapiens (human)Potency16.78890.004611.374133.4983AID624296
DNA polymerase kappa isoform 1Homo sapiens (human)Potency8.91250.031622.3146100.0000AID588579
histone acetyltransferase KAT2A isoform 1Homo sapiens (human)Potency12.58930.251215.843239.8107AID504327
Interferon betaHomo sapiens (human)Potency38.90180.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency38.90180.01238.964839.8107AID1645842
Cellular tumor antigen p53Homo sapiens (human)Potency22.88470.002319.595674.0614AID651631; AID720552
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency38.90180.01238.964839.8107AID1645842
cytochrome P450 2C9, partialHomo sapiens (human)Potency38.90180.01238.964839.8107AID1645842
[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)
Tyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)IC50 (µMol)300.00000.31804.00429.6000AID551432
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (219)

Processvia Protein(s)Taxonomy
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycle G2/M phase transitionCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
ER overload responseCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
mitophagyCellular tumor antigen p53Homo sapiens (human)
in utero embryonic developmentCellular tumor antigen p53Homo sapiens (human)
somitogenesisCellular tumor antigen p53Homo sapiens (human)
release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
hematopoietic progenitor cell differentiationCellular tumor antigen p53Homo sapiens (human)
T cell proliferation involved in immune responseCellular tumor antigen p53Homo sapiens (human)
B cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
T cell lineage commitmentCellular tumor antigen p53Homo sapiens (human)
response to ischemiaCellular tumor antigen p53Homo sapiens (human)
nucleotide-excision repairCellular tumor antigen p53Homo sapiens (human)
double-strand break repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
protein import into nucleusCellular tumor antigen p53Homo sapiens (human)
autophagyCellular tumor antigen p53Homo sapiens (human)
DNA damage responseCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrestCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediatorCellular tumor antigen p53Homo sapiens (human)
transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
Ras protein signal transductionCellular tumor antigen p53Homo sapiens (human)
gastrulationCellular tumor antigen p53Homo sapiens (human)
neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of neuroblast proliferationCellular tumor antigen p53Homo sapiens (human)
protein localizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA replicationCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell population proliferationCellular tumor antigen p53Homo sapiens (human)
determination of adult lifespanCellular tumor antigen p53Homo sapiens (human)
mRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
rRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
response to salt stressCellular tumor antigen p53Homo sapiens (human)
response to inorganic substanceCellular tumor antigen p53Homo sapiens (human)
response to X-rayCellular tumor antigen p53Homo sapiens (human)
response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
positive regulation of gene expressionCellular tumor antigen p53Homo sapiens (human)
cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic processCellular tumor antigen p53Homo sapiens (human)
glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
viral processCellular tumor antigen p53Homo sapiens (human)
glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
cerebellum developmentCellular tumor antigen p53Homo sapiens (human)
negative regulation of cell growthCellular tumor antigen p53Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayCellular tumor antigen p53Homo sapiens (human)
mitotic G1 DNA damage checkpoint signalingCellular tumor antigen p53Homo sapiens (human)
negative regulation of telomere maintenance via telomeraseCellular tumor antigen p53Homo sapiens (human)
T cell differentiation in thymusCellular tumor antigen p53Homo sapiens (human)
tumor necrosis factor-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
regulation of tissue remodelingCellular tumor antigen p53Homo sapiens (human)
cellular response to UVCellular tumor antigen p53Homo sapiens (human)
multicellular organism growthCellular tumor antigen p53Homo sapiens (human)
positive regulation of mitochondrial membrane permeabilityCellular tumor antigen p53Homo sapiens (human)
cellular response to glucose starvationCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of apoptotic processCellular tumor antigen p53Homo sapiens (human)
entrainment of circadian clock by photoperiodCellular tumor antigen p53Homo sapiens (human)
mitochondrial DNA repairCellular tumor antigen p53Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
transcription initiation-coupled chromatin remodelingCellular tumor antigen p53Homo sapiens (human)
negative regulation of proteolysisCellular tumor antigen p53Homo sapiens (human)
negative regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of DNA-templated transcriptionCellular tumor antigen p53Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assemblyCellular tumor antigen p53Homo sapiens (human)
positive regulation of transcription by RNA polymerase IICellular tumor antigen p53Homo sapiens (human)
response to antibioticCellular tumor antigen p53Homo sapiens (human)
fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
negative regulation of fibroblast proliferationCellular tumor antigen p53Homo sapiens (human)
circadian behaviorCellular tumor antigen p53Homo sapiens (human)
bone marrow developmentCellular tumor antigen p53Homo sapiens (human)
embryonic organ developmentCellular tumor antigen p53Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationCellular tumor antigen p53Homo sapiens (human)
protein stabilizationCellular tumor antigen p53Homo sapiens (human)
negative regulation of helicase activityCellular tumor antigen p53Homo sapiens (human)
protein tetramerizationCellular tumor antigen p53Homo sapiens (human)
chromosome organizationCellular tumor antigen p53Homo sapiens (human)
neuron apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of cell cycleCellular tumor antigen p53Homo sapiens (human)
hematopoietic stem cell differentiationCellular tumor antigen p53Homo sapiens (human)
negative regulation of glial cell proliferationCellular tumor antigen p53Homo sapiens (human)
type II interferon-mediated signaling pathwayCellular tumor antigen p53Homo sapiens (human)
cardiac septum morphogenesisCellular tumor antigen p53Homo sapiens (human)
positive regulation of programmed necrotic cell deathCellular tumor antigen p53Homo sapiens (human)
protein-containing complex assemblyCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stressCellular tumor antigen p53Homo sapiens (human)
thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of thymocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
necroptotic processCellular tumor antigen p53Homo sapiens (human)
cellular response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
cellular response to xenobiotic stimulusCellular tumor antigen p53Homo sapiens (human)
cellular response to ionizing radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to gamma radiationCellular tumor antigen p53Homo sapiens (human)
cellular response to UV-CCellular tumor antigen p53Homo sapiens (human)
stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
signal transduction by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
cellular response to actinomycin DCellular tumor antigen p53Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondriaCellular tumor antigen p53Homo sapiens (human)
cellular senescenceCellular tumor antigen p53Homo sapiens (human)
replicative senescenceCellular tumor antigen p53Homo sapiens (human)
oxidative stress-induced premature senescenceCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
oligodendrocyte apoptotic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of execution phase of apoptosisCellular tumor antigen p53Homo sapiens (human)
negative regulation of mitophagyCellular tumor antigen p53Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic processCellular tumor antigen p53Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediatorCellular tumor antigen p53Homo sapiens (human)
positive regulation of miRNA transcriptionCellular tumor antigen p53Homo sapiens (human)
negative regulation of G1 to G0 transitionCellular tumor antigen p53Homo sapiens (human)
negative regulation of miRNA processingCellular tumor antigen p53Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvateCellular tumor antigen p53Homo sapiens (human)
negative regulation of pentose-phosphate shuntCellular tumor antigen p53Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxiaCellular tumor antigen p53Homo sapiens (human)
regulation of fibroblast apoptotic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
positive regulation of reactive oxygen species metabolic processCellular tumor antigen p53Homo sapiens (human)
negative regulation of stem cell proliferationCellular tumor antigen p53Homo sapiens (human)
positive regulation of cellular senescenceCellular tumor antigen p53Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathwayCellular tumor antigen p53Homo sapiens (human)
DNA damage checkpoint signalingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein dephosphorylationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
triglyceride metabolic processTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
epidermal growth factor receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
integrin-mediated signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
axonogenesisTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
brain developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
heart developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
fibroblast growth factor receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
hormone-mediated signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cytokine-mediated signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cerebellar cortex formationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
platelet formationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
T cell costimulationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of chondrocyte differentiationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of type I interferon productionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
microvillus organizationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of interferon-beta productionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of interleukin-6 productionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of tumor necrosis factor productionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
regulation of cell adhesion mediated by integrinTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of cell adhesion mediated by integrinTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
multicellular organism growthTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
organ growthTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
peptidyl-tyrosine dephosphorylationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
megakaryocyte developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
atrioventricular canal developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
ERBB signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
hormone metabolic processTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
glucose homeostasisTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
regulation of protein-containing complex assemblyTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of ossificationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of mitotic cell cycleTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of glucose importTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of insulin receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of insulin secretionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
regulation of protein export from nucleusTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of hormone secretionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
platelet-derived growth factor receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
neurotrophin TRK receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
ephrin receptor signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
multicellular organismal reproductive processTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
genitalia developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
inner ear developmentTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
homeostasis of number of cells within a tissueTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of cortisol secretionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
Bergmann glial cell differentiationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
negative regulation of growth hormone secretionTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
face morphogenesisTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
regulation of type I interferon-mediated signaling pathwayTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
intestinal epithelial cell migrationTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cellular response to epidermal growth factor stimulusTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (62)

Processvia Protein(s)Taxonomy
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
transcription cis-regulatory region bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
cis-regulatory region sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
core promoter sequence-specific DNA bindingCellular tumor antigen p53Homo sapiens (human)
TFIID-class transcription factor complex bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specificCellular tumor antigen p53Homo sapiens (human)
protease bindingCellular tumor antigen p53Homo sapiens (human)
p53 bindingCellular tumor antigen p53Homo sapiens (human)
DNA bindingCellular tumor antigen p53Homo sapiens (human)
chromatin bindingCellular tumor antigen p53Homo sapiens (human)
DNA-binding transcription factor activityCellular tumor antigen p53Homo sapiens (human)
mRNA 3'-UTR bindingCellular tumor antigen p53Homo sapiens (human)
copper ion bindingCellular tumor antigen p53Homo sapiens (human)
protein bindingCellular tumor antigen p53Homo sapiens (human)
zinc ion bindingCellular tumor antigen p53Homo sapiens (human)
enzyme bindingCellular tumor antigen p53Homo sapiens (human)
receptor tyrosine kinase bindingCellular tumor antigen p53Homo sapiens (human)
ubiquitin protein ligase bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase regulator activityCellular tumor antigen p53Homo sapiens (human)
ATP-dependent DNA/DNA annealing activityCellular tumor antigen p53Homo sapiens (human)
identical protein bindingCellular tumor antigen p53Homo sapiens (human)
histone deacetylase bindingCellular tumor antigen p53Homo sapiens (human)
protein heterodimerization activityCellular tumor antigen p53Homo sapiens (human)
protein-folding chaperone bindingCellular tumor antigen p53Homo sapiens (human)
protein phosphatase 2A bindingCellular tumor antigen p53Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor bindingCellular tumor antigen p53Homo sapiens (human)
14-3-3 protein bindingCellular tumor antigen p53Homo sapiens (human)
MDM2/MDM4 family protein bindingCellular tumor antigen p53Homo sapiens (human)
disordered domain specific bindingCellular tumor antigen p53Homo sapiens (human)
general transcription initiation factor bindingCellular tumor antigen p53Homo sapiens (human)
molecular function activator activityCellular tumor antigen p53Homo sapiens (human)
promoter-specific chromatin bindingCellular tumor antigen p53Homo sapiens (human)
phosphotyrosine residue bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
phosphoprotein phosphatase activityTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein tyrosine phosphatase activityTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
non-membrane spanning protein tyrosine phosphatase activityTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
insulin receptor bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein kinase bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
signaling receptor complex adaptor activityTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cadherin bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cell adhesion molecule bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
peptide hormone receptor bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
molecular adaptor activityTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein tyrosine kinase bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
receptor tyrosine kinase bindingTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (36)

Processvia Protein(s)Taxonomy
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
nuclear bodyCellular tumor antigen p53Homo sapiens (human)
nucleusCellular tumor antigen p53Homo sapiens (human)
nucleoplasmCellular tumor antigen p53Homo sapiens (human)
replication forkCellular tumor antigen p53Homo sapiens (human)
nucleolusCellular tumor antigen p53Homo sapiens (human)
cytoplasmCellular tumor antigen p53Homo sapiens (human)
mitochondrionCellular tumor antigen p53Homo sapiens (human)
mitochondrial matrixCellular tumor antigen p53Homo sapiens (human)
endoplasmic reticulumCellular tumor antigen p53Homo sapiens (human)
centrosomeCellular tumor antigen p53Homo sapiens (human)
cytosolCellular tumor antigen p53Homo sapiens (human)
nuclear matrixCellular tumor antigen p53Homo sapiens (human)
PML bodyCellular tumor antigen p53Homo sapiens (human)
transcription repressor complexCellular tumor antigen p53Homo sapiens (human)
site of double-strand breakCellular tumor antigen p53Homo sapiens (human)
germ cell nucleusCellular tumor antigen p53Homo sapiens (human)
chromatinCellular tumor antigen p53Homo sapiens (human)
transcription regulator complexCellular tumor antigen p53Homo sapiens (human)
protein-containing complexCellular tumor antigen p53Homo sapiens (human)
cytoplasmTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
nucleusTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
nucleoplasmTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cytoplasmTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
cytosolTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
protein-containing complexTyrosine-protein phosphatase non-receptor type 11Homo sapiens (human)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (115)

Assay IDTitleYearJournalArticle
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1347158ZIKV-mCherry secondary 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.
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.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
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.
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.
AID1347153Confirmatory 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.
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.
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.
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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID1347164384 well plate NINDS Rhodamine confirmatory 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.
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.
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.
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.
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.
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.
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.
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.
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.
AID1347156DAPI mCherry counterscreen 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.
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.
AID1347149Furin counterscreen 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.
AID1347169Tertiary RLuc qRT-PCR qHTS assay 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.
AID1347161Confirmatory screen NINDS Rhodamine 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.
AID1347163384 well plate NINDS AMC confirmatory 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.
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.
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.
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.
AID1347167Vero cells viability 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.
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.
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.
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.
AID1347152Confirmatory screen NINDS 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.
AID1347168HepG2 cells viability 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.
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.
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.
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.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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).
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).
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID496824Antimicrobial activity against Toxoplasma gondii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
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
AID496831Antimicrobial activity against Cryptosporidium parvum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
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).
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID496817Antimicrobial activity against Trypanosoma cruzi2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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]
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID496830Antimicrobial activity against Leishmania major2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID496819Antimicrobial activity against Plasmodium falciparum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID496825Antimicrobial activity against Leishmania mexicana2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496827Antimicrobial activity against Leishmania amazonensis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID378865Antimitotic activity in human peripheral blood lymphocytes assessed as mitotic index at 1 uM2000Journal of natural products, Jan, Volume: 63, Issue:1
New prenylated anthraquinones and xanthones from Vismia guineensis.
AID497005Antimicrobial activity against Pneumocystis carinii2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
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]
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID496826Antimicrobial activity against Entamoeba histolytica2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
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).
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
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).
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID496823Antimicrobial activity against Trichomonas vaginalis2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
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).
AID680699TP_TRANSPORTER: increase in Vinblastine intracellular accumulation (Vinblastine: 1 uM, Estramustine: 50 uM) in SKVLB 1 cells1994Journal of the National Cancer Institute, May-04, Volume: 86, Issue:9
Modulation of the function of P-glycoprotein by estramustine.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID496832Antimicrobial activity against Trypanosoma brucei rhodesiense2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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).
AID496818Antimicrobial activity against Trypanosoma brucei brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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]
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).
AID87608Compound was evaluated for toxicity against HeLa S3 cells1986Journal of medicinal chemistry, Aug, Volume: 29, Issue:8
3,17 beta-Dihydroxy-20,21-epoxy-19-norpregna-1,3,5(10)-trienes: synthesis, rearrangement, cytotoxicity, and estrogen-receptor binding.
AID409956Inhibition of mouse brain MAOB2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
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).
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).
AID551432Inhibition of recombinant SHP22011Bioorganic & medicinal chemistry letters, Jan-15, Volume: 21, Issue:2
Shp2 protein tyrosine phosphatase inhibitor activity of estramustine phosphate and its triterpenoid analogs.
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]
AID496821Antimicrobial activity against Leishmania2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID496820Antimicrobial activity against Trypanosoma brucei2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
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).
AID73028Compound was evaluated for toxicity against GH3 cells; NT=Not tested1986Journal of medicinal chemistry, Aug, Volume: 29, Issue:8
3,17 beta-Dihydroxy-20,21-epoxy-19-norpregna-1,3,5(10)-trienes: synthesis, rearrangement, cytotoxicity, and estrogen-receptor binding.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
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]
AID496829Antimicrobial activity against Leishmania infantum2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID496828Antimicrobial activity against Leishmania donovani2010Bioorganic & medicinal chemistry, Mar-15, Volume: 18, Issue:6
Multi-target spectral moment QSAR versus ANN for antiparasitic drugs against different parasite species.
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.
AID1347170Vero cells viability counterscreen for qRT-PCR qHTS assay of selected 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.
AID1347172Secondary qRT-PCR qHTS assay for selected 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.
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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (928)

TimeframeStudies, This Drug (%)All Drugs %
pre-1990338 (36.42)18.7374
1990's231 (24.89)18.2507
2000's264 (28.45)29.6817
2010's84 (9.05)24.3611
2020's11 (1.19)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 40.05

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 strong demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index40.05 (24.57)
Research Supply Index7.16 (2.92)
Research Growth Index4.27 (4.65)
Search Engine Demand Index63.62 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (40.05)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials291 (29.19%)5.53%
Reviews146 (14.64%)6.00%
Case Studies59 (5.92%)4.05%
Observational0 (0.00%)0.25%
Other501 (50.25%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (50)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
Phase II Study of Weekly Paclitaxel by 1-HR Infusion Plus Estramustine in Metastatic Hormone-Refractory Prostate Carcinoma [NCT00003614]Phase 20 participants Interventional1999-02-04Completed
Phase II Evaluation of Early Oral Estramustine, Oral Etoposide and Intravenous Paclitaxel in Combination With Hormone Therapy in Patients With High-Risk Metastatic Adenocarinoma of the Prostate [NCT00028769]Phase 241 participants (Actual)Interventional2001-12-31Completed
A Prospective Randomized Phase III, Trial Comparing Consolidation Therapy With or Without Strontium-89 Following Induction Chemotherapy in Androgen-Independent Prostate Cancer [NCT00024167]Phase 3265 participants (Actual)Interventional2002-04-30Terminated(stopped due to Terminated due to slow accrual)
[NCT02866955]Phase 2100 participants (Actual)Interventional2011-06-15Completed
Efficacy and Safety of Estracyt® in Metastatic Breast Cancer Hormonal Estrogen Receptor (HER 2) Negative, Hormone Receptor (HR) Positive. [NCT02853071]Phase 20 participants (Actual)Interventional2017-01-31Withdrawn(stopped due to withdrawal industrial)
A Phase III Randomized Trial for Evaluating Second Line Hormonal Therapy (Ketoconazole/Hydrocortisone) Versus Paclitaxel/Estramustine Combination Chemotherapy on Progression Free Survival in Asymptomatic Patients With a Rising PSA After Hormonal Therapy f [NCT00027859]Phase 30 participants Interventional2003-10-08Completed
Combination of Docetaxel + Estramustine + Hydrocortisone Versus Docetaxel + Prednisone in Patients With Advanced Prostate Cancer Who Have Relapse in Biochemistry Whilst Androgenic Blockage [NCT00705822]Phase 354 participants (Actual)Interventional2006-08-31Terminated(stopped due to low recruitment rate)
A Phase II Pilot Study of Estramustine, Docetaxel, and Carboplatin for Patients With Hormone Refractory Prostate Cancer Progressing After Mitoxantrone-Based Chemotherapy. [NCT00183924]Phase 220 participants (Actual)Interventional2001-03-31Completed
A Randomized, Phase II Trial of Weekly Paclitaxel, Low-Dose Estramustine, and Carboplatin Administered Either Weekly or Every Four Weeks in the Treatment of Hormone Refractory Prostate Carcinoma [NCT00193193]Phase 2100 participants Interventional2000-08-31Completed
Adjuvant Chemotherapy (Docetaxel and Estramustine Phosphate) for High Risk Localized Prostate Cancer [NCT00193271]Phase 230 participants Interventional2004-08-31Completed
Phase I/II Study of Paclitaxel, Estramustine Phosphate and Thalidomide for Patients With Metastatic Androgen-Independent Prostate Carcinoma (AI-PCa) [NCT00038246]Phase 1/Phase 240 participants (Actual)Interventional2000-10-31Completed
Phase II Study of the Activity of Weekly Paclitaxel, Topotecan Plus Oral Estramustine Phosphate in Metastatic Hormone-Refractory Prostate Carcinoma [NCT00084565]Phase 20 participants (Actual)Interventional2003-11-30Withdrawn(stopped due to Study was never activated at Fox Chase Cancer Center.)
Phase I/II Evaluation of Oral Estramustine and Oral Vinorelbine on an Intermittent Schedule in Patients With Hormone-Refractory Adenocarcinoma of the Prostate [NCT00151086]Phase 1/Phase 233 participants (Actual)Interventional2001-12-31Completed
A Phase II Trial of Epirubicin With Estramustine Phosphate and Celecoxib for the Treatment of Hormone Resistant Prostate Cancer (HRPC) [NCT00218205]Phase 228 participants Interventional2002-07-31Recruiting
Randomized Phase Ii Trial Of Weekly Docetaxel, Estramustine And Prednisone Versus Docetaxel And Prednisone In Patient With Hormone-Resistant Prostate Cancer [NCT00541281]Phase 2150 participants (Actual)Interventional2003-12-31Completed
Phase II Evaluation of Docetaxel Combined With Estramustine Phosphate in Patients With Metastatic Breast Cancer [NCT00003066]Phase 240 participants (Anticipated)Interventional1997-02-28Active, not recruiting
A Randomized Phase II Trial of Taxol/VP-16/Estramustine vs. Ketoconazole/Doxorubicin/Vinblastine/Estramustine in Androgen Independent Prostate Cancer [NCT00003084]Phase 275 participants (Actual)Interventional1997-12-31Completed
Liposomal Doxorubicin and Estramustine Phosphate: A Phase II Study in Taxane Resistant, Hormone Refractory Advanced Prostate Cancer [NCT00132756]Phase 1/Phase 230 participants Interventional2003-12-31Terminated
An Evaluation of Estramustine, Docetaxel and Zoledronate in Patients With Hormone-Refractory Adenocarcinoma of the Prostate [NCT00151073]Phase 228 participants (Actual)Interventional2002-04-30Completed
Docetaxel, Estramustine and Short Term Androgen Withdrawal for Patients With a Rising PSA After Definitive Local Treatment [NCT00165399]Phase 262 participants (Actual)Interventional2004-03-31Completed
Phase II Trial Of Sequential Estramustine/Paclitaxel Followed By Doxorubicin/Ketoconazole In Patients With Androgen-Independent Prostate Cancer [NCT00014352]Phase 20 participants Interventional2000-09-30Completed
A Phase II Study Of Estramustine, Docetaxel, And Bevacizumab (IND # 7921, NSC # 704865) In Men With Hormone Refractory Prostate Cancer [NCT00016107]Phase 272 participants (Actual)Interventional2001-06-30Completed
A Phase II Trial Combining Estramustine, Docetaxel And Thalidomide In Patients With Androgen-Independent Metastatic Prostate Cancer [NCT00083005]Phase 260 participants (Anticipated)Interventional2004-03-31Completed
Phase II Study of Paclitaxel and Estramustine Phosphate in Patients With Relapsed Non-Hodgkin's Lymphoma [NCT00021372]Phase 225 participants (Actual)Interventional1996-02-29Completed
A Phase I And Randomized Phase 2 Trial Of Epothilone B Analogue BMS 247550 (NSC # 710428) Administered Every 21 Days With Or Without Oral Estramustine Phosphate In Patients With Androgen Independent Prostate Cancer [NCT00025194]Phase 1/Phase 20 participants Interventional2001-07-31Completed
A Phase III Randomized Study of Patients With High Risk, Hormone-Naive Prostate Cancer: Androgen Blockade With 4 Cycles of Immediate Chemotherapy Versus Androgen Blockade With Delayed Chemotherapy [NCT00030654]Phase 321 participants (Actual)Interventional2002-10-31Completed
A Phase II Study Of Estramustine, Docetaxel, And Exisulind (IND #64733) In Men With Hormone Refractory Prostate Cancer [NCT00052845]Phase 280 participants (Actual)Interventional2002-11-30Completed
Phase I/II Study of Intravenous Estramustine Phosphate Combined With Taxol in Patients With Hormone Refractory Adenocarcinoma of the Prostate [NCT00038168]Phase 1/Phase 214 participants (Actual)Interventional2000-06-30Completed
A Phase II Clinical Trial of Taxotere, Emcyt and Thalidomide (TET) for the Treatment of Hormone-Refractory Prostate Cancer [NCT00046826]Phase 20 participants Interventional2001-09-30Completed
Phase II Evaluation of Early Oral Estramustine, Oral Etoposide and Intravenous Paclitaxel in Patients With Hormonally Responsive Adenocarcinoma of the Prostate [NCT00151060]Phase 228 participants (Actual)Interventional1998-12-31Completed
A Phase II Trial of 13-Cis Retinoic Acid, Alpha Interferon, Taxotere, and Estramustine (R.I.T.E.) for the Treatment of Hormone Refractory Prostate Cancer [NCT00176527]Phase 240 participants (Anticipated)Interventional2002-11-30Terminated(stopped due to accrual goal met)
Phase III Randomized Study Of Adjuvant Hormonal Therapy With And Without Docetaxel And Estramustine In Patients With Advanced Prostate Cancer Or With A High Risk Of Relapse [NCT00055731]Phase 3413 participants (Actual)Interventional2002-11-14Completed
Neoadjuvant Androgen Deprivation Therapy and Chemotherapy Followed by Radical Prostatectomy in Patients With Prostate Cancer [NCT02494713]Phase 24 participants (Actual)Interventional2015-10-31Terminated(stopped due to slow enrollment; resource re-allocation)
A PHASE I TRIAL OF ESTRAMUSTINE PHOSPHATE AND DOXORUBICIN IN HORMONE REFRACTORY METASTATIC PROSTATE CANCER [NCT00002721]Phase 118 participants (Actual)Interventional1995-03-31Completed
PHASE I/II STUDY OF DOCETAXEL (TAXOTERE) AND ESTRAMUSTINE COMBINATION CHEMOTHERAPY IN PATIENTS WITH PROSTATE CANCER [NCT00002775]Phase 1/Phase 237 participants (Anticipated)Interventional1998-02-28Active, not recruiting
Phase I/II Study of Weekly Intravenous Estramustine Phosphate in Combination With Paclitaxel and Carboplatin in Patients With Advanced Prostate Cancer [NCT00003394]Phase 1/Phase 218 participants (Anticipated)Interventional1998-04-30Completed
Phase II Study Of Neo-Adjuvant Paclitaxel, Estramustine And Carboplatin (TEC) Plus Androgen Ablation Prior To Radiation Therapy In Patients With Poor Prognosis Localized Prostate Cancer [NCT00016913]Phase 234 participants (Actual)Interventional2001-05-31Completed
A Phase II Trial of Combination Vinorelbine-Estramustine With or Without Prednisone for High Risk and Recurrent, Advanced and Metastatic Renal Cell Carcinoma [NCT00003584]Phase 235 participants (Anticipated)Interventional1998-07-31Completed
Safety and Efficacy of One Hour Weekly Taxol Infusion and Estramustine in Hormone Refractory Prostate Cancer [NCT00005048]Phase 10 participants Interventional1997-04-30Completed
A Phase II Study of Estramustine, Docetaxel, and Carboplatin With G-CSF Support in Men With Hormone Refractory Prostate Cancer [NCT00005810]Phase 240 participants (Actual)Interventional2000-03-31Completed
A Phase I/II Study of Paclitaxel, Estramustine Phosphate, and Vinorelbine (PaclEVin) [NCT00004105]Phase 1/Phase 20 participants Interventional1998-09-30Completed
Treatment of Prostate Cancer by Induction of Alternate Cell Death Pathways: A Phase I Trial of Docetaxel, Estramustine, Mitoxantrone and Prednisone [NCT00003633]Phase 112 participants (Anticipated)Interventional1998-08-31Active, not recruiting
A Phase II Trial of Weekly Paclitaxel Plus Oral Estramustine in Patients With Hormone Refractory Prostate Cancer [NCT00003717]Phase 217 participants (Anticipated)Interventional1998-10-31Active, not recruiting
Phase 2 Study of Androgen Deprivation Therapy (ADT) Plus Chemotherapy as Initial Treatment for Local Failures or Advanced Prostate Cancer [NCT02560051]Phase 219 participants (Actual)Interventional2015-11-30Terminated(stopped due to Slow accrual; resource re-allocation)
A Phase I Study of Estramustine, Taxotere and Carboplatin (ETP) in Patients With Horomone Refractory Prostate Cancer [NCT00005627]Phase 10 participants Interventional1999-03-31Completed
A Randomized Phase II Trial of Mitoxantrone, Estramustine and Navelbine or 13-cis Retinoic Acid, Interferon and Paclitaxel in Patients With Metatstatic Hormone Refractory Prostate Cancer [NCT00005847]Phase 20 participants Interventional2001-04-05Completed
A Phase III Protocol of Androgen Suppression (AS) and Radiation Therapy (RT) vs AS and RT Followed by Chemotherapy With Paclitaxel, Estramustine, and Etoposide (TEE) for Localized, High-Risk, Prostate Cancer [NCT00004054]Phase 3397 participants (Actual)Interventional2000-01-31Completed
A Phase 3 Trial of Androgen Ablation Alone vs. Chemo/Hormonal Therapy as Initial Treatment of Unresectable/Metastatic Adenocarcinoma of the Prostate [NCT00002855]Phase 3306 participants (Actual)Interventional1996-08-31Completed
Docetaxel and Estramustine Versus Mitoxantrone and Prednisone for Advanced, Hormone Refractory Prostate Cancer [NCT00004001]Phase 3770 participants (Actual)Interventional1999-10-31Completed
Docetaxel Followed by Radical Prostatectomy in Patients With High Risk Localized Prostate Cancer [NCT01250717]Phase 228 participants (Actual)Interventional2001-01-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00004054 (5) [back to overview]Disease-free Survival Rate at 5 Years
NCT00004054 (5) [back to overview]Overall Survival (5-year Rate Reported)
NCT00004054 (5) [back to overview]Rate of Biochemical Failure at 5 Years
NCT00004054 (5) [back to overview]Rate of Distant Metastasis at Five Years
NCT00004054 (5) [back to overview]Rate of Local Progression at 5 Years
NCT00016913 (3) [back to overview]Progression-free Survival (PFS)
NCT00016913 (3) [back to overview]Time to Prostate-specific Antigen Failure
NCT00016913 (3) [back to overview]Toxicity
NCT00024167 (2) [back to overview]Overall Survival From Randomization
NCT00024167 (2) [back to overview]Overall Survival From Registration
NCT00028769 (3) [back to overview]Overall Survival (OS)
NCT00028769 (3) [back to overview]Progression-free Survival
NCT00028769 (3) [back to overview]Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT01250717 (1) [back to overview]Pathologic Complete Response Was Assessed by Rigorous Pathological Examination by One of Two Pathologists
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Volume of the Prostate Tumor as Assessed by Multiparametric Prostate Magnetic Resonance Imaging (mpMRI)
NCT02494713 (13) [back to overview]Efficacy as Measured by Volume of the Prostate Tumor as Assessed by Multiparametric Prostate Magnetic Resonance Imaging (mpMRI)
NCT02494713 (13) [back to overview]Safety of Drug Regimen as Measured by Number of Adverse Events
NCT02494713 (13) [back to overview]Surgical Morbidity as Measured by Number of Adverse Events
NCT02494713 (13) [back to overview]Efficacy as Measured by Pathologic Response
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02494713 (13) [back to overview]Efficacy as Measured by Prostate-specific Antigen (PSA) Levels
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale
NCT02560051 (17) [back to overview]Efficacy as Measured by Number of Participants With Pathology/Biopsy Positive for Disease
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale
NCT02560051 (17) [back to overview]Safety of Drug Regimen as Measured by Number of Adverse Events
NCT02560051 (17) [back to overview]Efficacy as Measured by Number Who Progressed
NCT02560051 (17) [back to overview]Efficacy as Measured by Number Who PSA Progressed
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Efficacy as Measured by PSA Level
NCT02560051 (17) [back to overview]Quality of Life Measure by FACT-P Scale

Disease-free Survival Rate at 5 Years

Disease-free survival (DFS) was measured from the date of randomization to the date of documentation of progression (local, distant, biochemical failure), death, or last follow-up (censored). The Kaplan-Meier method was used to estimate DFS rates. (NCT00004054)
Timeframe: From randomization to last follow-up. Analysis occurs after all patients have been potentially followed for 5 years. Maximum follow-up at time of analysis was 13.3 years.

Interventionpercentage of participants (Number)
Hormones and RT39.1
Hormones and RT Plus Chemotherapy42.9

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Overall Survival (5-year Rate Reported)

Survival time is defined as time from randomization to date of death from any cause and is estimated by the Kaplan-Meier method. Patients last known to be alive are censored at date of last contact. This analysis was planned to occur when all patients had been potentially followed for 5 years. (NCT00004054)
Timeframe: From the date of randomization to the date of death or last follow-up. Analysis occurs after all patients have been potentially followed for 5 years.

Interventionpercentage of participants (Number)
Hormones and RT84.9
Hormones and RT Plus Chemotherapy87.2

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Rate of Biochemical Failure at 5 Years

Biochemical failure uses the American Society for Radiation Oncology (ASTRO) definition of prostate-specific antigen (PSA) rises on three consecutive occasions, with biochemical failure date being midway between the last non-rising PSA and the first rise in PSA. Time to biochemical failure is defined as time from randomization to biochemical failure, last known follow-up (censored), or death (competing risk). Biochemical failure rates are estimated using the cumulative incidence method. (NCT00004054)
Timeframe: From randomization to last follow-up. Analysis occurs after all patients have been potentially followed for 5 years. Maximum follow-up at time of analysis was 13.3 years.

Interventionpercentage of participants (Number)
Hormones and RT48.0
Hormones and RT Plus Chemotherapy47.9

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Rate of Distant Metastasis at Five Years

Distant metastasis (DM) is defined as documented metastatic disease. Time to distant metastasis is defined as time from randomization to distant metastatic disease, last known follow-up (censored), or death (competing risk). Distant metastasis rates are estimated using the cumulative incidence method. (NCT00004054)
Timeframe: From randomization to last follow-up. Analysis occurs after all patients have been potentially followed for 5 years. Maximum follow-up at time of analysis was 13.3 years.

Interventionpercentage of participants (Number)
Hormones and RT10.4
Hormones and RT Plus Chemotherapy8.3

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Rate of Local Progression at 5 Years

Local progression is defined as documented clinical local and/or regional progression. Time to local progression is defined as time from randomization to local progression, last known follow-up (censored), or death (competing risk). Local progression rates are estimated using the cumulative incidence method. (NCT00004054)
Timeframe: From randomization to last follow-up. Analysis occurs after all patients have been potentially followed for 5 years. Maximum follow-up at time of analysis was 13.3 years.

Interventionpercentage of participants (Number)
Hormones and RT5.8
Hormones and RT Plus Chemotherapy4.1

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Progression-free Survival (PFS)

PFS was defined as the time between treatment initiation and the date of disease progression (PSA, bone, tumor) or death, whichever occurred first. PSA progression is defined as 2 consecutive rising PSAs (a rise of at least 0.2 ng/mL) above 1.0 ng/mL. (NCT00016913)
Timeframe: registration to progression, up to 5.5 years from registration

Interventionmonths (Median)
Neo-Adj ChemoTx + Ablation Prior to RT12.1

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Time to Prostate-specific Antigen Failure

PSA progression was defined in 2 ways. The CALGB PSA progression was defined as 2 consecutive rises in PSA with a rise of at least 0.2 ng/mL and above 1.0 ng/mL after radiation therapy; the date of PSA failure is taken as the midpoint between the last PSA before the rise and the first of the 2 PSAs that documented the rise. In addition, PSA progression was used according to the American Society for Therapeutic Radiology and Oncology 1996 (ASTRO) criteria and defined as 3 consecutive rises in PSA after radiation therapy. The date of PSA failure was taken as the midpoint between the time of the lowest PSA measure after irradiation and the first of the 3 consecutive rises. (NCT00016913)
Timeframe: PSA was measured every 4 weeks during chemotherapy, at least every 12 weeks post radiation for 2 years, and every 6 months thereafter until PSA failure date (Up to 5.5 years).

Interventionmonths (Median)
CALGB criteriaASTRO criteria
Neo-Adj ChemoTx + Ablation Prior to RT17.112.1

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Toxicity

Patients were evaluated for acute toxicities defined as grade 3 or greater cardiovascular (including venous thrombosis), gastrointestinal, or genitourinary toxicity occurring during the period starting from treatment initiation until 90 days or less after the completion of radiotherapy. The same toxicity measures were monitored at >90 days after the completion of radiotherapy. (NCT00016913)
Timeframe: 90 days and 1 year post treatment

InterventionEvents (Number)
Grade 3+ Toxicity <=90 days post radiotherapyGrade 3+ Toxicity >90 days post radiotherapy
Neo-Adj ChemoTx + Ablation Prior to RT20

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Overall Survival From Randomization

Overall survival (OS) was computed using the number of months from the date of randomization to the date of death. Participants still alive were censored at the last follow-up date. Kaplan-Meier methodology was used to evaluate OS. (NCT00024167)
Timeframe: Followed every 4 weeks from randomization until death, up to 7 years.

Interventionmonths (Median)
Induction Treatment + Strontium-8924.2
Induction Treatment + No Strontium-8922.8

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Overall Survival From Registration

Overall survival (OS) was computed using the number of months from the date of registration to the date of death. Participants still alive were censored at the last follow-up date. Kaplan-Meier methodology was used to evaluate OS. (NCT00024167)
Timeframe: Followed every 4 weeks from registration until death, up to 7 years.

Interventionmonths (Median)
Induction Treatment + Strontium-8927.9
Induction Treatment + No Strontium-8926.6

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Overall Survival (OS)

Overall survival is defined from the date of registration to date of death from any cause (NCT00028769)
Timeframe: 0-5 years

Interventionmonths (Median)
CAD + Chemo38

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Progression-free Survival

Measured from time of registration to time of first documentation of progression determined from the prostate-specific antigen (PSA) level, clinical criteria, or symptomatic deterioration. PSA progression is defined as a 25% increase greater than baseline. If the patient's PSA level had decrease during the study, a 25% increase from the nadir PSA level, with absolute value of >=5 ng/mL is considered progression. CLinical progress is defined as the appearance of any new lesion at any site or death without documented progression. Symptomatic deterioration is defined as a global deterioration of the health status requiring discontinuation of treatment without objective evidence of progression. (NCT00028769)
Timeframe: 0-5 years (assessed every 3 months if no progression when the chemotherapy had been finished. Once off chemotherapy, assessed every 3 months until progression)

Interventionmonths (Median)
CAD + Chemo13

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Pathologic Complete Response Was Assessed by Rigorous Pathological Examination by One of Two Pathologists

One of two pathologists (SR, EG), assigned the Gleason scores for each patient from pre-treatment prostate biopsies and assessed pathological staging on post- prostatectomy specimens. Staging including a description of all tumor foci within the gland, presence or absence of perineural invasion and/or lymphovascular invasion, presence of extraprostatic extension of tumor (including seminal vesicle invasion), and margin status. The pathologists reviewed the presence or absence of cancer in each prostate gland removed on the study patients. RECIST has to my knowledge not been used for pathological examination in neoadjuvant studies. 0 out of 28 participants acheived complete response. RECIST is not appropriate as cancer within the gland at the time of treatment is not measurable by RECIST. The primary outcome is a pathological complete response. (NCT01250717)
Timeframe: status post prostectomy

Interventionparticipants (Number)
Docetaxel Followed by Radical Prostatectomy0

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: baseline

Interventionng/mL (Median)
ADT + Chemotherapy58.7

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: Cycle 2 Day 1, about 8 weeks after treatment initiation (but before prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.4

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: Cycle 2 Day 57, about 16 weeks after treatment initiation (but before prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.15

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: Day 133, about 19 weeks after treatment initiation (but before prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.055

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Efficacy as Measured by Volume of the Prostate Tumor as Assessed by Multiparametric Prostate Magnetic Resonance Imaging (mpMRI)

The volume of the prostate tumor was measured by a radiologist's assessment of multiparametric prostate magnetic resonance imaging. (NCT02494713)
Timeframe: baseline

Interventioncc (Median)
ADT + Chemotherapy19.3

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Efficacy as Measured by Volume of the Prostate Tumor as Assessed by Multiparametric Prostate Magnetic Resonance Imaging (mpMRI)

The volume of the prostate tumor was measured by a radiologist's assessment of multiparametric prostate magnetic resonance imaging. (NCT02494713)
Timeframe: post treatment but prior to prostatectomy (about 25 days after the end of treatment)

Interventioncc (Median)
ADT + Chemotherapy3.75

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Safety of Drug Regimen as Measured by Number of Adverse Events

Number of adverse events was measured as a count of all participant adverse events that occurred from the time participant first initiates ADT plus chemotherapy until participant's completion of neoadjuvant ADT plus chemotherapy. (NCT02494713)
Timeframe: From the time participant first initiates ADT plus chemotherapy until participant's completion of neoadjuvant ADT plus chemotherapy.

Interventionadverse event (Number)
ADT + Chemotherapy119

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Surgical Morbidity as Measured by Number of Adverse Events

Number of adverse events was measured as a count of all participant adverse events that occurred from the time participant first initiates ADT plus chemotherapy until the participant was taken off-study or the study was stopped, an average of 20 months (NCT02494713)
Timeframe: From the time the participant signs the informed consent until the participant was taken off-study or the study was stopped, an average of 20 months

Interventionadverse event (Number)
ADT + Chemotherapy119

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Efficacy as Measured by Pathologic Response

Pathologic response is defined by percentage of tumor burden remaining at time of prostate removal. Percentage of tumor burden is measured based on a pathologist's assessment of the prostate tissue removed and visual estimate of how much tumor there is in the prostate. (NCT02494713)
Timeframe: Day of prostate removal, which is about 5 months following the day participant signed consent.

Interventionpercentage of tumor burden remaining (Median)
ADT + Chemotherapy30

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: about 20 weeks after treatment initiation (day of prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.01

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: about 32 weeks after treatment initiation (about 12 weeks after prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.01

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: about 44 weeks after treatment initiation (about 24 weeks after prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.35

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Efficacy as Measured by Prostate-specific Antigen (PSA) Levels

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02494713)
Timeframe: about 68 weeks after treatment initiation (about 48 weeks after prostatectomy)

Interventionng/mL (Median)
ADT + Chemotherapy0.1

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: Cycle 2 Day 1, which is about 8 weeks after treatment initiation

Interventionng/mL (Median)
Definitive Local Therapy0.01
Nodal Only/Low-volume Bone0.3
High Volume/no Prior tx3.8

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: Cycle 3 Day 1, which is about 16 weeks after treatment initiation

Interventionng/mL (Median)
Definitive Local Therapy0.01
Nodal Only/Low-volume Bone0.1
High Volume/no Prior tx0.9

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: Cycle 4 Day 1, which is about 24 weeks after treatment initiation

Interventionng/mL (Median)
Nodal Only/Low-volume Bone0.01
High Volume/no Prior tx0.55

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: Cycle 5 Day 1, which is about about 32 weeks after treatment initiation

Interventionng/mL (Median)
High Volume/no Prior tx0.5

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Quality of Life Measure by FACT-P Scale

"The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL.~The time point is about 12 weeks after completion of the last cycle. For the arm completing 3 cycles, the time point is 36 weeks after treatment initiation. For the arm completing 4 cycles, the time point is 44 weeks after treatment initiation. For the arm completing 5 cycles, the time point is 52 weeks after treatment initiation." (NCT02560051)
Timeframe: about 12 weeks after completion of the last cycle

Interventionunits on a scale (Median)
Definitive Local Therapy94
Nodal Only/Low-volume Bone118
High Volume/no Prior tx99

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Quality of Life Measure by FACT-P Scale

The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL. (NCT02560051)
Timeframe: post cycle 1, which is about 8 weeks after treatment initiation

Interventionunits on a scale (Median)
Definitive Local Therapy97
Nodal Only/Low-volume Bone99
High Volume/no Prior tx105

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Efficacy as Measured by Number of Participants With Pathology/Biopsy Positive for Disease

(NCT02560051)
Timeframe: about 10 months after treatment initiation

InterventionParticipants (Count of Participants)
Definitive Local Therapy0
Nodal Only/Low-volume Bone3
High Volume/no Prior tx3

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Quality of Life Measure by FACT-P Scale

The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL. (NCT02560051)
Timeframe: post cycle 3, which is about 24 weeks after treatment initiation

Interventionunits on a scale (Median)
Definitive Local Therapy79
Nodal Only/Low-volume Bone94
High Volume/no Prior tx114

[back to top]

Quality of Life Measure by FACT-P Scale

The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL. (NCT02560051)
Timeframe: post cycle 4, which is about 32 weeks after treatment initiation

Interventionunits on a scale (Median)
Nodal Only/Low-volume Bone96
High Volume/no Prior tx113

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Quality of Life Measure by FACT-P Scale

The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL. (NCT02560051)
Timeframe: post cycle 5, which is about about 40 weeks after treatment initiation

Interventionunits on a scale (Median)
High Volume/no Prior tx107

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Safety of Drug Regimen as Measured by Number of Adverse Events

(NCT02560051)
Timeframe: From the time the participant signs the informed consent until the participant was taken off-study or the study was stopped, an average of 10 months

Interventionadverse event (Number)
Definitive Local Therapy115
Nodal Only/Low-volume Bone270
High Volume/no Prior tx166

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Efficacy as Measured by Number Who Progressed

Progression defined as increase in Prostate Specific Antigen (PSA) >0.3 ng/mL over 2 measurements or larger/new lesion (NCT02560051)
Timeframe: From the time the participant signs the informed consent until the participant was taken off-study or the study was stopped, an average of 10 months

InterventionParticipants (Count of Participants)
Definitive Local Therapy0
Nodal Only/Low-volume Bone0
High Volume/no Prior tx2

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Efficacy as Measured by Number Who PSA Progressed

PSA progression defined as increase in Prostate Specific Antigen (PSA) >0.3 ng/mL over 2 measurements (NCT02560051)
Timeframe: From the time the participant signs the informed consent until the participant was taken off-study or the study was stopped, an average of 10 months

InterventionParticipants (Count of Participants)
Definitive Local Therapy0
Nodal Only/Low-volume Bone0
High Volume/no Prior tx1

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Efficacy as Measured by PSA Level

"Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood.~The time point is the end of treatment, which is about about 8 weeks after the start of the last cycle. For the arm completing 3 cycles, the time point is 24 weeks after treatment initiation. For the arm completing 4 cycles, the time point is 32 weeks after treatment initiation. For the arm completing 5 cycles, the time point is 40 weeks after treatment initiation." (NCT02560051)
Timeframe: end of treatment, which is about about 8 weeks after the start of the last cycle

Interventionng/mL (Median)
Definitive Local Therapy0.01
Nodal Only/Low-volume Bone0.01
High Volume/no Prior tx1.4

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: baseline

Interventionng/mL (Median)
Definitive Local Therapy5.7
Nodal Only/Low-volume Bone15.8
High Volume/no Prior tx90.7

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Efficacy as Measured by PSA Level

Prostate-specific antigen, or PSA, is a protein produced by normal, as well as malignant, cells of the prostate gland. The PSA test measures the level of PSA in a man's blood. For this test, a blood sample is sent to a laboratory for analysis. The results are reported as nanograms of PSA per milliliter (ng/mL) of blood. (NCT02560051)
Timeframe: Cycle 1 Day 1, which is the day of treatment initiation

Interventionng/mL (Median)
Definitive Local Therapy5.7
Nodal Only/Low-volume Bone9.7
High Volume/no Prior tx90.7

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Quality of Life Measure by FACT-P Scale

The Functional Assessment of Cancer Therapy-Prostate (FACT-P) scale is a tool used for assessing the health-related quality of life (QoL) in men with prostate cancer. It consists of 27 core items which assess patient function in four domains (Physical, Social/Family, Emotional, and Functional well-being), and it is further supplemented by 12 site specific items to assess for prostate-related symptoms. Each item is rated on a 0 to 4 Likert type scale, and then combined to produce a global QoL score, with a range of scores of 0 to 156. Higher scores represent better QoL. (NCT02560051)
Timeframe: post cycle 2, which is about 16 weeks after treatment initiation

Interventionunits on a scale (Median)
Definitive Local Therapy94
Nodal Only/Low-volume Bone97
High Volume/no Prior tx102

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