razoxane profile

Razoxane: An antimitotic agent with immunosuppressive properties. [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

ID Source	ID
PubMed CID	30623
CHEMBL ID	444186
CHEBI ID	50225
SCHEMBL ID	9089
MeSH ID	M0018535

Synonym
2, 4,4'-propylenedi-
2, 4,4'-(1-methyl-1,2-ethanediyl)bis-, (.+-.)-
mls002920046 ,
(.+-.)-1,5-dioxopiperazinyl)propane
2, 4,4'-(1-methyl-1,2-ethanediyl)bis-, (+-)-
nsc 129943
(+-)-1,5-dioxopiperazinyl)propane
(+-)-(3,3',5'-tetraoxo)-1,2-dipiperazinopropane
propane,2-bis(3,5-dioxopiperazin-1-yl)-
2, 4,4'-propylenedi-, (.+-.)-
2, 4,4'-propylenedi-, (+-)-
nsc-129943
.+-.-(3,3',5'-tetraoxo)-1,2-dipiperazinopropane
AC-1422
AKOS015837545
4,4'-propane-1,2-diyldipiperazine-2,6-dione
21416-67-1
icrf-159
razoxana
CHEBI:50225 ,
razoxane
(+,-)-1,2-bis(3,5-dioxopiperazine-1-yl)propane
razoxanum
icrf 159
(+/-)-4,4'-propylenedi-2,6-piperazinedione
razoxin
4-[2-(3,5-dioxopiperazin-1-yl)propyl]piperazine-2,6-dione
NSC129943 ,
21416-87-5
4,4'-propylenebis(piperazine-2,6-dione)
ici 59118
tepirone
1,2-bis(3,5-dioxo-1-piperazinyl)propane
(+-)-1,2-bis(3,5-dioxopiperazin-1-yl)propane
propylenediazmintetraessigsaeure-diimid
einecs 244-379-2
brn 0821182
4,4'-propylenebis(2,6-piperazinedione)
2,6-piperazinedione, 4,4'-(1-methyl-1,2-ethanediyl)bis-
ccris 344
ai3-52845
razoxana [inn-spanish]
troxozone
nsc 169780
2,6-piperazinedione, 4,4'-propylenedi-
nci-c01627
razoxanum [inn-latin]
NCGC00164737-01
NCI60_000672
smr001797645
cardioxane (tn)
razoxane (inn)
D08471
CHEMBL444186
ici-59118
FT-0653845
FT-0651500
NCGC00164737-05
NCGC00164737-04
NCGC00164737-06
NCGC00164737-07
NCGC00164737-03
NCGC00164737-02
eucardion
tox21_200258
cas-21416-67-1
NCGC00257812-01
dtxsid0020733 ,
dtxcid20733
desrazoxane
dyzoxane
razoxane [inn:ban]
5ar83pr647 ,
unii-5ar83pr647
(+-)-4.4'-propylenedi-2,6-piperazindion
4,4'-(propane-1,2-diyl)bis(piperazine-2,6-dione)
AM20090190
SCHEMBL9089
razoxane [who-dd]
razoxane [inn]
83713-23-9
razoxane [mi]
razoxane [mart.]
1,2-bis(3,5-dioxopiperazin-1-yl)propane
1,2-bis(3,5-dioxopiperazin-1-yl)-propane
(+)-razoxin
(+)-razoxane
AS-67684
razoxane, >98% (hplc)
J-014040
4,4'-(propane-1,2-diyl)dipiperazine-2,6-dione
BCP17033
Q3930720
mfcd00430424
HMS3745O07
C74037
2,6-piperazinedione,4,4-(1-methyl-1,2-ethanediyl)bis-
(+/-)-1,2-bis(3,5-dioxopiperazin-1-yl)propane
(+/-)-1,2-bis(3,5-dioxopiperazinyl)propane
CS-0068173
HY-119425

Excerpt	Reference	Relevance
"Dexrazoxane is a derivative of the powerful metal-chelating agent ethyl enediamine tetra acetic acid. "	( Utility of dexrazoxane for the reduction of anthracycline-induced cardiotoxicity. Jones, RL, 2008)	1.33
"Dexrazoxane (DZR) is a clinically approved agent for preventive treatment of doxorubicin-induced cardiotoxicity. "	( Cardioprotective effect of dexrazoxane in a rat model of myocardial infarction: anti-apoptosis and promoting angiogenesis. Chen, Y; Li, K; Ng, PC; Pong, NH; Shen, J; Sung, RY; Xiang, P; Zhou, L, 2011)	1.28
"Dexrazoxane is a cardioprotectant that significantly reduces the incidence of adverse cardiac events in women with advanced breast cancer treated with doxorubicin-containing regimens."	( Dexrazoxane as a cardioprotectant in children receiving anthracyclines. Balis, FM; Ginsberg, JP; Sepe, DM, 2010)	1.5
"Dexrazoxane is a cardioprotectant drug used to reduce the risk of cardiotoxicity in human patients."	( Safety of concurrent administration of dexrazoxane and doxorubicin in the canine cancer patient. Dervisis, NG; FitzPatrick, WM; Kitchell, BE, 2010)	1.14
"Dexrazoxane is an established treatment option in extravasation of the classic anthracyclines such as doxorubicin, epirubicin, and daunorubicin. "	( Treatment of experimental extravasation of amrubicin, liposomal doxorubicin, and mitoxantrone with dexrazoxane. Jensen, PB; Langer, SW; Sehested, M; Thougaard, AV, 2012)	1.22
"Dexrazoxane is an antioxidant prodrug that on hydrolysis is converted into an intracellular iron chelator. "	( Effect of dexrazoxane on homocysteine-induced endothelial dysfunction in normal subjects. Dimayuga, C; Hudaihed, A; Katz, SD; Zheng, H, 2002)	1.31
"Dexrazoxane is a cardioprotective antioxidant that is clinically used to reduce the cardiotoxicity of the chemotherapeutic drug doxorubicin. "	( Dexrazoxane (ICRF-187) protects cardiac myocytes against hypoxia-reoxygenation damage. Hasinoff, BB, 2002)	1.56
"Dexrazoxane (DXR) is a cardioprotectant approved for use with DOX."	( Gender-dependent reductions in vertebrae length, bone mineral density and content by doxorubicin are not reduced by dexrazoxane in young rats: effect on growth plate and intervertebral discs. Antoniou, J; Chalifour, LE; Demers, CN; Héon, S; Kirby, GM; Mwale, F; Servant, N; Wang, C, 2005)	1.05
"Dexrazoxane (DXR) is an iron-binding compound and the only approved cardioprotectant for use with DOX."	( Amifostine and dexrazoxane enhance the rapid loss of bone mass and further deterioration of vertebrae architecture in female rats. Antoniou, J; Chalifour, LE; Ciobanu, I; Demers, CN; Héon, S; Mwale, F; Servant, N, 2005)	1.18
"Dexrazoxane is a prodrug analog of the metal chelator EDTA that most likely acts by removing iron from the iron-doxorubicin complex, thus preventing formation of damaging reactive oxygen species."	( Dexrazoxane use in the prevention of anthracycline extravasation injury. Hasinoff, BB, 2006)	1.47
"Dexrazoxane proved to be an effective and well-tolerated acute treatment with only one out of 54 assessable patients requiring surgical resection (1.8%)."	( Treatment of anthracycline extravasation with Savene (dexrazoxane): results from two prospective clinical multicentre studies. Buter, J; Dahlstrøm, K; de Wit, M; Eidtmann, H; Giaccone, G; Jensen, PB; Knoblauch, P; Langer, SW; Mouridsen, HT; Rasmussen, A; Rosti, G, 2007)	1.21
"Dexrazoxane is a cardioprotective iron chelator that interferes with ROS production."	( Dexrazoxane prevents doxorubicin-induced long-term cardiotoxicity and protects myocardial mitochondria from genetic and functional lesions in rats. Geist, A; Haberstroh, J; Ketelsen, UP; Lebrecht, D; Setzer, B; Walker, UA, 2007)	1.47
"Dexrazoxane is a prodrug analog of the metal chelator EDTA that likely acts by removing iron from the iron-anthracycline complex, thus preventing formation of damaging reactive oxygen species."	( The use of dexrazoxane for the prevention of anthracycline extravasation injury. Hasinoff, BB, 2008)	1.22
"Dexrazoxane is a drug used to prevent anthracycline-induced cardiotoxicity. "	( Absence of secondary malignant neoplasms in children with high-risk acute lymphoblastic leukemia treated with dexrazoxane. Asselin, BL; Athale, UH; Barry, EV; Clavell, LA; Cohen, HJ; Dahlberg, SE; Larsen, EC; Lipshultz, SE; Moghrabi, A; Neuberg, DS; Sallan, SE; Samson, Y; Schorin, MA; Silverman, LB; Vrooman, LM, 2008)	1.18
"Razoxane is an effective drug in the systemic treatment of psoriasis, with an initial response rate of 97%. "	( Razoxane: a review of 6 years' therapy in psoriasis. Horton, JJ; Wells, RS, 1983)	3.15
"Dexrazoxane (ICRF-187) is a catalytic inhibitor of the nuclear enzyme DNA topoisomerase II (topo II). "	( Improved targeting of brain tumors using dexrazoxane rescue of topoisomerase II combined with supralethal doses of etoposide and teniposide. Holm, B; Jensen, PB; Sehested, M, 1998)	1.18
"Dexrazoxane is a synthetic bisdiketopiperazine two-ringed compound which hydrolyzes to an EDTA analog. "	( Clinical pharmacology of dexrazoxane. Hochster, HS, 1998)	1.22
"Dexrazoxane is a valuable drug for protecting against cardiac toxicity in patients receiving anthracycline-based chemotherapy. "	( Dexrazoxane. A review of its use as a cardioprotective agent in patients receiving anthracycline-based chemotherapy. Spencer, CM; Wiseman, LR, 1998)	1.54
"Dexrazoxane is a valuable drug in amelioration of chemotherapy induced cardiotoxicity, both in adult and pediatric patients. "	( [Dexrazoxane. Current status and prospectives of cardiotoxicity of chemotherapy]. Lopez, M, )	1.31
"Dexrazoxane (ICRF-187) is an inhibitor of the catalytic activity of DNA topoisomerase II (topo II) that does not stabilize DNA-topo II covalent complexes. "	( Induction of apoptosis by dexrazoxane (ICRF-187) through caspases in the absence of c-jun expression and c-Jun NH2-terminal kinase 1 (JNK1) activation in VM-26-resistant CEM cells. Beck, WT; Khélifa, T, 1999)	1.22
"Dexrazoxane is a potent metal ion chelator as well as being a catalytic inhibitor of DNA topoisomerase II."	( Dexrazoxane is a potent and specific inhibitor of anthracycline induced subcutaneous lesions in mice. Jensen, PB; Langer, SW; Sehested, M, 2001)	1.45
"Dexrazoxane is a bidentate chelator of divalent cations. "	( Phase I trial of 96-hour continuous infusion of dexrazoxane in patients with advanced malignancies. Chow, W; Doroshow, JH; Gandara, D; Groshen, S; Johnson, K; Lenz, HJ; Leong, L; Margolin, K; Morgan, R; Raschko, J; Shibata, S; Somlo, G; Synold, TW; Tetef, ML; Yen, Y, 2001)	1.18
"Razoxane is an antitumor agent structurally related to EDTA. "	( Mode of action of razoxane: inhibition of basement membrane collagen-degradation by a malignant tumor enzyme. Karakiulakis, G; Maragoudakis, ME; Missirlis, E, 1989)	2.05

Excerpt	Reference	Relevance
"Dexrazoxane has been shown in several clinical trials to prevent the development of this serious toxicity."	( Cardioprotective effect of dexrazoxane in patients with breast cancer treated with anthracyclines in adjuvant setting: a 10-year single institution experience. Bosso, G; Ceste, M; de Conciliis, E; Ferrero, G; Ferro, S; Giaretto, L; Lanfranco, C; Manfredi, R; Miglietta, L; Milanese, S; Parello, G; Simoni, C; Testore, F, 2008)	1.15
"Dexrazoxane has been shown to prevent the QT prolongation induced by another anthracycline, epirubicin, but has not yet been reported to prevent that induced by doxorubicin."	( Dexrazoxane protects the heart from acute doxorubicin-induced QT prolongation: a key role for I(Ks). Bois, P; Dilly, S; Ducroq, J; Faivre, JF; Guilbot, S; Laemmel, E; Le Grand, M; Moha ou Maati, H; Pons-Himbert, C; Stücker, O, 2010)	1.5
"Dexrazoxane has in vitro antioxidant capacity. "	( In vitro and in vivo study on the antioxidant activity of dexrazoxane. Antonelli, A; Carpi, A; Cervetti, G; Fallahi, P; Franzoni, F; Galetta, F; Petrini, M; Regoli, F; Santoro, G; Tocchini, L, 2010)	1.22
"Dexrazoxane has the potential to minimize tissue damage and treatment delays after an anthracycline extravasation. "	( Successful experience utilizing dexrazoxane treatment for an anthracycline extravasation. Gay, WE; Tyson, AM, 2010)	1.26
"Dexrazoxane has cardioprotective activity."	( The effect of dexrazoxane for clinical and subclinical cardiotoxicity in children with acute myeloid leukemia. Gallegos-Castorena, S; Gonzalez-Ramella, O; Sánchez-Medina, J, 2010)	1.21
"Dexrazoxane has been approved as a cardioprotective agent and as an antidote in extravasation of anthracyclines."	( [Dexrazoxane in anthracycline induced cardiotoxicity and extravasation]. Beijnen, JH; Goey, AK; Huitema, AD; Schellens, JH, 2010)	1.43
"Dexrazoxane has been reported to be protective against anthracycline induced subcutaneous ulceration in mice. "	( Treatment of anthracycline extravasation in mice with dexrazoxane with or without DMSO and hydrocortisone. Jensen, PB; Langer, SW; Sehested, M; Thougaard, AV, 2006)	1.2
"Dexrazoxane has two biological activities: it is a prodrug that is hydrolyzed to an iron chelating EDTA-type structure and it is also a strong inhibitor of topoisomerase II."	( Dexrazoxane: how it works in cardiac and tumor cells. Is it a prodrug or is it a drug? Hasinoff, BB; Herman, EH, 2007)	1.47
"Dexrazoxane has been in clinical use for more than 25 years for prevention of cardiotoxicity in anthracycline based anticancer therapy. "	( Other uses of dexrazoxane: Savene, the first proven antidote against anthracycline extravasation injuries. Jensen, PB; Langer, SW; Sehested, M, 2007)	1.3
"Dexrazoxane has proved to be successful and superior over amifostine against such an evolution of doxorubicin cardiomyopathy."	( Effects of dexrazoxane and amifostine on evolution of Doxorubicin cardiomyopathy in vivo. Bjelogrlic, SK; Jokanovic, M; Jovic, V; Radic, J; Radulovic, S, 2007)	1.21
"Dexrazoxane (ICRF-187) has recently been demonstrated to reduce cardiac toxicity induced by chemotherapy with anthracyclines, although the reason for this phenomenon has remained obscure thus far. "	( Modulation of transferrin receptor expression by dexrazoxane (ICRF-187) via activation of iron regulatory protein. Brock, J; Grünewald, K; Kastner, S; Thaler, J; Weiss, G, 1997)	1.17
"Dexrazoxane has been used successfully to reduce cardiac toxicity in patients receiving anthracycline-based chemotherapy for cancer (predominantly women with advanced breast cancer). "	( Dexrazoxane. A review of its use as a cardioprotective agent in patients receiving anthracycline-based chemotherapy. Spencer, CM; Wiseman, LR, 1998)	1.54
"Dexrazoxane has been shown to reduce anthracycline-induced cardiotoxicity. "	( [Dexrazoxane. Current status and prospectives of cardiotoxicity of chemotherapy]. Lopez, M, )	1.31
"Dexrazoxane has been demonstrated to reduce the cardiac toxicity associated with long term, chronic use of doxorubicin."	( High-dose doxorubicin, dexrazoxane, and GM-CSF in malignant mesothelioma: a phase II study-Cancer and Leukemia Group B 9631. Green, MR; Herndon, JE; Kindler, HL; Kosty, MP; Vogelzang, NJ, 2001)	1.12

Excerpt	Reference	Relevance
"Dexrazoxane pre-treatment significantly reduced the etoposide-induced micronuclei formation, chromosomal aberrations, and also the suppression of erythroblast proliferation in bone marrow cells of mice. "	( Protection of mouse bone marrow from etoposide-induced genomic damage by dexrazoxane. Al-Anteet, AA; Al-Harbi, MM; Al-Rasheed, NM; Alhaider, AA; Attia, SM, 2009)	1.2
"Dexrazoxane-treated patients revealed better exercise tolerance; however the haemodynamic response to the stress was no different in both sub-groups."	( Long-term serial echocardiographic examination of late anthracycline cardiotoxicity and its prevention by dexrazoxane in paediatric patients. Blazek, B; Elbl, L; Hrstkova, H; Michalek, J; Tomaskova, I, 2005)	1.05
"Dexrazoxane pretreatment protected against the daunorubicin-induced decrease in atrial dF/dt."	( Prevention of chronic anthracycline cardiotoxicity in the adult Fischer 344 rat by dexrazoxane and effects on iron metabolism. Charlier, H; Cusack, BJ; Gambliel, H; Hadjokas, N; Musser, B; Olson, RD; Shadle, SE, 2006)	1.07
"The razoxane-treated patients experienced no significant toxicity apart from a readily reversible mild leukopenia in 52% while gastrointestinal symptoms necessitated stopping the drug in only four patients."	( A controlled prospective trial of adjuvant razoxane in resectable colorectal cancer. Cassell, PC; Ellis, H; Evans, MG; Gilbert, JM; Hellmann, K; Stoodley, BJ; Wastell, C, 1981)	1.01
"Dexrazoxane pre-treatment (50 mg kg(-1); 1 h prior to each daunorubicin injection) prevented the decrease in RyR2/GAPDH mRNA ratio and histopathologic lesions in daunorubicin-treated rats."	( Prevention by dexrazoxane of down-regulation of ryanodine receptor gene expression in anthracycline cardiomyopathy in the rat. Bauer, FK; Burke, BE; Cusack, BJ; Gambliel, H; Olson, RD, 2000)	1.16
"Dexrazoxane treatment caused DNA endoreduplication resulting in large highly polyploid cells."	( The catalytic DNA topoisomerase II inhibitor dexrazoxane (ICRF-187) induces differentiation and apoptosis in human leukemia K562 cells. Abram, ME; Allan, WP; Barnabé, N; Hasinoff, BB; Khélifa, T; Yalowich, JC, 2001)	1.08
"Razoxane treatment also induces PGA and high c-jun mRNA levels for 4 days, but thereafter a decay of c-jun expression occurs."	( Stable induction of c-jun mRNA expression in normal human keratinocytes by agents that induce predifferentiation growth arrest. Blatti, SP; Scott, RE, 1992)	1
"Pretreatment with razoxane (ICRF 159) in these animals did not appear to alter these major metabolic enzymes."	( Effect of razoxane (ICRF 159) on daunomycin (NSC 82151) metabolism and DNA complexation. Finch, M; Wang, GM, 1980)	0.99

Excerpt	Reference	Relevance
" A significant difference in body-weight increase and survival was observed between the treatment groups: ADR-529 injected prior to the first DXR dose significantly protected animals from DXR toxicity, but this schedule was significantly more toxic than the administration of ADR-529 beginning with the third or sixth DXR dose."	( Reducing doxorubicin cardiotoxicity in the rat using deferred treatment with ADR-529. Agen, C; Bernardini, N; Costa, M; Danesi, R; Del Tacca, M; Della Torre, P, 1992)	0.28
"Loss of body weight, cardiomyopathy, and nephropathy were the main toxic manifestations found when male spontaneously hypertensive rats (SHR) and genetically related Wistar-Kyoto (WKY) rats were given 1 mg/kg doxorubicin iv once a week for 12 weeks."	( Protective effect of ICRF-187 on doxorubicin-induced cardiac and renal toxicity in spontaneously hypertensive (SHR) and normotensive (WKY) rats. el-Hage, A; Ferrans, VJ; Herman, EH, 1988)	0.27
" We conclude that ICRF-187 offers significant protection against cardiac toxicity caused by doxorubicin, without affecting the antitumor effect of doxorubicin or the incidence of noncardiac toxic reactions."	( Protective effect of the bispiperazinedione ICRF-187 against doxorubicin-induced cardiac toxicity in women with advanced breast cancer. Dubin, N; Ferrans, V; Green, MD; Kramer, E; Rey, M; Sanger, J; Speyer, JL; Stecy, P; Ward, C; Zeleniuch-Jacquotte, A, 1988)	0.27
" The bisdioxopiperazine compound, dexrazoxane (ICRF-187, ADR-529), has been shown to prevent this cumulative side effect of the anthracyclines."	( Cardiotoxicity and cardioprotection during chemotherapy. Hochster, H; Speyer, J; Wasserheit, C, 1995)	0.56
"All animal and human reports involving doxorubicin-induced cardiac adverse effects were searched using MEDLINE combined with a fan search of relevant papers."	( Dexrazoxane in the prevention of doxorubicin-induced cardiotoxicity. Nesser, ME; Seifert, CF; Thompson, DF, 1994)	0.91
" Irreversible cardiomyopathy is a serious and dose-limiting side effect after chronic administration."	( Comparison of different iron chelators as protective agents against acute doxorubicin-induced cardiotoxicity. Bast, A; van Acker, SA; van Asbeck, BS; van der Vijgh, WJ; Voest, EE, 1994)	0.29
"This study demonstrates that dexrazoxane can be safely combined with escalating doses of epirubicin at dose ratios of 5 to 9:1 without having an adverse impact on toxicity."	( Comparative study of the pharmacokinetics and toxicity of high-dose epirubicin with or without dexrazoxane in patients with advanced malignancy. Basser, RL; Cebon, J; Duggan, G; Green, MD; Mihaly, G; Rosenthal, MA; Sobol, MM, 1994)	0.79
" Statistical analysis showed that razoxane treatment had no effect either beneficial or adverse on the rates of recurrence or on five year survival of patients with colo-rectal cancer."	( An evaluation of the effectiveness and safety of razoxane when used as an adjunct to surgery in colo-rectal cancer. Report of a controlled randomised study of 603 patients. Fielding, JW; Kingston, RD; Palmer, MK, 1993)	0.82
" A comparative study (using the identical frequency of the dosing scheme and S alpha T segment as the decisive parameter) has revealed that antimet-as another original substance of the diketopiperazines group-also involves (though less significantly) protective effects against the toxic action of adriamycin."	( Preclinical comparison of bis-diketopiperazine-propane (dexrazoxane) and bis-diketopiperazine-ethane (antimet) on the adriamycin-cardiotoxic effect. Grossmann, V; Kvĕtina, J; Safárová, M; Svoboda, Z, 1997)	0.54
" Instead, patients in the control arms of some of the trials have been exposed to more prolonged use or increased dosage of toxic chemotherapy that placed them at greater risk of the toxicity the protective agent was designed to prevent (eg, cardiotoxicity in trials of dexrazoxane, myelosuppression or thrombocytopenia in trials of growth factors)."	( Design and interpretation of clinical trials that evaluate agents that may offer protection from the toxic effects of cancer chemotherapy. Phillips, KA; Tannock, IF, 1998)	0.48
" The use of DEX did not add to the toxicity of the anthracyclines, nor was there clear evidence of an adverse impact of the agent on antitumor activity of the chemotherapeutic regimen."	( European trials with dexrazoxane in amelioration of doxorubicin and epirubicin-induced cardiotoxicity. Lopez, M; Vici, P, 1998)	0.61
" The drug is thought to reduce cardiac toxicity by binding to free and bound iron, thus reducing the formation of anthracycline-iron complexes and the generation of free radicals which are toxic to cardiac tissue."	( [Dexrazoxane. Current status and prospectives of cardiotoxicity of chemotherapy]. Lopez, M, )	0.69
" The frequency of cardiomyopathy may be reduced by modifying the schedule of administration, patients selection considering risk factors, careful cardiac monitoring during chemotherapy, using less toxic doxorubicin analogues and liposomal formulation."	( [Cardiac toxicity in cancer therapy]. Gisterek, I; Mazur, G; Wróbel, T; Włodarska, I; Zymliński, R; Łacko, A, 2002)	0.31
" Recently, high dose-intense chemotherapy with G-CSF and stem cell transplantation, and mediastinal irradiation, produce even more toxic effects on the heart."	( [Chemotherapy-induced cardiac toxicity and management]. Komagata, H; Sakai, H, 2003)	0.32
"Cardiotoxicity is a well-known side effect of several cytotoxic drugs, especially of the anthracyclines and can lead to long term morbidity."	( Cardiotoxicity of cytotoxic drugs. Guchelaar, HJ; Richel, DJ; Schimmel, KJ; van den Brink, RB, 2004)	0.32
"Anthracyclines, such as doxorubicin and daunorubicin, continue to be widely used in the treatment of cancer, although they share the adverse effect of chronic, cumulative dose-related cardiotoxicity."	( Prevention of chronic anthracycline cardiotoxicity in the adult Fischer 344 rat by dexrazoxane and effects on iron metabolism. Charlier, H; Cusack, BJ; Gambliel, H; Hadjokas, N; Musser, B; Olson, RD; Shadle, SE, 2006)	0.56
" However, for each individual patient, care providers should weigh the cardioprotective effect of dexrazoxane against the possible risk of adverse effects including a lower response rate."	( Prevention of anthracycline-induced cardiotoxicity in children: the evidence. Caron, HN; Kremer, LC; van Dalen, EC, 2007)	0.56
" Although infrequent, cumulative dose-dependent cardiotoxicity is nevertheless a significant side effect of this therapy resulting in reduced cardiac reserve or even frank cardiac failure."	( Managing cardiotoxicity in anthracycline-treated breast cancers. Green, MD; Ng, R, 2007)	0.34
" To maximize the benefits of these drugs, a high-risk population has been identified and new strategies have been investigated to minimize toxic effects, including limiting the cumulative dose, controlling the rate of administration and using liposomal preparations and novel anthracycline analogues."	( Anthracycline-induced cardiotoxicity: course, pathophysiology, prevention and management. Alvarez, JA; Barry, E; Lipshultz, SE; Miller, TL; Scully, RE, 2007)	0.34
" Possible adverse effects of dexrazoxane when administered as a cardioprotective agent are a decreased antitumor effect of anthracyclines and the onset of secondary malignancies in children."	( [Dexrazoxane in anthracycline induced cardiotoxicity and extravasation]. Beijnen, JH; Goey, AK; Huitema, AD; Schellens, JH, 2010)	1.2
"Cardiotoxicity was an unanticipated side effect elicited by the clinical use of imatinib (Imb)."	( A multifaceted evaluation of imatinib-induced cardiotoxicity in the rat. Agee, S; Estis, J; Hasinoff, B; Herman, EH; Knapton, A; Lipshultz, S; Lu, QA; Rosen, E; Rosenzweig, B; Thompson, K; Todd, JA; Zhang, J, 2011)	0.37
" Anthracycline--and nonanthracycline-induced cardiac toxicity--clinically significant and frequent adverse event of conservative treatment of cancer."	( [Cardiotoxicity of conservative treatment of solid tumors]. Askol'skiĭ, AV; Kasap, NV; Klimanov, MIu; Lial'kin, SA; Maĭdanevich, NN; Sivak, LA, )	0.13
" A study published in 1984 by Camerman and colleagues proposed that the therapeutic effects of bimolane could be due to ICRF-154, an impurity present within the bimolane samples that may also be responsible for the toxic effects attributed to bimolane."	( A comparative study of the cytotoxic and genotoxic effects of ICRF-154 and bimolane, two catalytic inhibitors of topoisomerase II. Eastmond, DA; Hasegawa, LS; Vuong, MC, 2013)	0.39

Excerpt	Reference	Relevance
" Doxorubicin's estimated terminal half-life was 39."	( Pharmacokinetics of the cardioprotector ADR-529 (ICRF-187) in escalating doses combined with fixed-dose doxorubicin. Blum, RH; Green, M; Hochster, H; Liebes, L; Meyers, M; Oratz, R; Speyer, JL; Wadler, S; Wernz, JC, 1992)	0.28
" Pharmacokinetic analysis showed that the children had a larger volume of distribution per kilogram of body weight in the central compartment and total body and a more rapid total-body clearance than adults."	( Phase I study of ICRF-187 in pediatric cancer patients and comparison of its pharmacokinetics in children and adults. Earhart, RH; Glaubiger, DL; Gribble, TJ; Holcenberg, JS; Kamen, BA; Pratt, CB; Tutsch, KD; Ungerleider, RS, 1986)	0.27
" Studies are need to determine the optimal dose ratio for cardioprotection and to explore further the pharmacokinetic interactions of the two drugs at increasing doses of epirubicin supported by hematopoietic growth factors."	( Comparative study of the pharmacokinetics and toxicity of high-dose epirubicin with or without dexrazoxane in patients with advanced malignancy. Basser, RL; Cebon, J; Duggan, G; Green, MD; Mihaly, G; Rosenthal, MA; Sobol, MM, 1994)	0.51
" The pharmacokinetic analysis showed that pretreatment with dexrazoxane (100 mg/ kg) reduced the area under plasma concentration-time curve of doxorubicin, its mean residence time and plasma clearance significantly."	( Interaction of dexrazoxane with red blood cells and hemoglobin alters pharmacokinetics of doxorubicin. Boroujerdi, M; Vaidyanathan, S, 2000)	0.88
" Dexrazoxane pharmacokinetic parameters were derived by standard noncompartmental methods."	( Pharmacokinetics of dexrazoxane in subjects with impaired kidney function. Aronoff, GR; Brier, ME; Fang, A; Gaylor, SK; Glue, P; McGovren, JP, 2011)	1.24

Excerpt	Reference	Relevance
"Our objectives in this study were to determine the maximum tolerated dose of ADR-529 (which uses a different vehicle than ICRF-187) when given with a fixed doxorubicin dose and to determine whether ADR-529 alters doxorubicin pharmacokinetics."	( Pharmacokinetics of the cardioprotector ADR-529 (ICRF-187) in escalating doses combined with fixed-dose doxorubicin. Blum, RH; Green, M; Hochster, H; Liebes, L; Meyers, M; Oratz, R; Speyer, JL; Wadler, S; Wernz, JC, 1992)	0.28
"Myelotoxicity was dose limiting for ADR-529 at 600-750 mg/m2 when given with a fixed dose of doxorubicin at 60 mg/m2 (dose ratios of ADR-529 to doxorubicin ranged from 10:1 to 12."	( Pharmacokinetics of the cardioprotector ADR-529 (ICRF-187) in escalating doses combined with fixed-dose doxorubicin. Blum, RH; Green, M; Hochster, H; Liebes, L; Meyers, M; Oratz, R; Speyer, JL; Wadler, S; Wernz, JC, 1992)	0.28
"We recommend that an ADR-529 dose of 600 mg/m2 be given with single-agent doxorubicin at a dose of 60 mg/m2 in future studies."	( Pharmacokinetics of the cardioprotector ADR-529 (ICRF-187) in escalating doses combined with fixed-dose doxorubicin. Blum, RH; Green, M; Hochster, H; Liebes, L; Meyers, M; Oratz, R; Speyer, JL; Wadler, S; Wernz, JC, 1992)	0.28
"We studied the effects of ICRF-154 in combination with 11 anticancer agents on four human leukaemia cell lines."	( The effects of ICRF-154 in combination with other anticancer agents in vitro. Akutsu, M; Kano, Y; Miura, Y; Narita, T; Sakamoto, S; Suda, K; Suzuki, K, 1992)	0.28
" Chronic treatment with these drugs or each combined with ICRF-187 did not change the antioxidant levels relative to the control values."	( Comparative study of doxorubicin, mitoxantrone, and epirubicin in combination with ICRF-187 (ADR-529) in a chronic cardiotoxicity animal model. Alderton, PM; Green, MD; Gross, J, 1992)	0.28
" ICRF-187 caused no significant change in tumor growth delay induced by either ADR alone or ADR combined with WBH."	( Protective effect of ICRF-187 against normal tissue injury induced by adriamycin in combination with whole body hyperthermia. Baba, H; Bull, JM; Newman, RA; Ohno, S; Siddik, ZH; Stephens, LC; Strebel, FR, 1991)	0.28
" However, the drug administered in combination with an antimetastatic, 1,2-bis(3,5-dioxopiperazin-1-yl)ethane (ICRF-154), resulted in an increase in survival time."	( Intratumor chemotherapy in combination with a systemic antimetastatic drug in the treatment of Lewis-lung carcinoma. De-Oliveira, MM; Giannotti Filho, O; Joussef, AC; Nakamura, IT, 1985)	0.27
"We have investigated the effect of ICRF-159 on the toxicity of daunorubicin (DR) and doxorubicin (DX) given iv, and the effectiveness of ICRF-159 combined with DR or DX on the growth of transplantable MLV-M (murine leukemia virus-Moloney) leukemia, MS-2 solid sarcoma, and pulmonary MS-2 metastases in mice."	( Studies in mice treated with ICRF-159 combined with daunorubicin or doxorubicin. Casazza, AM; Di Marco, A; Giuliani, F; Savi, G, )	0.13
"The purpose of this study was to determine the maximal tolerable dose (MTD) of epirubicin and ADR-529 given in combination with cyclophosphamide, 5-fluorouracil, and tamoxifen."	( The cardioprotector ADR-529 and high-dose epirubicin given in combination with cyclophosphamide, 5-fluorouracil, and tamoxifen: a phase I study in metastatic breast cancer. Bastholt, L; Gjedde, SB; Jakobsen, P; Mirza, MR; Mouridsen, HT; Rose, C; Sørensen, B, 1994)	0.29
"6-fold when combined with ICRF-187 (B."	( Improved targeting of brain tumors using dexrazoxane rescue of topoisomerase II combined with supralethal doses of etoposide and teniposide. Holm, B; Jensen, PB; Sehested, M, 1998)	0.56
" The anthracyclines doxorubicin, daunorubicin, and idarubicin were individually combined with DEX to study in vitro effects in leukemic myeloid cell lines."	( Dexrazoxane in combination with anthracyclines lead to a synergistic cytotoxic response in acute myelogenous leukemia cell lines. Freireich, EJ; Jendiroba, D; Keyhani, A; Liu, B; Pagliaro, L; Pearlman, M, 2003)	0.94
" The mobilizing regimen consisted of high-dose epirubicin 150 mg/m(2), preceded by dexrazoxane 1000 mg/m(2) (day 1), given in combination with paclitaxel 175 mg/m(2) (day 2), plus filgrastim."	( High-dose epirubicin, preceded by dexrazoxane, given in combination with paclitaxel plus filgrastim provides an effective mobilizing regimen to support three courses of high-dose dense chemotherapy in patients with high-risk stage II-IIIA breast cancer. Baioni, M; Ballardini, M; De Giorgi, U; Ferrari, E; Marangolo, M; Minzi, MR; Rosti, G; Zaniboni, A; Zornetta, L, 2003)	0.82
"To evaluate left ventricular (LV) systolic function by means of echocardiography in patients with osteosarcoma treated with doxorubicin alone or in combination with dexrazoxane."	( Left ventricular systolic function assessed by echocardiography in children and adolescents with osteosarcoma treated with doxorubicin alone or in combination with dexrazoxane. Campos Filho, O; Carvalho, AC; de Matos Neto, RP; Gomes, Lde F; Moisés, VA; Oporto, VM; Paiva, MG; Petrilli, AS; Silva, CM, 2006)	0.72
"Data in this study show that in patients with osteosarcoma treated with doxorubicin alone or combined with dexrazoxane, the LV systolic function, as assessed by the fractional percentage of systolic shortening mean, showed a better performance in the group that received dexrazoxane."	( Left ventricular systolic function assessed by echocardiography in children and adolescents with osteosarcoma treated with doxorubicin alone or in combination with dexrazoxane. Campos Filho, O; Carvalho, AC; de Matos Neto, RP; Gomes, Lde F; Moisés, VA; Oporto, VM; Paiva, MG; Petrilli, AS; Silva, CM, 2006)	0.74

Excerpt	Reference	Relevance
"The bioavailability of the antineoplastic agent, ICRF-159, has been examined in 12 patients receiving the drug in single and subdivided dose schedules in an attempt to account for the differences in toxicity found with the different schedules clinically."	( The bioavailability in man of ICRF-159 a new oral antineoplastic agent. Alford, DA; Allen, LM; Creaven, PJ, 1975)	0.25
" Recent clinical trials suggest that oral mesna has adequate bioavailability (roughly 50% by urinary thiol measurements) to prevent urotoxicity in high-dose ifosfamide regimens."	( Chemoprotectants for cancer chemotherapy. Dorr, RT, 1991)	0.28
" However, when given by this route at high doses, poor bioavailability was noted."	( Bis-diketopiperazine derivatives in clinical oncology: ICRF-159. Bruno, S; Macdonald, JS; Marsoni, S; Penta, J; Poster, DS, 1980)	0.26
" The drug is well absorbed from small intestine."	( [Topoisomerase inhibitors developing in Japan]. Furue, H, 1993)	0.29

Excerpt	Relevance	Reference
"Maximal dosing of cytotoxic chemotherapy drugs is often limited by the development of severe nonmyelosuppressive toxicities."	( Chemoprotectants for cancer chemotherapy. Dorr, RT, 1991)	0.28
") was cytotoxic to the bone marrow cells (which limited the analysis) but an increase in micronucleated polychromatic erythrocytes was observed in razoxane dosed animals (5-fold compared to control value)."	( The mutagenic activity of razoxane (ICRF 159): an anticancer agent. Albanese, R; Watkins, PA, 1985)	0.77
" At the dosage regimen used in the present experiments, doxorubicin, NAC, or ICRF-187 alone or in combination did not cause alterations in lungs, liver, kidney, or small intestine."	( Comparison of the effectiveness of (+/-)-1,2-bis(3,5-dioxopiperazinyl-1-yl)propane (ICRF-187) and N-acetylcysteine in preventing chronic doxorubicin cardiotoxicity in beagles. Ferrans, VJ; Herman, EH; Myers, CE; Van Vleet, JF, 1985)	0.27
" Repeated dosage regimens had the greatest effect on circulating blood cells, and anemia and neutropenia were most prominent after three series of five daily doses with rest periods between series."	( Preclinical toxicologic evaluation of ICRF-187 in dogs. Henry, MC; Levine, BS; Port, CD; Rosen, E, 1980)	0.26
" The dose-response surface is explored by regression analysis of experimental data, and after the estimation of the underlying hazard function the quality of the fit of the model is assessed."	( Survival analysis of drug combinations using a hazards model with time-dependent covariates. Carter, WH; Stablein, DM; Wampler, GL, 1980)	0.26
" At the dosage regimen used in the present experiments, doxorubicin did not induce lesions in lungs, liver, kidney, diaphragm, small intestine, or skeletal muscles."	( Reduction of chronic doxorubicin cardiotoxicity in dogs by pretreatment with (+/-)-1,2-bis(3,5-dioxopiperazinyl-1-yl)propane (ICRF-187). Ferrans, VJ; Herman, EH, 1981)	0.26
" In a dose-response protocol, diethylstilbestrol was inhibitory to the primary R3327MAT-Lu tumor, thereby also inhibiting the formation of lung metastases."	( Inhibition of the R3327MAT-Lu prostatic tumor by diethylstilbestrol and 1,2-bis(3,5-dioxopiperazin-1-yl)propane. Fair, WR; Heston, WD; Kadmon, D; Lazan, DW, 1982)	0.26
" The dosage of razoxane was 150 mg/m2 daily orally starting 5 days before the first irradiation."	( Inoperable recurrent rectal cancer: results of a prospective trial with radiation therapy and razoxane. Eiter, H; Hergan, K; Rhomberg, W; Schneider, B, 1994)	0.86
" Cardioxane was applied at a dosage of 1000 mg/m2 as a 15-min infusion in Ringer lactate solution 30 min before doxorubicin administration."	( Cardioprotection with ICRF-187 (Cardioxane) in patients with advanced breast cancer having cardiac risk factors for doxorubicin cardiotoxicity, treated with the FDC regimen. Bosnjak, S; Jelić, S; Kreacić, M; Milanović, N; Nesković-Konstantinović, Z; Radulović, S; Ristović, Z; Vuletić, L, 1995)	0.29
" Further research is needed to clearly demonstrate the effect dexrazoxane has on the antitumor effects of combination chemotherapy while defining optimal dosing strategies to minimize myelosuppression and maximize cardioprotection."	( Dexrazoxane in the prevention of doxorubicin-induced cardiotoxicity. Nesser, ME; Seifert, CF; Thompson, DF, 1994)	1.15
" In addition, ICRF-187 allowed for 50% greater cumulative dosing in normal mice that, nonetheless, showed extensive histological heart damage 7 wk after dosing."	( Characterization of experimental mitoxantrone cardiotoxicity and its partial inhibition by ICRF-187 in cultured neonatal rat heart cells. Alberts, DS; Dawson, BV; Dorr, RT; Hendrix, M; Shipp, NG, 1993)	0.29
" Direct perfusion of DaunoXome in isolated hearts of untreated animals resulted in a 12-fold reduction of the accumulation of daunorubicin in heart tissue as compared to the perfusion of free daunorubicin, and did not cause alterations in cardiac function at a dosage for which free daunorubicin induced major alterations."	( Development of the model of rat isolated perfused heart for the evaluation of anthracycline cardiotoxicity and its circumvention. Besse, P; Bonoron-Adèle, S; Gouverneur, G; Pouna, P; Robert, J; Tariosse, L, 1996)	0.29
" A comparative study (using the identical frequency of the dosing scheme and S alpha T segment as the decisive parameter) has revealed that antimet-as another original substance of the diketopiperazines group-also involves (though less significantly) protective effects against the toxic action of adriamycin."	( Preclinical comparison of bis-diketopiperazine-propane (dexrazoxane) and bis-diketopiperazine-ethane (antimet) on the adriamycin-cardiotoxic effect. Grossmann, V; Kvĕtina, J; Safárová, M; Svoboda, Z, 1997)	0.54
" IRP activation, stabilisation of trf-rec mRNA and increased surface expression of the protein in response to ICRF-187, follow a dose-response relationship."	( Modulation of transferrin receptor expression by dexrazoxane (ICRF-187) via activation of iron regulatory protein. Brock, J; Grünewald, K; Kastner, S; Thaler, J; Weiss, G, 1997)	0.55
" Instead, patients in the control arms of some of the trials have been exposed to more prolonged use or increased dosage of toxic chemotherapy that placed them at greater risk of the toxicity the protective agent was designed to prevent (eg, cardiotoxicity in trials of dexrazoxane, myelosuppression or thrombocytopenia in trials of growth factors)."	( Design and interpretation of clinical trials that evaluate agents that may offer protection from the toxic effects of cancer chemotherapy. Phillips, KA; Tannock, IF, 1998)	0.48
" Clinical trials in women with advanced breast cancer have found that patients given dexrazoxane (about 30 minutes prior to anthracycline therapy; dexrazoxane to doxorubicin dosage ratio 20:1 or 10:1) have a significantly lower overall incidence of cardiac events than placebo recipients (14 or 15% vs 31%) when the drug is initiated at the same time as doxorubicin."	( Dexrazoxane. A review of its use as a cardioprotective agent in patients receiving anthracycline-based chemotherapy. Spencer, CM; Wiseman, LR, 1998)	1.14
" METHODS FOR REDUCING TOXICITY: There are several methods by which one can reduce the toxicity of cancer chemotherapy, such as the application of rationally designed dosage schedules, alternative routes of administration, biochemical modulation, and the development of drug camers and analogs."	( [Anticancer chemotherapy. Prevention of complications]. Brion, N; Paule, B, 1998)	0.3
"Mesna: (1) Mesna, dosed as detailed in these guidelines, is recommended to decrease the incidence of standard-dose ifosfamide-associated urothelial toxicity."	( American Society of Clinical Oncology clinical practice guidelines for the use of chemotherapy and radiotherapy protectants. Broder, G; Cohen, GI; Gradishar, WJ; Green, DM; Hensley, ML; Langdon, RJ; Lindley, C; Meropol, NJ; Mitchell, RB; Negrin, R; Pfister, DG; Schuchter, LM; Szatrowski, TP; Thigpen, JT; Von Hoff, D; Wasserman, TH; Winer, EP, 1999)	0.3
"After determining the lethal dosage of Pro and Raz, we assessed and compared the inhibitory effects of Pro and Raz against primary tumor growth and metastatic occurrences of LLC at the dosage of LD5."	( Antitumor effects of two bisdioxopiperazines against two experimental lung cancer models in vivo. Ding, J; Lu, DY; Xu, B, 2004)	0.32
" Coadministration of the topoisomerase II catalytic inhibitor dexrazoxane in mice allows for more than 3-fold higher dosing of etoposide."	( Combining etoposide and dexrazoxane synergizes with radiotherapy and improves survival in mice with central nervous system tumors. Dejligbjerg, M; Hofland, KF; Jensen, LH; Jensen, PB; Kristjansen, PE; Rengtved, P; Sehested, M; Thougaard, AV, 2005)	0.86
" In animal experiments, Pro and Raz were active against primary tumor growth (35-50 %) and significantly inhibited pulmonary metastasis of LLC (inhibition > 90 %) at dosage below LD(5)."	( Medicinal chemistry of probimane and MST-16: comparison of anticancer effects between bisdioxopiperazines. Ding, J; Huang, M; Lu, DY; Xu, B; Xu, CH; Zhu, H, 2006)	0.33
"Treatment of endothelial cells with dexrazoxane resulted in a dose-response inhibition of cell growth lasting for up to 5 days after a single dose of the drug."	( Induction of thrombospondin-1 partially mediates the anti-angiogenic activity of dexrazoxane. Barker, J; Bicknell, R; Herbert, JM; Maloney, SL; Nagy, Z; Rabai, EM; Suchting, S; Sullivan, DC; Sundar, S, 2009)	0.85
" Modeling demonstrated that equivalent exposure (AUC(0-inf)) could be achieved if dosing were reduced by 50% in subjects with CL(CR) less than 40 mL/min compared with control subjects (CL(CR) >80 mL/min)."	( Pharmacokinetics of dexrazoxane in subjects with impaired kidney function. Aronoff, GR; Brier, ME; Fang, A; Gaylor, SK; Glue, P; McGovren, JP, 2011)	0.68
" The most effective dosage and timing of administration are unknown; however, there is evidence to suggest that administration within 6 hours after the event is warranted."	( Dexrazoxane treatment of doxorubicin extravasation injury in four dogs. Endicott, MM; Northrup, NC; Saba, CF; Venable, RO, 2012)	1
" Anthracyclines are widely used to treat these leukemias, but dosing is limited by cardiotoxicity."	( Dexrazoxane use in pediatric patients with acute lymphoblastic or myeloid leukemia from 1999 and 2009: analysis of a national cohort of patients in the Pediatric Health Information Systems database. Aplenc, R; Fisher, BT; Huang, YS; Li, Y; Seif, AE; Torp, K; Walker, DM, 2013)	1.01

Class	Description
N-alkylpiperazine
[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	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
TDP1 protein	Homo sapiens (human)	Potency	26.1011	0.0008	11.3822	44.6684	AID686978; AID686979
GLI family zinc finger 3	Homo sapiens (human)	Potency	6.6850	0.0007	14.5928	83.7951	AID1259369; AID1259392
AR protein	Homo sapiens (human)	Potency	47.3258	0.0002	21.2231	8,912.5098	AID743040
apical membrane antigen 1, AMA1	Plasmodium falciparum 3D7	Potency	22.3872	0.7079	12.1943	39.8107	AID720542
pregnane X nuclear receptor	Homo sapiens (human)	Potency	47.3258	0.0054	28.0263	1,258.9301	AID1346982
vitamin D (1,25- dihydroxyvitamin D3) receptor	Homo sapiens (human)	Potency	60.1320	0.0237	23.2282	63.5986	AID743223
euchromatic histone-lysine N-methyltransferase 2	Homo sapiens (human)	Potency	2.8184	0.0355	20.9770	89.1251	AID504332
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_a	Homo sapiens (human)	Potency	84.1586	0.0017	23.8393	78.1014	AID743083
vitamin D3 receptor isoform VDRA	Homo sapiens (human)	Potency	35.4813	0.3548	28.0659	89.1251	AID504847
flap endonuclease 1	Homo sapiens (human)	Potency	3.1623	0.1337	25.4129	89.1251	AID588795
serine/threonine-protein kinase PLK1	Homo sapiens (human)	Potency	26.6795	0.1683	16.4040	67.0158	AID720504
DNA polymerase iota isoform a (long)	Homo sapiens (human)	Potency	2.2387	0.0501	27.0736	89.1251	AID588590
peripheral myelin protein 22	Rattus norvegicus (Norway rat)	Potency	18.1056	0.0056	12.3677	36.1254	AID624032
lamin isoform A-delta10	Homo sapiens (human)	Potency	11.2202	0.8913	12.0676	28.1838	AID1487
Cellular tumor antigen p53	Homo sapiens (human)	Potency	13.4267	0.0023	19.5956	74.0614	AID651631; AID720552
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Protein	Taxonomy	Measurement	Average	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
Replicase polyprotein 1ab	Betacoronavirus England 1	IC50 (µMol)	10.0000	0.0040	3.4388	9.5100	AID1640022
Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2	IC50 (µMol)	3.1900	0.0002	2.4585	9.9600	AID1640021
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle G2/M phase transition	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
ER overload response	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
in utero embryonic development	Cellular tumor antigen p53	Homo sapiens (human)
somitogenesis	Cellular tumor antigen p53	Homo sapiens (human)
release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic progenitor cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
T cell proliferation involved in immune response	Cellular tumor antigen p53	Homo sapiens (human)
B cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
T cell lineage commitment	Cellular tumor antigen p53	Homo sapiens (human)
response to ischemia	Cellular tumor antigen p53	Homo sapiens (human)
nucleotide-excision repair	Cellular tumor antigen p53	Homo sapiens (human)
double-strand break repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
protein import into nucleus	Cellular tumor antigen p53	Homo sapiens (human)
autophagy	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in cell cycle arrest	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator resulting in transcription of p21 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
Ras protein signal transduction	Cellular tumor antigen p53	Homo sapiens (human)
gastrulation	Cellular tumor antigen p53	Homo sapiens (human)
neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of neuroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
protein localization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA replication	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell population proliferation	Cellular tumor antigen p53	Homo sapiens (human)
determination of adult lifespan	Cellular tumor antigen p53	Homo sapiens (human)
mRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
rRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
response to salt stress	Cellular tumor antigen p53	Homo sapiens (human)
response to inorganic substance	Cellular tumor antigen p53	Homo sapiens (human)
response to X-ray	Cellular tumor antigen p53	Homo sapiens (human)
response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of gene expression	Cellular tumor antigen p53	Homo sapiens (human)
cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cardiac muscle cell apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
viral process	Cellular tumor antigen p53	Homo sapiens (human)
glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
cerebellum development	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of cell growth	Cellular tumor antigen p53	Homo sapiens (human)
DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
mitotic G1 DNA damage checkpoint signaling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of telomere maintenance via telomerase	Cellular tumor antigen p53	Homo sapiens (human)
T cell differentiation in thymus	Cellular tumor antigen p53	Homo sapiens (human)
tumor necrosis factor-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
regulation of tissue remodeling	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV	Cellular tumor antigen p53	Homo sapiens (human)
multicellular organism growth	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of mitochondrial membrane permeability	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to glucose starvation	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
entrainment of circadian clock by photoperiod	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial DNA repair	Cellular tumor antigen p53	Homo sapiens (human)
regulation of DNA damage response, signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
transcription initiation-coupled chromatin remodeling	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of proteolysis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of DNA-templated transcription	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of RNA polymerase II transcription preinitiation complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of transcription by RNA polymerase II	Cellular tumor antigen p53	Homo sapiens (human)
response to antibiotic	Cellular tumor antigen p53	Homo sapiens (human)
fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of fibroblast proliferation	Cellular tumor antigen p53	Homo sapiens (human)
circadian behavior	Cellular tumor antigen p53	Homo sapiens (human)
bone marrow development	Cellular tumor antigen p53	Homo sapiens (human)
embryonic organ development	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylation	Cellular tumor antigen p53	Homo sapiens (human)
protein stabilization	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of helicase activity	Cellular tumor antigen p53	Homo sapiens (human)
protein tetramerization	Cellular tumor antigen p53	Homo sapiens (human)
chromosome organization	Cellular tumor antigen p53	Homo sapiens (human)
neuron apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of cell cycle	Cellular tumor antigen p53	Homo sapiens (human)
hematopoietic stem cell differentiation	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glial cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
type II interferon-mediated signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
cardiac septum morphogenesis	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of programmed necrotic cell death	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex assembly	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to endoplasmic reticulum stress	Cellular tumor antigen p53	Homo sapiens (human)
thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of thymocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
necroptotic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to xenobiotic stimulus	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to ionizing radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to gamma radiation	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to UV-C	Cellular tumor antigen p53	Homo sapiens (human)
stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
signal transduction by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
cellular response to actinomycin D	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of release of cytochrome c from mitochondria	Cellular tumor antigen p53	Homo sapiens (human)
cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
replicative senescence	Cellular tumor antigen p53	Homo sapiens (human)
oxidative stress-induced premature senescence	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
oligodendrocyte apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of execution phase of apoptosis	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of mitophagy	Cellular tumor antigen p53	Homo sapiens (human)
regulation of mitochondrial membrane permeability involved in apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
regulation of intrinsic apoptotic signaling pathway by p53 class mediator	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of miRNA transcription	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of G1 to G0 transition	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of miRNA processing	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of glucose catabolic process to lactate via pyruvate	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of pentose-phosphate shunt	Cellular tumor antigen p53	Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to hypoxia	Cellular tumor antigen p53	Homo sapiens (human)
regulation of fibroblast apoptotic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of reactive oxygen species metabolic process	Cellular tumor antigen p53	Homo sapiens (human)
negative regulation of stem cell proliferation	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of cellular senescence	Cellular tumor antigen p53	Homo sapiens (human)
positive regulation of intrinsic apoptotic signaling pathway	Cellular tumor antigen p53	Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
transcription cis-regulatory region binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
cis-regulatory region sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
core promoter sequence-specific DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
TFIID-class transcription factor complex binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription repressor activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription activator activity, RNA polymerase II-specific	Cellular tumor antigen p53	Homo sapiens (human)
protease binding	Cellular tumor antigen p53	Homo sapiens (human)
p53 binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA binding	Cellular tumor antigen p53	Homo sapiens (human)
chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
DNA-binding transcription factor activity	Cellular tumor antigen p53	Homo sapiens (human)
mRNA 3'-UTR binding	Cellular tumor antigen p53	Homo sapiens (human)
copper ion binding	Cellular tumor antigen p53	Homo sapiens (human)
protein binding	Cellular tumor antigen p53	Homo sapiens (human)
zinc ion binding	Cellular tumor antigen p53	Homo sapiens (human)
enzyme binding	Cellular tumor antigen p53	Homo sapiens (human)
receptor tyrosine kinase binding	Cellular tumor antigen p53	Homo sapiens (human)
ubiquitin protein ligase binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase regulator activity	Cellular tumor antigen p53	Homo sapiens (human)
ATP-dependent DNA/DNA annealing activity	Cellular tumor antigen p53	Homo sapiens (human)
identical protein binding	Cellular tumor antigen p53	Homo sapiens (human)
histone deacetylase binding	Cellular tumor antigen p53	Homo sapiens (human)
protein heterodimerization activity	Cellular tumor antigen p53	Homo sapiens (human)
protein-folding chaperone binding	Cellular tumor antigen p53	Homo sapiens (human)
protein phosphatase 2A binding	Cellular tumor antigen p53	Homo sapiens (human)
RNA polymerase II-specific DNA-binding transcription factor binding	Cellular tumor antigen p53	Homo sapiens (human)
14-3-3 protein binding	Cellular tumor antigen p53	Homo sapiens (human)
MDM2/MDM4 family protein binding	Cellular tumor antigen p53	Homo sapiens (human)
disordered domain specific binding	Cellular tumor antigen p53	Homo sapiens (human)
general transcription initiation factor binding	Cellular tumor antigen p53	Homo sapiens (human)
molecular function activator activity	Cellular tumor antigen p53	Homo sapiens (human)
promoter-specific chromatin binding	Cellular tumor antigen p53	Homo sapiens (human)
3'-5'-RNA exonuclease activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
RNA-dependent RNA polymerase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
cysteine-type endopeptidase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
mRNA 5'-cap (guanine-N7-)-methyltransferase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
mRNA (nucleoside-2'-O-)-methyltransferase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
mRNA guanylyltransferase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
RNA endonuclease activity, producing 3'-phosphomonoesters	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
ISG15-specific peptidase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
5'-3' RNA helicase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
protein guanylyltransferase activity	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
[Information is prepared from geneontology information from the June-17-2024 release]

Process	via Protein(s)	Taxonomy
nuclear body	Cellular tumor antigen p53	Homo sapiens (human)
nucleus	Cellular tumor antigen p53	Homo sapiens (human)
nucleoplasm	Cellular tumor antigen p53	Homo sapiens (human)
replication fork	Cellular tumor antigen p53	Homo sapiens (human)
nucleolus	Cellular tumor antigen p53	Homo sapiens (human)
cytoplasm	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrion	Cellular tumor antigen p53	Homo sapiens (human)
mitochondrial matrix	Cellular tumor antigen p53	Homo sapiens (human)
endoplasmic reticulum	Cellular tumor antigen p53	Homo sapiens (human)
centrosome	Cellular tumor antigen p53	Homo sapiens (human)
cytosol	Cellular tumor antigen p53	Homo sapiens (human)
nuclear matrix	Cellular tumor antigen p53	Homo sapiens (human)
PML body	Cellular tumor antigen p53	Homo sapiens (human)
transcription repressor complex	Cellular tumor antigen p53	Homo sapiens (human)
site of double-strand break	Cellular tumor antigen p53	Homo sapiens (human)
germ cell nucleus	Cellular tumor antigen p53	Homo sapiens (human)
chromatin	Cellular tumor antigen p53	Homo sapiens (human)
transcription regulator complex	Cellular tumor antigen p53	Homo sapiens (human)
protein-containing complex	Cellular tumor antigen p53	Homo sapiens (human)
double membrane vesicle viral factory outer membrane	Replicase polyprotein 1ab	Severe acute respiratory syndrome coronavirus 2
[Information is prepared from geneontology information from the June-17-2024 release]

Assay ID	Title	Year	Journal	Article
AID504749	qHTS profiling for inhibitors of Plasmodium falciparum proliferation	2011	Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043	Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID651635	Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Current protocols in cytometry, Oct, Volume: Chapter 13	Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2006	Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5	Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497	High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set	2010	Assay and drug development technologies, Feb, Volume: 8, Issue:1	High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID409954	Inhibition of mouse brain MAOA	2008	Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21	Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID588220	Literature-mined public compounds from Kruhlak et al phospholipidosis modelling dataset	2008	Toxicology mechanisms and methods, , Volume: 18, Issue:2-3	Development of a phospholipidosis database and predictive quantitative structure-activity relationship (QSAR) models.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	241 (32.26)	18.7374
1990's	209 (27.98)	18.2507
2000's	215 (28.78)	29.6817
2010's	74 (9.91)	24.3611
2020's	8 (1.07)	2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Publication Type	This drug (%)	All Drugs (%)
Trials	115 (13.96%)	5.53%
Reviews	110 (13.35%)	6.00%
Case Studies	48 (5.83%)	4.05%
Observational	0 (0.00%)	0.25%
Other	551 (66.87%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (48)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Pilot Study of Pre-Operative Treatment of Newly-Diagnosed, Surgically-Resectable Osteosarcoma With Doxorubicin, Ifosfamide, Etoposide, and Cisplatin With Early Metabolic Assessment of Response [NCT01258634]	Phase 1	2 participants (Actual)	Interventional	2010-07-31	Terminated(stopped due to PI no longer affiliated with institution; only 2 subjects enrolled)
Randomized Phase II Study of Vincristine, Doxorubicin, Cyclophosphamide and Dexrazoxane (VACdxr) With or Without ImmTher for Newly Diagnosed High Risk Ewing's Sarcoma [NCT00038142]	Phase 2	46 participants (Actual)	Interventional	1997-11-30	Terminated(stopped due to Low Accrual)
Prevention of Heart Failure Induced by Doxorubicin With Early Administration of Dexrazoxane in Patients With Breast Cancer [NCT03930680]	Phase 1	25 participants (Anticipated)	Interventional	2021-09-14	Recruiting
Risk-Adapted Focal Proton Beam Radiation and/or Surgery in Patients With Low, Intermediate and High Risk Rhabdomyosarcoma Receiving Standard or Intensified Chemotherapy [NCT01871766]	Phase 2	98 participants (Actual)	Interventional	2013-12-04	Active, not recruiting
A Phase 3 Randomized Trial for Patients With De Novo AML Comparing Standard Therapy Including Gemtuzumab Ozogamicin (GO) to CPX-351 With GO, and the Addition of the FLT3 Inhibitor Gilteritinib for Patients With FLT3 Mutations [NCT04293562]	Phase 3	1,400 participants (Anticipated)	Interventional	2020-07-21	Recruiting
Efficacy of Olaratumab and Rechallenge With Doxorubicin in Anthracycline Pretreated, Advanced Soft Tissue Sarcoma Patients. An Exploratory Phase-II Study [NCT03698227]	Phase 2	2 participants (Actual)	Interventional	2018-11-12	Terminated(stopped due to Lack of efficacy on olaratumab)
International Phase 3 Trial in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ALL) Testing Imatinib in Combination With Two Different Cytotoxic Chemotherapy Backbones [NCT03007147]	Phase 3	475 participants (Anticipated)	Interventional	2017-08-08	Recruiting
Treatment of Children With All Stages of Hepatoblastoma With Temsirolimus (NSC#683864) Added to High Risk Stratum Treatment [NCT00980460]	Phase 3	236 participants (Actual)	Interventional	2009-09-14	Active, not recruiting
A Phase 3 Study of 131I-Metaiodobenzylguanidine (131I-MIBG) or ALK Inhibitor Therapy Added to Intensive Therapy for Children With Newly Diagnosed High-Risk Neuroblastoma (NBL) [NCT03126916]	Phase 3	724 participants (Anticipated)	Interventional	2018-05-14	Active, not recruiting
Intensive Treatment For T-CELL Acute Lymphoblastic Leukemia and Advanced Stage Lymphoblastic Non-Hodgkin's Lymphoma: A Pediatric Oncology Group Phase III Study [NCT01230983]	Phase 3	573 participants (Actual)	Interventional	1996-06-30	Completed
Feasibility and Dose Discovery Analysis of Zoledronic Acid With Concurrent Chemotherapy in the Treatment of Newly Diagnosed Metastatic Osteosarcoma [NCT00742924]	Phase 1	24 participants (Actual)	Interventional	2008-08-31	Completed
A Phase II Trial of Irinotecan and Temozolomide in Combination With Existing High Dose Alkylator Based Chemotherapy for Treatment of Patients With Newly Diagnosed Ewing Sarcoma [NCT01864109]	Phase 2	83 participants (Actual)	Interventional	2013-05-31	Active, not recruiting
A Phase 3 Study of Dinutuximab Added to Intensive Multimodal Therapy for Children With Newly Diagnosed High-Risk Neuroblastoma [NCT06172296]	Phase 3	478 participants (Anticipated)	Interventional	2024-02-14	Not yet recruiting
Randomized Phase II Trial Of Interventional Therapy Investigate Cardiac Protection of Dexrazoxane In Women With Breast Cancer Having Experienced Grade 1 Cardiotoxicity During Prior Anthracycline-based Chemotherapy. [NCT00955890]	Phase 2	12 participants (Actual)	Interventional	2009-06-30	Terminated(stopped due to Enrolled too slow)
A Feasibility Pilot and Phase II Study Of Chemoimmunotherapy With Epratuzumab (IND #12034) for Children With Relapsed CD22-Positive Acute Lymphoblastic Leukemia (ALL) [NCT00098839]	Phase 1/Phase 2	134 participants (Actual)	Interventional	2005-02-28	Completed
A Phase I Study of Obatoclax (Pan Anti-Apoptotic BCL-2 Family Small Molecule Inhibitor), in Combination With Vincristine/Doxorubicin/Dexrazoxane, in Children With Relapsed/Refractory Solid Tumors or Leukemia [NCT00933985]	Phase 1	22 participants (Actual)	Interventional	2009-06-30	Terminated
Outpatient Chemotherapy in Pediatric Osteosarcoma: Doxorubicin With Cisplatin, High-Dose Methotrexate, and Additional Risk-Adapted Outpatient Chemotherapy [NCT00673179]		7 participants (Actual)	Interventional	2008-05-31	Terminated(stopped due to Low accrual.)
A Clinical Trial on TopotectTM (Dexrazoxane) in the Treatment of Accidental Extravasation of Anthracycline Anti-cancer Agents [NCT00548561]	Phase 2/Phase 3	23 participants (Actual)	Interventional	2001-06-30	Completed
Phase I Study of Cis-Diamminedicholoroplatinum in Combination With ICRF-187 in the Treatment of Advanced Malignancies [NCT00550901]	Phase 1	25 participants (Anticipated)	Interventional	2001-02-28	Completed
A Pilot Induction Regimen Incorporating Chimeric 14.18 Antibody (ch14.18, Dinutuximab) (NSC# 764038) and Sargramostim (GM-CSF) for the Treatment of Newly Diagnosed High-Risk Neuroblastoma [NCT03786783]	Phase 2	42 participants (Actual)	Interventional	2019-01-14	Active, not recruiting
A 2X2X2 Factorial Randomized Phase III Trial Of Multimodality Therapy Comparing 4 Cycles Of Doxorubicin And Cyclophosphamide With Or Without Dexrazoxane (AC+/-Z) Followed By 12 Weeks Of Weekly Paclitaxel With Or Without Trastuzumab (T+/-H) Followed By Loc [NCT00016276]	Phase 3	396 participants (Actual)	Interventional	2001-05-31	Terminated(stopped due to Administratively complete.)
Treatment of Childhood Acute Lymphoblastic Leukemia [NCT00165087]	Phase 3	491 participants	Interventional	1996-01-31	Terminated(stopped due to Terminated by IRB for continuing review)
A Clinical Trial on Topotect® (Dexrazoxane) in the Treatment of Accidental Extravasation of Anthracycline Anti-cancer Agents [NCT00548704]	Phase 2/Phase 3	57 participants (Actual)	Interventional	2002-04-30	Completed
A Phase II Trial of Epigenetic Priming in Patients With Newly Diagnosed Acute Myeloid Leukemia [NCT03164057]	Phase 2	206 participants (Actual)	Interventional	2017-06-15	Active, not recruiting
A Feasibility Trial of Everolimus (RAD001),an mTOR Inhibitor, Given in Combination With Multiagent Re-Induction Chemotherapy in Pediatric Patients With Relapsed Acute Lymphoblastic Leukemia (ALL) [NCT01523977]	Phase 1	22 participants (Actual)	Interventional	2011-11-30	Completed
A Phase 1 Study of Crizotinib in Combination With Conventional Chemotherapy for Relapsed or Refractory Solid Tumors or Anaplastic Large Cell Lymphoma [NCT01606878]	Phase 1	46 participants (Actual)	Interventional	2013-04-29	Completed
A Phase I Study of Venetoclax in Combination With Cytotoxic Chemotherapy, Including Calaspargase Pegol, for Children, Adolescents and Young Adults With High-Risk Hematologic Malignancies [NCT05292664]	Phase 1	92 participants (Anticipated)	Interventional	2023-03-29	Recruiting
Treatment of Acute Lymphoblastic Leukemia in Children [NCT00400946]	Phase 3	800 participants (Actual)	Interventional	2005-04-30	Completed
Marched Pair Study of the Standard Chemotherapy 4doxorubicin Plus Cyclophosphamide(AC) 60 + 4 Docetaxel Protocol Versus 4 PLD C35+4 Docetaxel in Neoadjuvant Chemotherapy of Breast Cancer [NCT02953184]	Phase 2	160 participants (Anticipated)	Interventional	2016-11-30	Recruiting
A Phase III Randomized Trial of Adding Vincristine-Topotecan-Cyclophosphamide to Standard Chemotherapy in Initial Treatment of Non-Metastatic Ewing Sarcoma [NCT00334867]	Phase 3	0 participants (Actual)	Interventional	2005-12-31	Withdrawn(stopped due to withdrawn)
Intravenous Erwinase for Patients With Relapsed/Refractory Acute Lymphoblastic Leukemia and Allergy to E. Coli Asparaginase (IND 104224) [NCT00928200]	Phase 1	1 participants (Actual)	Interventional	2009-04-13	Terminated(stopped due to Study was terminated due to lack of accrual.)
A Pilot Phase II Trial Of Irinotecan Plus Carboplatin, And Irinotecan Maintenance Therapy (High-Risk Patients Only), Integrated Into The Upfront Therapy Of Newly Diagnosed Patients With Intermediate - And High-Risk Rhabdomyosarcoma [NCT00077285]	Phase 2	65 participants (Anticipated)	Interventional	2003-10-31	Active, not recruiting
Osteosarcoma: Outcome of Therapy Based on Histologic Response. A Collaborative Effort of the POB/NCI, Texas Children's Hospital and University of Oklahoma. [NCT00019864]	Phase 2	100 participants (Anticipated)	Interventional	2000-03-31	Terminated
A Phase I Trial Of G3139 (BCL-2 Antisense, NSC# 683428, IND# 58842) Combined With Cytotoxic Chemotherapy In Relapsed Childhood Solid Tumors [NCT00039481]	Phase 1	15 participants (Actual)	Interventional	2002-11-30	Completed
Cardioprotection With Dexrazoxane in Acute Myeloid Leukemia (AML), High-Risk Myelodysplastic Syndrome (MDS), Myeloid Blast Phase of Chronic Myeloid Leukemia (CML), Ph+ AML, and Myeloid Blast Phase of Myeloproliferative Neoplasms [NCT03589729]	Phase 2	100 participants (Anticipated)	Interventional	2018-09-19	Recruiting
Use of the Cardioprotectant Dexrazoxane During Congenital Heart Surgery [NCT04997291]	Phase 1	12 participants (Anticipated)	Interventional	2021-04-09	Recruiting
Use of the Cardioprotectant Dexrazoxane During Congenital Heart Surgery: Proposal for Pilot Investigation [NCT02519335]	Phase 1	12 participants (Actual)	Interventional	2014-09-30	Terminated(stopped due to PI no longer at this facility)
Phase II Trial of Neoadjuvant Dose-Dense Doxorubicin, Ifosfamide, and Irinotecan (CPT-11) for Advanced Soft Tissue and Recurrent Bone Sarcomas [NCT00544778]	Phase 2	7 participants (Actual)	Interventional	2001-08-31	Terminated(stopped due to The study was terminated prematurely due to withdrawal of support by the sponsor.)
A Phase III Randomized Trial of Adding Vincristine-Topotecan-Cyclophosphamide to Standard Chemotherapy in Initial Treatment of Non-Metastatic Ewing Sarcoma [NCT01231906]	Phase 3	642 participants (Actual)	Interventional	2010-11-22	Active, not recruiting
A Phase II Proof of Concept Study Evaluating the Reduction of Mitoxantrone-induced Cardiotoxicity and Neurological Outcome in the Combined Use of Mitoxantrone and Dexrazoxane (Cardioxane®) in Multiple Sclerosis (MSCardioPro) [NCT01627938]	Phase 2	50 participants (Anticipated)	Interventional	2012-04-30	Active, not recruiting
Advanced Stage Hodgkins Disease - A Pediatric Oncology Group Phase III Study [NCT00005578]	Phase 3	219 participants (Actual)	Interventional	1997-03-31	Completed
RESPONSE DEPENDENT TREATMENT OF STAGES IA, IIA AND IIIA HODGKIN'S DISEASE WITH DBVE AND LOW DOSE INVOLVED FIELD IRRADIATION WITH OR WITHOUT ZINECARD: A PEDIATRIC ONCOLOGY GROUP PHASE III STUDY [NCT00002827]	Phase 3	294 participants (Actual)	Interventional	1996-10-31	Completed
Protocol for Patients With Newly-Diagnosed Non-Metastatic Osteosarcoma - A POG/CCG Pilot Intergroup Study [NCT00003937]	Phase 3	253 participants (Actual)	Interventional	1999-09-30	Completed
Randomized Phase II Study of Vincristine, Doxorubicin, Cyclophosphamide and Dexrazoxane With and Without ImmTher for Newly Diagnosed High Risk Ewing's Sarcoma [NCT00003667]	Phase 2	0 participants	Interventional	1998-09-30	Completed
A Non-Inferiority Study of Doxorubicin With Upfront Dexrazoxane for the Treatment of Advanced or Metastatic Soft Tissue Sarcoma [NCT02584309]	Phase 2	73 participants (Actual)	Interventional	2016-02-22	Completed
A Phase II Study of Intrathecal and Systemic Chemotherapy With Radiation Therapy for Children With Central Nervous System Atypical Teratoid/Rhabdoid Tumor (AT/RT) Tumor [NCT00084838]	Phase 2	25 participants (Actual)	Interventional	2003-02-28	Completed
A Multicenter, Open Label, Single-arm Study of KDX-0811(Dexrazoxane) in the Treatment of Accidental Extravasation of Anthracycline Anti-cancer Agents [NCT01596088]	Phase 1/Phase 2	2 participants (Actual)	Interventional		Completed
Treatment of Newly Diagnosed Acute Lymphoblastic Leukemia in Children and Adolescents [NCT03020030]	Phase 3	560 participants (Actual)	Interventional	2017-03-03	Active, not recruiting
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT00084838 (19) [back to overview]	Pre-Radiation Therapy Chemotherapeutic Response
NCT00084838 (19) [back to overview]	Grade 3-4 Infection/Febrile Neutropenia Events
NCT00084838 (19) [back to overview]	Grade 3-4 Hepatic Events
NCT00084838 (19) [back to overview]	Grade 3-4 Hemorrhage Events
NCT00084838 (19) [back to overview]	Grade 3-4 Gastrointestinal Events
NCT00084838 (19) [back to overview]	Grade 3-4 Dermatology Events
NCT00084838 (19) [back to overview]	Grade 3-4 Neurology Events
NCT00084838 (19) [back to overview]	Grade 3-4 Auditory/Hearing Events
NCT00084838 (19) [back to overview]	Grade 3-4 Allergy/Immunology
NCT00084838 (19) [back to overview]	2-yr Overall Survival
NCT00084838 (19) [back to overview]	Grade 3-4 Constitutional Events
NCT00084838 (19) [back to overview]	Grade 3-4 Cardiovascular Events
NCT00084838 (19) [back to overview]	Grade 3-4 Blood/Bone Marrow Events
NCT00084838 (19) [back to overview]	Grade 3-4 Metabolic/Laboratory Events
NCT00084838 (19) [back to overview]	Grade 3-4 Muscloskeletal Events
NCT00084838 (19) [back to overview]	Grade 3-4 Pain Events
NCT00084838 (19) [back to overview]	Grade 3-4 Pulmonary Events
NCT00084838 (19) [back to overview]	Grade 3-4 Renal/Genitourinary Events
NCT00084838 (19) [back to overview]	Grade 3/4 Events
NCT00098839 (4) [back to overview]	Remission Re-induction (CR2) Rate
NCT00098839 (4) [back to overview]	Event-free Survival Rate
NCT00098839 (4) [back to overview]	Pharmacokinetics
NCT00098839 (4) [back to overview]	Rate of Minimal Residual Disease (MRD) < 0.01%
NCT00400946 (10) [back to overview]	Induction Therapeutic Nadir Serum Asparaginase Activity Rate
NCT00400946 (10) [back to overview]	Post-Induction Nadir Serum Asparaginase Activity Level
NCT00400946 (10) [back to overview]	5-Year Disease-Free Survival
NCT00400946 (10) [back to overview]	5-year Disease-Free Survival by CNS Directed Treatment Group
NCT00400946 (10) [back to overview]	5-Year Disease-Free Survival by MRD Day 32 Status
NCT00400946 (10) [back to overview]	Asparaginase-Related Toxicity Rate
NCT00400946 (10) [back to overview]	Induction Infection Toxicity Rate
NCT00400946 (10) [back to overview]	Post-Induction Therapeutic Nadir Serum Asparaginase Activity Rate
NCT00400946 (10) [back to overview]	Induction Serum Asparaginase Activity Level
NCT00400946 (10) [back to overview]	5-Year Disease-Free Survival by Bone Marrow Day 18 Status
NCT00544778 (1) [back to overview]	Response Rate
NCT00742924 (1) [back to overview]	Limiting Toxicity
NCT00928200 (1) [back to overview]	Occurrence of a Dose-Limiting Toxicity
NCT00980460 (5) [back to overview]	Number of Cycles on Which Grade 3 or Higher Adverse Events Coded According to CTC AE Version 5 Were Observed
NCT00980460 (5) [back to overview]	Disease Status at the End of 2 Courses of Therapy
NCT00980460 (5) [back to overview]	Number of Deaths
NCT00980460 (5) [back to overview]	Feasibility of Referral for Liver Transplantation
NCT00980460 (5) [back to overview]	Event-free Survival
NCT01231906 (1) [back to overview]	Event-Free Survival
NCT01596088 (1) [back to overview]	Adverse Events
NCT02584309 (5) [back to overview]	Cardiac-related Mortality
NCT02584309 (5) [back to overview]	Progression-free Survival (PFS) (Arm 1 Only)
NCT02584309 (5) [back to overview]	Percentage of Patients With Heart Failure or Cardiomyopathy
NCT02584309 (5) [back to overview]	Ability of 3D Echocardiogram to Serve as an Early Marker of Cardiac Dysfunction Compared to 2D Echocardiogram Modified Simpson's Biplane Method of LVEF
NCT02584309 (5) [back to overview]	Early Detection of Cardiac Dysfunction by 2D Echocardiography Ventricular Strain Compared to 2D Echocardiography Ejection Fraction
NCT03786783 (5) [back to overview]	Response Rate
NCT03786783 (5) [back to overview]	Percentage of Participants With Unacceptable Toxicity
NCT03786783 (5) [back to overview]	Overall Survival
NCT03786783 (5) [back to overview]	Event-free Survival
NCT03786783 (5) [back to overview]	"Percentage of Participants Who Are Feasibility Failure"

Pre-Radiation Therapy Chemotherapeutic Response

"Response pre-RT/post-CT was defined as follows with overall response defined as achieving PR or CR.~Complete Response (CR): Complete resolution of all initially demonstrable tumor on MRI or CT evaluation w/o appearance of any new areas of disease; negative CSF cytology. Partial Response (PR): >/= 50% decrease in the sum of the products of the maximum perpendicular diameters of the tumor (sum LD) relative to baseline w/o appearance of any new areas of disease; CSF cytology unchanged from that at diagnosis or clearing after being initially positive Stable Disease (SD): <50% decrease in the sum LD w/o appearance of any new areas of disease; CSF cytology unchanged from that at diagnosis or clearing after being initially positive Progressive Disease (PD): >/= 25% increase in the sum LD relative to baseline, or the appearance of any new areas of disease or appearance of positive cytology after two consecutive negative samples." (NCT00084838)
Timeframe: Assessed at study entry and pre-RT/post-CT at week 7.

Intervention	proportion of evaluable patients (Number)
Multi-agent Intrathecal and Systemic CT With RT (Modified IRS	0.58

Intervention	proportion of participants (Number)
Reinduction Chemoimmunotherapy With Epratuzumab Once Weekly	.646
Reinduction Chemoimmunotherapy With Epratuzumab Twice Weekly	.660

Intervention	Proportion of participants (Number)
Reinduction Chemoimmunotherapy With Epratuzumab Once Weekly	.604
Reinduction Chemoimmunotherapy With Epratuzumab Twice Weekly	.640

Intervention	Proportion of participants (Number)
Reinduction Chemoimmunotherapy With Epratuzumab Once Weekly	.195
Reinduction Chemoimmunotherapy With Epratuzumab Twice Weekly	.295

Intervention	percentage of participants (Number)
	Day 4 NSAA Rate	Day 11 NSAA Rate	Day 18 NSAA Rate	Day 25 NSAA Rate
Overall	97	96	87	12

Intervention	IU/mL (Mean)
	Week 5 NSAA Level	Week 11 NSAA Level	Week 17 NSAA Level	Week 23 NSAA Level	Week 29 NSAA Level
Intramuscular Native E Coli L-asparaginase (IM-EC)	0.129	0.143	0.159	0.180	0.123
Intravenous PEG-asparaginase (IV-PEG)	0.726	0.773	0.787	0.757	0.806

Intervention	probability (Number)
CNS-1	.89
CNS-2	.89
CNS-3	1.00
Traumatic Tap With Blasts	.84
Traumatic Tap Without Blasts	.87

Intervention	IU/mL (Median)
	Day 4 NSAA Level	Day 11 NSAA Level	Day 18 NSAA Level	Day 25 NSAA Level
Overall	.694	.505	.211	.048

Intervention	probability (Number)
M1 Day 18 Bone Marrow Status	.89
M2/M3 Day 18 Bone Marrow Status	.78
Hypocellular Day 18 Bone Marrow Status	.88

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

Intervention	Cycles (Number)
	Hearing impaired	Diarrhea	Enterocolitis	Nausea	Small intestinal obstruction	Vomiting	Abdominal distension	Abdominal pain	Colitis	Anal mucositis	Ascites	Malabsorption	Mucositis oral	Constipation	Dental caries	Typhlitis	Duodenal obstruction	Esophageal hemorrhage	Gastritis	Illeus	Oral pain	Small intestinal mucositis	Colonic hemorrhage	Dysphagia	Esophagitis	Gastroparesis	Gastric fistula	Gastrointestinal disorders - Other, specify	Obstruction gastric	Rectal mucositis	Fever	General disorders and administration site conditions - Other, specify	Pain	Multi-organ failure	Irritability	Infusion related reaction	Hypothermia	Catheter related infection	Infections and infestations - Other, specify	Mucosal infection	Otitis media	Urinary tract infection	Biliary tract infection	Abdominal infection	Bladder infection	Enterocolitis infectious	Duodenal infection	Upper respiratory infection	Eye infection	Wound infection	Sepsis	Lung infection	Peritoneal infection	Skin infection	Small intestine infection	Periorbital infection	Alanine aminotransferase increased	Aspartate aminotransferase increased	Activated partial thromboplastin time prolonged	Alkaline phosphatase increased	Blood bilirubin increased	Creatinine increased	GGT increased	Weight loss	Fibronogen decreased	Ejection fraction decreased	Investigations - Other, specify	White blood cell decreased	INR increased	CPK increased	Cholesterol high	Electrocardiogram QT corrected interval prolonged	Lipase increased	Serum amylase increased	Anorexia	Dehydration	Hyperglycemia	Hyperkalemia	Hypermagnesemia	Hypernatremia	Hypokalemia	Hyponatremia	Acidosis	Alkalosis	Hypocalcemia	Hypoalbuminemia	Hypomagnesemia	Hypophosphatemia	Tumor lysis syndrome	Hypercalcemia	Hypoglycemia	Hypertriglyceridemia	Metabolism and nutrition disorders - Other, specify	Peripheral sensory neuropathy	Oculomotor nerve disorder	Abducens nerve disorder	Peripheral motor neuropathy	Syncope	Dysphasia	Depressed level of consciousness	Seizure	Apnea	Atelectasis	Dyspnea	Bronchospasm	Hypoxia	Pleural effusion	Pulmonary edema	Stridor	Respiratory failure	Epistaxis	Wheezing	Hypertension	Hematoma	Hypotension	Vascular disorders - Other, specify	Thromboembolic event	Left ventricular systolic dysfunction	Cardiac arrest	Right ventricular dysfunction	Ventricular tachycardia	Cardiac disorders - Other, specify	Sinus tachycardia	Heart failure	Myocardial infarction	Biliary fistula	Hepatobiliary disorders - Other, specify	Hepatic hemorrhage	Portal vein thrombosis	Portal hypertension	Biliary anastomotic leak	Postoperative hemorrhage	Gastrointestinal anastomotic leak	Intraoperative hemorrhage	Arthralgia	Generalized muscle weakness	Back pain	Bone pain	Muscle weakness lower limb	Agitation	Hallucinations	Insomnia	Acute kidney injury	Renal and urinary disorders - Other, specify	Renal calculi	Proteinuria	Erythema multiforme	Skin and subcutaneous tissue disorders - Other, specify	Rash maculo-papular	Eye disorders - Other, specify	Surgical and medical procedures - Other, specify	Tumor pain	Allergic reaction	Anaphylaxis	Immune system disorders - Other, specify
High-risk Group (Regimen H)	4	15	1	3	0	5	0	6	1	0	0	0	6	0	0	1	0	0	0	0	0	0	0	0	0	0	1	1	1	1	9	0	4	2	1	1	1	0	9	0	0	3	0	0	0	5	0	2	0	0	3	1	0	7	0	1	6	19	1	1	5	1	6	6	1	1	0	0	0	1	1	1	1	1	17	12	10	5	0	3	29	10	1	3	2	1	2	19	0	0	1	4	1	1	0	0	2	0	0	1	1	0	0	3	0	6	1	0	0	1	1	1	4	0	5	0	1	0	0	0	0	0	4	1	0	0	1	1	0	0	0	0	0	1	0	0	0	0	0	0	0	1	0	0	0	1	0	1	2	0	0	0	2	2	1
High-risk Group (Regimen W)	4	15	0	10	0	13	3	9	1	0	0	0	8	1	0	2	0	0	1	4	1	0	1	1	1	1	0	0	0	0	1	0	1	0	0	0	0	1	27	1	1	0	0	0	0	4	0	2	0	0	0	0	0	1	0	0	9	10	3	0	2	0	1	4	0	0	0	1	1	0	0	0	0	0	20	3	5	3	0	0	12	6	0	0	4	3	3	7	0	1	1	0	0	2	0	2	3	0	1	0	0	0	0	1	0	2	2	0	0	0	2	0	2	1	3	1	1	1	3	0	0	1	1	1	1	0	0	1	0	1	1	1	2	0	0	0	0	0	0	1	0	0	0	1	0	0	0	0	1	0	0	1	0	0	0
Intermediate-risk Group (Regimen F)	20	15	0	10	1	24	1	10	3	1	1	1	44	2	1	2	1	1	1	3	4	1	0	0	0	0	0	0	0	0	9	1	6	1	0	0	0	8	38	0	0	3	1	1	2	8	1	4	1	1	5	2	1	1	1	0	28	37	2	1	7	3	7	6	2	1	1	0	0	0	0	0	0	0	30	13	15	12	4	1	48	22	4	1	7	3	11	21	2	0	0	0	0	5	3	1	7	1	0	0	0	0	2	2	1	10	2	1	1	2	0	0	6	1	3	2	0	1	1	2	1	0	0	0	0	1	1	2	1	0	1	1	0	0	1	2	1	1	1	4	1	0	9	3	1	0	1	2	3	1	1	0	0	0	0
Low-risk Group (Regimen T)	1	4	1	1	1	2	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	1	0	0	0	0	0	0	1	4	1	1	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	1	1	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	1	3	2	2	2	2	4	1	0	0	0	0	0	0	0	0	0	0	0	2	0	0	0	0	0	0	0	1	0	0	0	0	0	0	0	0	0	0	3	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0	0

Intervention	participants (Number)
	RECIST PR, no AFP response	AFP response, no RECIST response	RECIST response, AFP response	no AFP response, no RECIST response
High-risk Group (Regimen H)	3	10	4	18
High-risk Group (Regimen W)	3	5	6	16

Intervention	Percent Probability (Number)
Very Low-risk Group	100
Low-risk Group (Regimen T)	87.21
Intermediate-risk Group (Regimen F)	87.03
High-risk Group (Regimen W)	43.61
High-risk Group (Regimen H)	46.38

Intervention	Percent Probability (Number)
Arm A (Combination Chemotherapy)	77.64
Arm B (Combination Chemotherapy, Topotecan Hydrochloride)	78.79

Intervention	Participants (Count of Participants)
Arm 1: Doxorubicin and Upfront Dexrazoxane	0
Arm 2: Control (Doxorubicin and Standard of Care Dexrazoxane)	0

Intervention	Participants (Count of Participants)
	Moderate cancer therapy related cardiac dysfunction (CTRCD)	Mild cancer therapy related cardiac dysfunction (CTRCD)	Heart failure with mildly reduced ejection fraction (HfmrEF)	Heart failure with preserved ejection fraction (HFpEF)
Arm 1: Doxorubicin and Upfront Dexrazoxane	4	25	0	17
Arm 2: Control (Doxorubicin and Standard of Care Dexrazoxane)	0	4	0	1

Intervention	Participants (Count of Participants)
	Patients with moderate CTRCD by 2D echo71922604		Patients with moderate CTRCD by 2D echo71922605	Patients without moderate CTRCD by 2D echo71922604	Patients without moderate CTRCD by 2D echo71922605
	Early dysfunction noted on 3D Echo	No early dysfunction noted on 3D echo
Arm 1: Doxorubicin and Upfront Dexrazoxane	0
Arm 1: Doxorubicin and Upfront Dexrazoxane	1
Arm 1: Doxorubicin and Upfront Dexrazoxane	7
Arm 2: Control (Doxorubicin and Standard of Care Dexrazoxane)	0
Arm 1: Doxorubicin and Upfront Dexrazoxane	38
Arm 2: Control (Doxorubicin and Standard of Care Dexrazoxane)	9

razoxane

Description

Cross-References

Synonyms (101)

Research Excerpts

Overview

Effects

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Drug Classes (1)

Protein Targets (17)

Potency Measurements

Inhibition Measurements

Biological Processes (124)

Molecular Functions (44)

Ceullar Components (20)

Bioassays (13)

Research

Studies (747)

Market Indicators

Research Demand Index: 19.11

Study Types

Clinical Trials (48)

Trial Overview

Trial Outcomes

Pre-Radiation Therapy Chemotherapeutic Response

Grade 3-4 Infection/Febrile Neutropenia Events

Grade 3-4 Hepatic Events

Grade 3-4 Hemorrhage Events

Grade 3-4 Gastrointestinal Events

Grade 3-4 Dermatology Events

Grade 3-4 Neurology Events

Grade 3-4 Auditory/Hearing Events

Grade 3-4 Allergy/Immunology

2-yr Overall Survival

Grade 3-4 Constitutional Events

Grade 3-4 Cardiovascular Events

Grade 3-4 Blood/Bone Marrow Events

Grade 3-4 Metabolic/Laboratory Events

Grade 3-4 Muscloskeletal Events

Grade 3-4 Pain Events

Grade 3-4 Pulmonary Events

Grade 3-4 Renal/Genitourinary Events

Grade 3/4 Events

Remission Re-induction (CR2) Rate

Event-free Survival Rate

Pharmacokinetics

Rate of Minimal Residual Disease (MRD) < 0.01%

Induction Therapeutic Nadir Serum Asparaginase Activity Rate

Post-Induction Nadir Serum Asparaginase Activity Level

5-Year Disease-Free Survival

5-year Disease-Free Survival by CNS Directed Treatment Group

5-Year Disease-Free Survival by MRD Day 32 Status

Asparaginase-Related Toxicity Rate

Induction Infection Toxicity Rate

Post-Induction Therapeutic Nadir Serum Asparaginase Activity Rate

Induction Serum Asparaginase Activity Level

5-Year Disease-Free Survival by Bone Marrow Day 18 Status

Response Rate

Limiting Toxicity

Occurrence of a Dose-Limiting Toxicity

Number of Cycles on Which Grade 3 or Higher Adverse Events Coded According to CTC AE Version 5 Were Observed

Disease Status at the End of 2 Courses of Therapy

Number of Deaths

Feasibility of Referral for Liver Transplantation

Event-free Survival

Event-Free Survival

Adverse Events

Cardiac-related Mortality

Progression-free Survival (PFS) (Arm 1 Only)

Percentage of Patients With Heart Failure or Cardiomyopathy

Ability of 3D Echocardiogram to Serve as an Early Marker of Cardiac Dysfunction Compared to 2D Echocardiogram Modified Simpson's Biplane Method of LVEF

Early Detection of Cardiac Dysfunction by 2D Echocardiography Ventricular Strain Compared to 2D Echocardiography Ejection Fraction

Response Rate

Percentage of Participants With Unacceptable Toxicity

Overall Survival