fotemustine profile

Fotemustine is an alkylating antineoplastic agent. It is a nitrogen mustard derivative that is used to treat malignant brain tumors, such as glioblastoma multiforme. Fotemustine is a lipophilic drug that can cross the blood-brain barrier, allowing it to reach the brain and central nervous system. It is administered intravenously and its mechanism of action involves the alkylation of DNA, which inhibits DNA replication and cell division. The synthesis of fotemustine involves the reaction of a nitrogen mustard with a cyclophosphamide derivative. Fotemustine is studied because it is a promising treatment option for malignant brain tumors, which are often resistant to conventional chemotherapy. Research is ongoing to investigate its efficacy, safety, and optimal dosing. Clinical trials are evaluating the use of fotemustine in combination with other chemotherapeutic agents, as well as its potential role in the treatment of other types of cancer.'

fotemustine: structure given in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

fotemustine : A racemate comprising equimolar amounts of (R)- and (S)-fotemustine. It is an alkylating agent used in the treatment of malignant melanoma. [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]

diethyl (1-{[(2-chloroethyl)(nitroso)carbamoyl]amino}ethyl)phosphonate : A member of the class of N-nitrosoureas that is ethyl diethylphosphonate in the hydrogen at position 1 of the ethyl group attached to the phosphorus has been replaced by a [(2-chloroethyl)(nitroso)carbamoyl]amino group. [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]

ID Source	ID
PubMed CID	104799
CHEMBL ID	549386
CHEBI ID	131852
SCHEMBL ID	8880
MeSH ID	M0153576

Synonym
servier-10036
s-10036
fotemustine
muphoran
fotemustinum [latin]
phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester
s 10036
ccris 6337
fotemustina [spanish]
c9h19cln3o5p
fotemustine (inn/ban)
muphoran (tn)
D07255
92118-27-9
diethyl-1-(3-(2-chloroethyl)-3-nitrosoureido)ethylphosphonate
(+-)-diethyl (1-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)phosphonate
mustoforan
s10036 ,
mustophorane
CHEMBL549386
diethyl (1-{[(2-chloroethyl)(nitroso)carbamoyl]amino}ethyl)phosphonate
CHEBI:131852
1-(2-chloroethyl)-3-(1-diethoxyphosphorylethyl)-1-nitrosourea
1-(2-chloroethyl)-3-(1-diethoxyphosphorylethyl)-1-nitroso-urea
A844148
AKOS015920275
unii-gq7jl9p5i2
fotemustina
hsdb 7762
fotemustinum
gq7jl9p5i2 ,
fotemustine [inn:ban]
FT-0630979
NCGC00346829-01
fotemustine [inn]
fotemustine [mi]
fotemustine [who-dd]
phosphonic acid, p-(1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester
fotemustine [mart.]
(+/-)-diethyl (1-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)phosphonate
fotemustine [hsdb]
diethyl (1-(3-(2-chloroethyl)-3-nitrosoureido)ethyl)phosphonate
HY-B0733
MLS006010716
smr002529685
MLS006010211
SCHEMBL8880
DS-1395
diethyl (1-{[n-(2-chloroethyl)-n'-oxohydrazinecarbonyl]amino}ethyl)phosphonate
sr-01000944936
SR-01000944936-1
fotemustine, >=98% (hplc)
diethyl 1-(3-(2-chloroethyl)-3-nitrosoureido)ethylphosphonate
BCP07342
Q1439555
6-amino-3-hydroxy(1h)indazole
DTXSID80869091
unii-qy93p3gn94
unii-upb2nn83ar
NCGC00346829-03
phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester, (-)-
QY93P3GN94 ,
191219-77-9
phosphonic acid, (1-((((2-chloroethyl)nitrosoamino)carbonyl)amino)ethyl)-, diethyl ester, (+)-
fotemustine, (-)-
fotemustine, (+)-
191220-84-5
UPB2NN83AR ,
fotemustene

Excerpt	Reference	Relevance
"Fotemustine (FTM) is a common treatment option for glioblastoma patients refractory to temozolomide (TMZ). "	( Efficacy and safety of second-line fotemustine in elderly patients with recurrent glioblastoma. Berardi, R; Burattini, L; Cascinu, S; Detti, B; Fabrini, MG; Iacovelli, R; Lolli, I; Perrone, F; Santoni, M; Savio, G; Scoccianti, S; Silvano, G, 2013)	2.11
"Fotemustine is a third-generation nitrosourea showing efficacy in various types of tumors such as melanoma and glioma. "	( An overview of fotemustine in high-grade gliomas: from single agent to association with bevacizumab. Bellu, L; Cecchin, D; Della Puppa, A; Farina, P; Lombardi, G; Pambuku, A; Zagonel, V, 2014)	2.2
"Fotemustine (FTM) is a third-generation nitrosourea showing efficacy in gliomas and it has been used with different schedules in adult patients."	( Clinical outcome of an alternative fotemustine schedule in elderly patients with recurrent glioblastoma: a mono-institutional retrospective study. Bellu, L; D'Avella, D; Della Puppa, A; Farina, M; Fiduccia, P; Lombardi, G; Pambuku, A; Zagonel, V, 2016)	1.43
"Fotemustine is a nitrosourea compound used for the treatment of malignant gliomas, especially in France. "	( Concurrent radiotherapy: fotemustine combination for newly diagnosed malignant glioma patients, a phase II study. Beauchesne, PD; Bernier, V; Carnin, C; Taillandier, L, 2009)	2.1
"Fotemustine is a cancer chemotherapeutic agent that belongs to an extremely active class of alkylating compounds."	( Antimutagenicity of amifostine against the anticancer drug fotemustine in the Drosophila somatic mutation and recombination (SMART) test. Aydemir, N; Bilaloglu, R; Celikler, S; Sevim, N; Vatan, O, )	1.1
"Fotemustine (FTMS) is a third-generation nitrosourea, in preclinical studies, FTMS compared favorably with carmustine (BCNU) and lomustine (CCNU) against several human tumor cell lines. "	( Lecture: fotemustine in brain tumors. Botturi, A; Ferrari, D; Gaviani, P; Lamperti, E; Salmaggi, A; Silvani, A; Simonetti, G, 2011)	2.23
"Fotemustine is a nitrosurea that has proved its efficacy in metastatic melanoma and particularly on cerebral metastases, given its high lipophilicity, facilitating its active penetration in all tissues including the central nervous system. "	( Fotemustine for the treatment of melanoma. Dréno, B; Quéreux, G, 2011)	3.25
"Fotemustine is a chemotherapy drug usually administered intravenously according to standard administration schedules."	( Initial experience with hepatic intraarterial fotemustine and interferon alpha 2b combination for treatment of liver tumors. Arcoria, D; Calì, S; DI Maggio, EM; Ferraù, F; Malaponte, E; Panebianco, V; Parisi, A; Romeo, P; Vasta, F; Vitale, FV, 2011)	1.35
"Fotemustine is an alkylating cytostatic drug belonging to the nitrosourea family and is used in particular in the treatment of disseminated malignant melanoma. "	( [New toxicity of fotemustine: diffuse interstitial lung disease]. Auffret, M; Bertrand, M; Gauthier, S; Mortier, L; Wémeau-Stervinou, L, 2012)	2.16
"Fotemustine is a nitrosourea with theoretic and preclinical advantages over the original analogs, carmustine and lomustine, in the treatment of brain tumors. "	( Phase I study of fotemustine in pediatric patients with refractory brain tumors. Baruchel, S; Bouffet, E; Gammon, J; Grant, RM; Hargrave, DR; Tariq, N, 2002)	2.1
"Fotemustine is a third generation chloroethylnitrosourea that has demonstrated significant antitumoral effects in malignant melanoma. "	( Cytotoxicity, DNA damage, and apoptosis induced by new fotemustine analogs on human melanoma cells in relation to O6-methylguanine DNA-methyltransferase expression. Cupissol, D; Cuq, P; Depeille, P; Evrard, A; Montero, JL; Passagne, I; Vian, L; Winum, JY, 2003)	2.01
"Fotemustine is a cytotoxic drug belonging to the group of nitrosourea derivatives, and is used in the treatment of metastatic melanoma, particularly when secondary brain lesions are present. "	( Neurological toxicity during metastatic melanoma treatment with fotemustine. Carlander, B; Guillot, B; Khalil, Z; Pageot, N, 2005)	2.01
"Fotemustine is a DNA-alkylating drug while vinorelbine is a semi-synthetic Vinca alkaloid."	( Genotoxic effects induced by fotemustine and vinorelbine in human lymphocytes. Aydemir, N; Bilaloğlu, R; Celikler, S, )	1.14
"Fotemustine is a cytotoxic alkylating agent, belonging to the group of nitrosourea family. "	( Focus on Fotemustine. Aquino, A; Bonmassar, E; De Rossi, A; De Vecchis, L; Laudisi, A; Leti, M; Marchesi, F; Rossi, L; Sini, V; Toppo, L; Torino, F; Tortorelli, G; Turriziani, M, 2006)	2.19
"Fotemustine (FM) is a new chloronitrosurea (CNU), chemically characterized by the graft of an aminophosphonic acid on the CNU radical, which makes it highly lipophilic. "	( Palliative therapy of melanoma patients with fotemustine. Inverse relationship between tumour load and treatment effectiveness. A multicentre phase II trial of the EORTC-Melanoma Cooperative Group (MCG). Bröcker, EB; Engel, E; Gérard, B; Glabbeke, MV; Israels, P; Kennes, C; Kleeberg, UR; Lejeune, F; Lentz, MA; Tilgen, W, 1995)	1.99
"Fotemustine (Fote) is a new aminoacid linked chloroethyl nitrosourea which has been shown to be useful in disseminated malignant melanoma. "	( [Tamoxifen increases cytotoxic effects of fotemustine. Experimental results on cell lines of human melanoma]. Barbé, V; Berlion, M; Berrile, J; Bizzari, JP; Fischel, JL; Formento, P; Milano, G, 1994)	2
"Fotemustine is a novel chloroethylnitrosourea, that readily penetrates the blood brain barrier. "	( Phase II trial of fotemustine in patients with metastatic malignant melanoma. Falkson, CI; Falkson, G; Falkson, HC, 1994)	2.07
"Fotemustine is a new chloroethylnitrosourea characterized by the grafting of a phosphonoalanine group onto a nitrosourea radical. "	( Fotemustine in the treatment of brain primary tumors and metastases. Berille, J; Bertrand, P; Bizzari, JP; Cour, V; Gerard, B; Giroux, B; Khayat, D; Sarkany, M, 1994)	3.17
"Fotemustine is a chemotherapeutic drug for the treatment of melanoma. "	( Chemical and glutathione conjugation-related degradation of fotemustine: formation and characterization of a glutathione conjugate of diethyl (1-isocyanatoethyl)phosphonate, a reactive metabolite of fotemustine. Brakenhoff, JP; Commandeur, JN; de Kanter, FJ; Luijten, WC; van Baar, BL; Vermeulen, NP, )	1.82
"Fotemustine is a new nitrosourea derivative whose activity has been demonstrated on metastatic melanoma with specific activity on brain metastases and also on poor prognosis lung cancers. "	( Cisplatin-fotemustine combination in inoperable non-small cell lung cancer: preliminary report of a French multicentre phase II trial. Baio, S; Berille, J; Le Cesne, A; Le Chevalier, T; Rivière, A, 1994)	2.13
"Fotemustine (Fote) is a new amino acid-linked chloroethyl nitrosourea which has been shown to be useful in disseminated malignant melanoma. "	( Tamoxifen enhances the cytotoxic effects of the nitrosourea fotemustine. Results on human melanoma cell lines. Barbé, V; Berlion, M; Berrile, J; Bizzari, JP; Fischel, JL; Formento, P; Milano, G, 1993)	1.97
"Fotemustine is a clinically used DNA-alkylating 2-chloro-ethyl-substituted N-nitrosourea, which sometimes shows signs of haematotoxicity and reversible liver and renal toxicity as toxic side-effects. "	( Molecular mechanisms of toxic effects of fotemustine in rat hepatocytes and subcellular rat liver fractions. Brakenhoff, JP; Commandeur, JN; Groot, EJ; Vermeulen, NP; Wormhoudt, LW, 1996)	2
"Fotemustine is a chloroethylnitrosourea with antitumor activity in disseminated melanoma and adult primary brain tumors. "	( Activity of fotemustine in medulloblastoma and malignant glioma xenografts in relation to O6-alkylguanine-DNA alkyltransferase and alkylpurine-DNA N-glycosylase activity. Boland, I; Gouyette, A; Lacroix, C; Lellouch-Tubiana, A; Margison, GP; Morizet, J; Parker, F; Pierre-Kahn, A; Poullain, MG; Terrier-Lacombe, MJ; Vassal, G; Vénuat, AM; Watson, AJ, 1998)	2.12
"Fotemustine is a relatively novel DNA-alkylating 2-chloroethyl-substituted N-nitrosourea (CENU) drug, clinically used for the treatment of disseminated malignant melanoma in different visceral and non-visceral tissues. "	( Toxicity of fotemustine in rat hepatocytes and mechanism-based protection against it. Brakenhoff, JP; Commandeur, JN; Groot, EJ; Li, QJ; Ramnatshing, S; Vermeulen, NP; Wormhoudt, LW, 1998)	2.12
"Fotemustine is a third-generation nitrosourea characterized by a phosphoalanine carrier group grafted onto the nitrosourea radical, which gives it a high lipophilicity and a better penetration through the cell membrane. "	( [Fotemustine (Muphoran) in 22 patients with relapses of high-grade cerebral gliomas]. Dam-Hieu, P; Labat, JP; Lucas, B; Malhaire, JP; Person, H; Simon, H, 1999)	2.66
"Fotemustine is a new nitrosourea which is active against disseminated malignant melanoma. "	( [Contribution of a new nitrosourea compound: fotemustine]. Boaziz, C, 1992)	1.99
"Fotemustine is a new chloronitrosourea which is active against disseminated malignant melanoma (DMM), and especially against cerebral metastases (CM). "	( Fotemustine: an overview of its clinical activity in disseminated malignant melanoma. Avril, MF; Bertrand, P; Bizzari, JP; Cour, V; Gerard, B; Khayat, D, 1992)	3.17
"Fotemustine is a new nitrosourea derivative that contains an alpha-aminophosphonic acid and has a short half-life and a high plasma clearance. "	( Hepatic intra-arterial infusion of fotemustine: pharmacokinetics. Cour, V; Fety, R; Lucas, C; Solere, P; Vignoud, J, 1992)	2
"Fotemustine is a highly reactive chloroethyl-nitrosourea anti-tumor drug that is currently undergoing phase III clinical trials in stage IV metastatic malignant melanoma. "	( Local treatment of cutaneous and subcutaneous metastatic malignant melanoma with fotemustine. Breitbart, EW; Mensing, H; Schallreuter, KU; Wood, JM, 1991)	1.95
"Fotemustine is a well tolerated active drug in recurrent malignant gliomas with an original and short treatment schedule."	( Phase II study of fotemustine in recurrent supratentorial malignant gliomas. Derlon, JM; Frenay, M; Giroux, B; Khoury, S; Namer, M, 1991)	1.34
"Fotemustine is a new nitrosourea which has shown some efficacy on disseminated malignant melanoma (DMM) (24.2% response rate (RR) among 153 patients in a Phase II trial) but little activity on hepatic metastasis (8.8% RR). "	( Fotemustine (S 10036) in the intra-arterial treatment of liver metastasis from malignant melanoma. A phase II Study. Aigner, K; Auclerc, G; Bizzari, JP; Borel, C; Bousquet, JC; Buthiau, D; Cohen-Alloro, G; Cour, V; Khayat, D; Weil, M, 1991)	3.17
"Fotemustine is a novel chloroethylnitrosourea derivative currently used in Phase III clinical trials for disseminated metastatic melanoma. "	( Sensitivity and resistance in human metastatic melanoma to the new chloroethylnitrosourea anti-tumor drug Fotemustine. Schallreuter, KU; Wood, JM, 1991)	1.94
"Fotemustine is a new chloronitrosourea recently developed by the French company Servier. "	( [Fotemustine, a new nitrosourea derivative. Current status of development]. Cour, V; Langenbahn, H, 1990)	2.63
"Fotemustine (S 10036) is a new anti-tumor nitrosourea characterized by a phosphonoalanine carrier group coupled to the nitrosourea moiety, which potentially increases the cellular penetration of the drug. "	( In vitro chemosensitivity testing of Fotemustine (S 10036), a new antitumor nitrosourea. Bizzari, JP; Deloffre, P; Etienne, MC; Fischel, JL; Formento, P; Frenay, M; Gioanni, J; Milano, G, 1990)	1.99
"Fotemustine is a new chloroethylnitrosourea which has recently entered a Phase II clinical trial. "	( Cytotoxicity and DNA damaging effects of a new nitrosourea, fotemustine, diethyl- 1-(3-(2-chloroethyl)-3-nitrosoureido) ethylphosphonate-S10036. Bizzari, JP; Catalin, J; Deloffre, P; Paraire, M; Rustum, Y; Tapiero, H; Tew, KD; Yin, MB, )	1.82
"Fotemustine (S 10036) is a new nitrosourea compound whose antitumoral activity has been demonstrated, particularly in disseminated malignant melanoma. "	( [Study of the clinical pharmacokinetics of fotemustine in various tumor indications]. Beerblock, K; Bizzari, JP; Deloffre, P; Lokiec, F; Lucas, C, 1989)	1.98

Excerpt	Reference	Relevance
"Fotemustine has shown therapeutic efficacy as single-drug second-line chemotherapy in treatment of TMZ pretreated patients."	( Second-line chemotherapy with fotemustine in temozolomide-pretreated patients with relapsing glioblastoma: a single institution experience. Ammannati, F; Biti, G; Bordi, L; Borghesi, S; Detti, B; Iannalfi, A; Leonulli, BG; Martinelli, F; Meattini, I; Sardaro, A; Scoccianti, S, 2008)	1.36
"Fotemustine therefore has no activity in advanced gastric cancer."	( Fotemustine in patients with advanced gastric cancer, a phase II trial from the EORTC-GITCCG (European Organization for Research and Treatment of Cancer, Gastrointestinal Tract Cancer Cooperative Group). Bleiberg, H; De Greve, J; Fabri, MC; Gerard, B; Kok, T; Paillot, B; Rougier, P; Van Glabbeke, M; van Pottelsberghe, C; Wagener, T, 1996)	2.46
"As fotemustine (FOT) has demonstrated activity on cerebral metastases, the rationale of this study was to replace carmustine by FOT in this four-drug regimen."	( Combined treatment with dacarbazine, cisplatin, fotemustine and tamoxifen in metastatic malignant melanoma. Bassères, N; Bizzari, JP; Bonerandi, JJ; Gérard, B; Grob, JJ; Richard, MA; Zarrour, H, 1998)	1.07
"Fotemustine has also been used in combination with dacarbazine (DTIC), in patients with DMM."	( Fotemustine: an overview of its clinical activity in disseminated malignant melanoma. Avril, MF; Bertrand, P; Bizzari, JP; Cour, V; Gerard, B; Khayat, D, 1992)	2.45
"Fotemustine has been administered to 10 patients with metastatic or redux soft sarcoma in a phase II pilot study. "	( [Fotemustine: a pilot phase II trial in sarcoma of the soft tissues]. Berille, J; Bizzari, JP; Jacquillat, C; Khayat, D; Spielmann, M; Tursz, T, 1991)	2.63
"14C Fotemustine has been used to determine its reactivity and metabolism in drug sensitive and resistant melanoma metastases and in cultures of sensitive and resistant clones of human melanoma cells."	( Sensitivity and resistance in human metastatic melanoma to the new chloroethylnitrosourea anti-tumor drug Fotemustine. Schallreuter, KU; Wood, JM, 1991)	0.98

Excerpt	Reference	Relevance
"fotemustine. Planned treatment duration was 6 months, starting with four weekly doses of 100 mg/m(2), and after a 5-week rest, repeated every 3 weeks."	( Adjuvant intra-arterial hepatic fotemustine for high-risk uveal melanoma patients. Denys, A; Goitein, G; Halkic, N; Leyvraz, S; Pampallona, S; Peters, S; Schalenbourg, A; Voelter, V; Zografos, L, 2008)	1.35
"With fotemustine-treated plasmid, the fotemustine-resistant subline did not exhibit an increased repair of directly fotemustine-induced DNA damage."	( Alterations of DNA repair in melanoma cell lines resistant to cisplatin, fotemustine, or etoposide. Diem, C; Emmert, S; Epe, B; Hellfritsch, D; Rünger, TM; Schadendorf, D, 2000)	0.99
"HIA treatment with fotemustine did not translate into an improved OS compared with IV treatment, despite better RR and PFS. "	( Hepatic intra-arterial versus intravenous fotemustine in patients with liver metastases from uveal melanoma (EORTC 18021): a multicentric randomized trial. Baurain, JF; Durando, X; Gurunath, RK; Jouary, T; Kaempgen, E; Keilholz, U; Leyvraz, S; Marshall, E; Negrier, S; Piperno-Neumann, S; Schadendorf, D; Scheulen, M; Suciu, S; Testori, A; Vermorken, JB; Zdzienicki, M, 2014)	1

Excerpt	Reference	Relevance
"Fotemustine is a clinically used DNA-alkylating 2-chloro-ethyl-substituted N-nitrosourea, which sometimes shows signs of haematotoxicity and reversible liver and renal toxicity as toxic side-effects."	( Molecular mechanisms of toxic effects of fotemustine in rat hepatocytes and subcellular rat liver fractions. Brakenhoff, JP; Commandeur, JN; Groot, EJ; Vermeulen, NP; Wormhoudt, LW, 1996)	2
" This adverse event should be managed with caution."	( Nitroso-urea-cisplatin-based chemotherapy associated with valproate: increase of haematologic toxicity. Bourg, V; Chichmanian, RM; Frenay, M; Lebrun, C; Thomas, P, 2001)	0.31
" However, its use is somewhat limited by its toxic side effects and chemoresistance caused by direct repair of O6-alkyl groups by the enzyme O6-methylguanine DNA-methyltransferase (MGMT)."	( Cytotoxicity, DNA damage, and apoptosis induced by new fotemustine analogs on human melanoma cells in relation to O6-methylguanine DNA-methyltransferase expression. Cupissol, D; Cuq, P; Depeille, P; Evrard, A; Montero, JL; Passagne, I; Vian, L; Winum, JY, 2003)	0.57
"This study showed that FTM is a valuable therapeutic option for elderly glioblastoma patients, with a safe toxicity profile."	( Efficacy and safety of second-line fotemustine in elderly patients with recurrent glioblastoma. Berardi, R; Burattini, L; Cascinu, S; Detti, B; Fabrini, MG; Iacovelli, R; Lolli, I; Perrone, F; Santoni, M; Savio, G; Scoccianti, S; Silvano, G, 2013)	0.67
" Treatment adverse events were mostly mild to moderate in intensity."	( Activity and safety of bevacizumab plus fotemustine for recurrent malignant gliomas. Carapella, CM; Carosi, MA; Cognetti, F; Fabi, A; Giannarelli, D; Marucci, L; Metro, G; Pace, A; Piludu, F; Pompili, A; Telera, S; Vaccaro, V; Vari, S; Vidiri, A; Villani, V, 2014)	0.67
" Grades 3-4 toxicity was 28 % (31 patients), being neutropenia (4 %) and thrombocytopenia (17 %) the most frequent adverse reactions."	( GEINOFOTE: efficacy and safety of fotemustine in patients with high-grade recurrent gliomas and poor performance status. Benavides, M; Berros, JP; Cano, JM; Ceballos, I; Covela, M; Fernández, I; Fuster, J; García Bueno, JM; García, A; Manneh, R; Moreno, V; Pérez-Segura, P; Quintanar, T; Sepúlveda, J; Vaz, MA, 2016)	0.71
"This study has shown that FTM is safe and has a comparable activity with other available therapeutic options of use in the treatment of recurrent HGG."	( GEINOFOTE: efficacy and safety of fotemustine in patients with high-grade recurrent gliomas and poor performance status. Benavides, M; Berros, JP; Cano, JM; Ceballos, I; Covela, M; Fernández, I; Fuster, J; García Bueno, JM; García, A; Manneh, R; Moreno, V; Pérez-Segura, P; Quintanar, T; Sepúlveda, J; Vaz, MA, 2016)	0.71
" We retrieved evidence on treatment-related grade III/IV adverse events, progression-free survival (PFS) and overall survival (OS)."	( A systematic literature review and network meta-analysis of effectiveness and safety outcomes in advanced melanoma. Franken, MG; Gheorghe, M; Haanen, JBAG; Leeneman, B; Uyl-de Groot, CA; van Baal, PHM, 2019)	0.51

Excerpt	Reference	Relevance
"Fotemustine is a new nitrosourea derivative that contains an alpha-aminophosphonic acid and has a short half-life and a high plasma clearance."	( Hepatic intra-arterial infusion of fotemustine: pharmacokinetics. Cour, V; Fety, R; Lucas, C; Solere, P; Vignoud, J, 1992)	2
"8 micrograms/ml, and declined monophasically with a half-life of about 24 min."	( Disposition, pharmacokinetics, and metabolism of 14C-fotemustine in cancer patients. Breen, M; Brownsill, R; Gordon, BH; Gray, AJ; Hiley, M; Ings, RM; Marchant, N; Richards, R; Taylor, AR; Wallace, D, 1990)	0.53
" Pharmacokinetic parameters of this drug were investigated during phase II clinical trials and compared according to tumor type."	( [Study of the clinical pharmacokinetics of fotemustine in various tumor indications]. Beerblock, K; Bizzari, JP; Deloffre, P; Lokiec, F; Lucas, C, 1989)	0.54
" In all, 40 pharmacokinetic determinations of fotemustine were made at dose levels ranging from 2 x 300 to 2 x 500 mg/m2."	( Phase I pharmacokinetics study of high-dose fotemustine and its metabolite 2-chloroethanol in patients with high-grade gliomas. Biron, P; Evene, E; Giroux, B; Gordon, B; Lucas, C; Mornex, F; Richards, R; Roux, N; Solere, P; Tranchand, B, 1993)	0.81
" Pharmacokinetic data were assessed during this Phase I-II study and reported here."	( Phase I-II and pharmacokinetic study of a new fotemustine schedule in advanced non-small cell lung cancer. Baud, M; Bérille, J; Chabot, G; Gouyette, A; Le Cesne, A; Le Chevalier, T; Lucas, C; Marty, M, 1995)	0.55
" No significant difference was noted in the AUC between days 1, 2 or 3 in any of the seven patients in whom a pharmacokinetic study of Fotemustine was performed."	( Phase I-II and pharmacokinetic study of a new fotemustine schedule in advanced non-small cell lung cancer. Baud, M; Bérille, J; Chabot, G; Gouyette, A; Le Cesne, A; Le Chevalier, T; Lucas, C; Marty, M, 1995)	0.75
"The nitrosourea, fotemustine, was given intravenously in 1 h constant-rate infusion to 66 patients in a multicentric study to assess both fotemustine pharmacokinetic behaviour and the pharmacokinetic-pharmacodynamic relationships."	( Pharmacokinetics and pharmacodynamics of nitrosourea fotemustine: a French cancer centre multicentric study. Fety, R; Iliadis, A; Launay-Iliadis, MC; Lokiec, F; Lucas, C; Milano, G; Tranchand, B, 1996)	0.88
" The pharmacokinetic parameters in renal-impaired patients were not significantly different from those in patients with normal renal function with a similar incidence of grade 3-4 toxicity in both groups."	( Clinical and pharmacokinetic phase II study of fotemustine in refractory and relapsing multiple myeloma patients. Ardiet, C; Berger, E; Bouafia, F; Coiffier, B; Dumontet, C; Guyotat, D; Jaubert, J; Lucas, C; Sebban, C; Tranchand, B, 2003)	0.58
" In total, 18 blood samples were collected for pharmacokinetic analysis (maximum plasma concentration, area under the concentration-time curve and total clearance) of D and F at 14 time points during therapy."	( Preliminary study on pharmacokinetics of dacarbazine and fotemustine in glioblastoma multiforme patients does not indicate gender-specific differences. Fazeny-Dörner, B; Mader, RM; Marosi, C; Piribauer, M; Rizovski, B; Stögermaier, B, 2004)	0.57

Excerpt	Reference	Relevance
"The aims of this phase I study in patients with recurrent malignant gliomas were to determine the maximum tolerated dose (MTD) and toxicity profile of fotemustine when combined with a fixed dose of procarbazine (PCZ), and to evaluate the extent of O6-alkylguanine-DNA alkyltransferase (ATase) depletion in circulating lymphocytes during treatment."	( Fotemustine combined with procarbazine in recurrent malignant gliomas: a phase I study with evaluation of lymphocyte 06-alkylguanine-DNA alkyltransferase activity. Berger, E; Boiardi, A; Ciusani, E; Giroux, B; Lucas, C; Margison, G; Silvani, A; Watson, A, 2001)	1.95
"The regimen, temozolomide combined with fotemustine, is an active and moderately safe first-line chemotherapy regimen with acceptable and easily manageable toxicities in patients with metastatic melanoma."	( Temozolomide in combination with fotemustine in patients with metastatic melanoma. Camlica, H; Tas, F; Topuz, E, 2008)	0.89
"To evaluate the efficacy of hypofractionated stereotactic radiotherapy performed as reirradiation in combination with fotemustine or bevacizumab as salvage treatment in patients with recurrent malignant glioma."	( Hypofractionated stereotactic radiotherapy in combination with bevacizumab or fotemustine for patients with progressive malignant gliomas. Agolli, L; Caporello, P; Enrici, RM; Esposito, V; Falco, T; Lanzetta, G; Minniti, G; Osti, MF; Scaringi, C, 2015)	0.85

Excerpt	Reference	Relevance
" After intraperitoneal administration the absolute bioavailability remains limited (22."	( Pharmacology of EAPB0203, a novel imidazo[1,2-a]quinoxaline derivative with anti-tumoral activity on melanoma. Bonnet, PA; Bressolle, FM; Cooper, JF; Deleuze-Masquéfa, C; Gattacceca, F; Khier, S; Margout, D; Moarbess, G; Pinguet, F; Solassol, I, 2010)	0.36
"The ATP-binding cassette transporter P-glycoprotein (P-gp) is known to limit both brain penetration and oral bioavailability of many chemotherapy drugs."	( A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein. Ambudkar, SV; Brimacombe, KR; Chen, L; Gottesman, MM; Guha, R; Hall, MD; Klumpp-Thomas, C; Lee, OW; Lee, TD; Lusvarghi, S; Robey, RW; Shen, M; Tebase, BG, 2019)	0.51

Excerpt	Relevance	Reference
" The thiolate-active site of RR from melanoma was inhibited by the new nitrosourea anti-tumour drug fotemustine (IC50 = 10(-4) M as determined from a dose-response study)."	( Ribonucleotide diphosphate reductase from human metastatic melanoma. Elgren, TE; Hogenkamp, HP; MacFarlan, S; Nelson, LS; Schallreuter, KU; Yan-Sze, I, 1992)	0.5
" Dosage was fotemustine 100 mg/m2 and dacarbazine 200 mg/m2 intravenously twice monthly on days 1 and 8, repeated for a maximum of six courses."	( Fotemustine plus dacarbazine in advanced stage III malignant melanoma. Binder, M; Dorffner, R; Glebowski, E; Pehamberger, H; Winkler, A; Wolff, K, 1992)	2.11
" In a panel of 12 human cancer cell lines [melanoma (4), ovary (2), head and neck (3), lung (1), bladder (1), breast (1)], the dose-response curves of S 10036 (0-100 microM) were similar to those obtained with equimolar concentrations of BCNU and CCNU; they indicated a moderately more marked effect for two and an equal effect for six melanoma cell lines with S 10036 as compared with BCNU."	( In vitro chemosensitivity testing of Fotemustine (S 10036), a new antitumor nitrosourea. Bizzari, JP; Deloffre, P; Etienne, MC; Fischel, JL; Formento, P; Frenay, M; Gioanni, J; Milano, G, 1990)	0.55
" We have recently shown wide interindividual variation in the depletion and subsequent regeneration of ATase in peripheral blood mononuclear cells (PMCs) following DTIC and this has now been extended to ascertain whether or not depletion is related to dosage of DTIC used and repeated treatment cycles of chemotherapy."	( Dosage and cycle effects of dacarbazine (DTIC) and fotemustine on O6-alkylguanine-DNA alkyltransferase in human peripheral blood mononuclear cells. Dougal, M; Lee, SM; Margison, GP; Thatcher, N, 1993)	0.54
" A statistically significant relationship was seen between the development of severe haematological toxicity (WHO > or = 3) with increasing dosage of DTIC and significant subclinical pulmonary damage was seen in 11 patients where the lung function was monitored during the course of treatment."	( Sequential administration of varying doses of dacarbazine and fotemustine in advanced malignant melanoma. Lee, SM; Margison, GP; Thatcher, N; Woodcock, AA, 1993)	0.53
" rIFN alpha 2a was administered at the dosage of 3 MIU subcutaneously 3 times a week until progression."	( Fotemustine and dacarbazine plus recombinant interferon alpha 2a in thetreatment of advanced melanoma. Caponigro, F; Casaretti, R; Comella, G; Comella, P; Daponte, A; Fiore, F; Frasci, G; Gravina, A; Ionna, F; Mozzillo, N; Parziale, AP; Presutti, F, 1997)	1.74
" For both GLA salts, cytotoxicity was manifested after 4 days of cell exposure and with very sharp dose-response curves."	( Cytotoxic effects of two gamma linoleic salts (lithium gammalinolenate or meglumine gammalinolenate) alone or associated with a nitrosourea: an experimental study on human glioblastoma cell lines. Bryce, R; Etienne, MC; Ferrero, JM; Fischel, JL; Formento, P; Ilc, K; Milano, G, 1999)	0.3
" Two patients in the first triplet had G3-G4 local toxicity, so that the scheduled F dosage was halved."	( Phase I-II study on isolation antiblastic fotemustine perfusion after dacarbazine chemosensitization for advanced melanoma of the extremities. De Salvo, GL; Foletto, M; Lejeune, FJ; Lise, M; Lopes, M; Mocellin, S; Pilati, PL; Pontes, L; Ribeiro, M; Rossi, CR, 2003)	0.58

Class	Description
organic phosphonate
N-nitrosoureas	A nitroso compound that is any urea in which one of the nitrogens is substituted by a nitroso group
organochlorine compound	An organochlorine compound is a compound containing at least one carbon-chlorine bond.
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein	Taxonomy	Measurement	Average (µ)	Min (ref.)	Avg (ref.)	Max (ref.)	Bioassay(s)
EWS/FLI fusion protein	Homo sapiens (human)	Potency	0.0148	0.0013	10.1577	42.8575	AID1259256
Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus	Potency	39.8107	0.0096	10.5250	35.4813	AID1479145
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Process	via Protein(s)	Taxonomy
virion membrane	Spike glycoprotein	Severe acute respiratory syndrome-related coronavirus
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (53)

Assay ID	Title	Year	Journal	Article
AID1508630	Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay	2021	Cell reports, 04-27, Volume: 35, Issue:4	A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1296008	Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening	2020	SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1	Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347083	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347103	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986	P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347108	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987	P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen	2019	Molecular pharmacology, 11, Volume: 96, Issue:5	A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347098	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347102	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347107	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845	Primary qHTS for Inhibitors of ATXN expression
AID1347086	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347100	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154	Primary screen GU AMC qHTS for Zika virus inhibitors	2020	Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49	Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347082	qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal	2020	Antiviral research, 01, Volume: 173	A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347094	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347101	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347095	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347096	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091	qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells	2018	Oncotarget, Jan-12, Volume: 9, Issue:4	Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347411	qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary	2020	ACS chemical biology, 07-17, Volume: 15, Issue:7	High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1079947	Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1079935	Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1079942	Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079933	Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1079931	Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID1079939	Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079940	Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID1079948	Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID1079934	Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1079944	Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID406725	Cytotoxicity against human RPMI7591 cells after 96 hrs by MTT assay	2008	Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13	In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1079949	Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079938	Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1079943	Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID406724	Cytotoxicity against human M4Be cells after 96 hrs by MTT assay	2008	Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13	In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1079946	Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID433907	Cytotoxicity against human A375 cells after 96 hrs by MTT assay	2009	European journal of medicinal chemistry, Sep, Volume: 44, Issue:9	New imidazo[1,2-a]quinoxaline derivatives: synthesis and in vitro activity against human melanoma.
AID1079936	Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1079937	Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1079941	Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID406723	Cytotoxicity against human A375 cells after 96 hrs by MTT assay	2008	Bioorganic & medicinal chemistry, Jul-01, Volume: 16, Issue:13	In vitro and in vivo anti-tumoral activities of imidazo[1,2-a]quinoxaline, imidazo[1,5-a]quinoxaline, and pyrazolo[1,5-a]quinoxaline derivatives.
AID1079932	Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID1079945	Animal toxicity known. [column 'TOXIC' in source]
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Timeframe	Studies, This Drug (%)	All Drugs %
pre-1990	9 (3.28)	18.7374
1990's	112 (40.88)	18.2507
2000's	77 (28.10)	29.6817
2010's	63 (22.99)	24.3611
2020's	13 (4.74)	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	84 (28.77%)	5.53%
Reviews	34 (11.64%)	6.00%
Case Studies	24 (8.22%)	4.05%
Observational	0 (0.00%)	0.25%
Other	150 (51.37%)	84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (9)

Trial Overview

Trial	Phase	Enrollment	Study Type	Start Date	Status
A Randomized, Phase III Study of Fotemustine Versus the Combination of Fotemustine and Ipilimumab or the Combination of Ipilimumab and Nivolumab in Patients With Metastatic Melanoma With Brain Metastasis [NCT02460068]	Phase 3	168 participants (Anticipated)	Interventional	2012-12-31	Recruiting
An Open-label Study to Assess the Anti-tumor Activity of Avastin in Combination With Fotemustine as First-line Therapy in Patients With Metastatic Melanoma [NCT01069627]	Phase 2	20 participants (Actual)	Interventional	2006-12-31	Completed
Phase II Study of the Predictive Value of the Expression of Tumoral MGMT With Respect to the Therapeutic Response of Fotemustine in Patients With Metastatic Malignant Melanoma [NCT00560118]	Phase 2	60 participants (Anticipated)	Interventional	2003-08-31	Completed
The Prospective Study of FTD Program and HD-MTX-Ara-C Program Contrast in the Treatment of PCNSL Lymphoma. [NCT05274139]	Phase 2	20 participants (Actual)	Interventional	2017-03-02	Completed
A Phase II Single-arm Study for the Treatment After Recurrence of Advanced Melanoma Patients Harboring the V600BRAF Mutation and Pretreated With Vemurafenib, With the Association of Vemurafenib Plus Fotemustine. [NCT01983124]	Phase 2	31 participants (Actual)	Interventional	2013-02-28	Completed
Intravenous Versus Intra-Arterial Fotemustine Chemotherapy in Patients With Liver Metastases From Uveal Melanoma: A Randomized Phase III Study of the EORTC Melanoma Group [NCT00110123]	Phase 3	171 participants (Actual)	Interventional	2005-01-31	Terminated(stopped due to low accrual)
Fotemustine and Dacarbazine Versus Dacarbazine +/- Alpha Interferon in Advanced Malignant Melanoma: Phase III Study [NCT01359956]	Phase 3	269 participants (Actual)	Interventional	2002-04-30	Completed
A Phase II Study of the Combination of Ipilimumab and Fotemustine in Patients With Unresectable Locally Advanced or Metastatic Malignant Melanoma [NCT01654692]	Phase 2	86 participants (Actual)	Interventional	2010-06-30	Completed
Randomized Non Comparative Phase II Trial With Bevacizumab and Fotemustine in the Treatment of Recurrent Glioblastoma [NCT01474239]	Phase 2	91 participants (Actual)	Interventional	2011-11-30	Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

Trial	Outcome
NCT01069627 (18) [back to overview]	Duration of CR - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Duration of CR - Time to Event
NCT01069627 (18) [back to overview]	Duration of Overall Response of CR or PR - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Duration of Overall Response of CR or PR - Time to Event
NCT01069627 (18) [back to overview]	Duration of Stable Disease - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Duration of Stable Disease - Time to Event
NCT01069627 (18) [back to overview]	OS - Time to Event
NCT01069627 (18) [back to overview]	Overall Survival (OS) - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Percentage of Participants With Clinical Benefit of CR, PR, or Stable Disease (SD)
NCT01069627 (18) [back to overview]	Percentage of Participants With Complete Response (CR) or Partial Response (PR)
NCT01069627 (18) [back to overview]	Time to CR - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Time to CR - Time To Event
NCT01069627 (18) [back to overview]	Time to Overall Response of CR or PR - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Time to Overall Response of CR or PR - Time to Event
NCT01069627 (18) [back to overview]	Time to Progression (TTP) - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	Time to Treatment Failure (TTF) - Percentage of Participants With an Event
NCT01069627 (18) [back to overview]	TTF - Time to Event
NCT01069627 (18) [back to overview]	TTP - Time to Event
NCT01359956 (4) [back to overview]	Overall Response Rate (ORR)
NCT01359956 (4) [back to overview]	Overall Survival (OS)
NCT01359956 (4) [back to overview]	Progression Free Survival (PFS)
NCT01359956 (4) [back to overview]	Treatment Related Toxicity
NCT01474239 (16) [back to overview]	Overall Survival (OS)
NCT01474239 (16) [back to overview]	Percentage of Participants Alive 12 Months After Start of Treatment
NCT01474239 (16) [back to overview]	Percentage of Participants Alive 30 Days After Last Dose of Study Drug
NCT01474239 (16) [back to overview]	Percentage of Participants Alive 6 Months After Start of Treatment
NCT01474239 (16) [back to overview]	Percentage of Participants Alive 9 Months After Start of Treatment
NCT01474239 (16) [back to overview]	Percentage of Participants Who Were Alive and Progression Free 6 Months After Start of Treatment
NCT01474239 (16) [back to overview]	Percentage of Participants With Corticosteroid Initiation During the Study Period
NCT01474239 (16) [back to overview]	Percentage of Participants With Karnofsky Performance Status (KPS) Deterioration
NCT01474239 (16) [back to overview]	Percentage of Participants With World Health Organization (WHO) Performance Status (PS) Deterioration
NCT01474239 (16) [back to overview]	Progression-Free Survival (PFS)
NCT01474239 (16) [back to overview]	Time to Corticosteroid Initiation
NCT01474239 (16) [back to overview]	Time to Karnofsky Performance Status (KPS) Deterioration
NCT01474239 (16) [back to overview]	Time to WHO PS Deterioration
NCT01474239 (16) [back to overview]	Change From Screening in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30) Scores at Weeks 8, 16, 24, 32, 40, 48, 56, 64, and 72
NCT01474239 (16) [back to overview]	Percentage of Participants in Each Class of Corticosteroid Use
NCT01474239 (16) [back to overview]	Percentage of Participants With a Best Overall Response of Complete Response (CR) or Partial Response (PR)

Duration of CR - Percentage of Participants With an Event

Evaluated only for participants whose best overall response was CR. The start date was the date of first documented CR and the end date was defined as the date of first documented progression of disease, or death. Participants who did not experience progression of disease were censored at last tumor assessment date or at maximum follow-up. (NCT01069627)
Timeframe: Baseline, every 9 weeks during study treatment, and every 3 months during follow-up, up to 36 months

Intervention	percentage of participants (Number)
Bevacizumab + Fotemustine	0

Intervention	participants (Number)
Fotemustine/Dacarbazine/Interferon + Fotemustine/Dacarbazine	32
Dacarbazine/Interferon + Dacarbazine	33
Fotemustine/Dacarbazine/Interferon+Dacarbazine/Interferon	34
Fotemustine/Dacarbazine + Dacarbazine	31

Intervention	units on a scale (Mean)
	Physical Functioning (Fn): Screening (n=58,31)	Physical Fn: Change at Week 8 (n=27,16)	Physical Fn: Change at Week 16 (n=15,7)	Physical Fn: Change at Week 24 (n=14,1)	Physical Fn: Change at Week 32 (n=7,2)	Physical Fn: Change at Week 40 (n=9,1)	Physical Fn: Change at Week 48 (n=4,1)	Physical Fn: Change at Week 56 (n=4,0)	Physical Fn: Change at Week 64 (n=1,0)	Physical Fn: Change at Week 72 (n=1,0)	Role Fn: Screening (n=58,31)	Role Fn: Change at Week 8 (n=27,16)	Role Fn: Change at Week 16 (n=15,7)	Role Fn: Change at Week 24 (n=14,1)	Role Fn: Change at Week 32 (n=7,2)	Role Fn: Change at Week 40 (n=9,1)	Role Fn: Change at Week 48 (n=4,1)	Role Fn: Change at Week 56 (n=4,0)	Role Fn: Change at Week 64 (n=1,0)	Role Fn: Change at Week 72 (n=1,0)	Emotional Fn: Screening (n=58,31)	Emotional Fn: Change at Week 8 (n=27,16)	Emotional Fn: Change at Week 16 (n=15,7)	Emotional Fn: Change at Week 24 (n=14,1)	Emotional Fn: Change at Week 32 (n=7,2)	Emotional Fn: Change at Week 40 (n=9,1)	Emotional Fn: Change at Week 48 (n=4,1)	Emotional Fn: Change at Week 56 (n=4,0)	Emotional Fn: Change at Week 64 (n=1,0)	Emotional Fn: Change at Week 72 (n=1,0)	Cognitive Fn: Screening (n=58,31)	Cognitive Fn: Change at Week 8 (n=27,16)	Cognitive Fn: Change at Week 16 (n=15,7)	Cognitive Fn: Change at Week 24 (n=14,1)	Cognitive Fn: Change at Week 32 (n=7,2)	Cognitive Fn: Change at Week 40 (n=9,1)	Cognitive Fn: Change at Week 48 (n=4,1)	Cognitive Fn: Change at Week 56 (n=4,0)	Cognitive Fn: Change at Week 64 (n=1,0)	Cognitive Fn: Change at Week 72 (n=1,0)	Social Fn: Screening (n=58,31)	Social Fn: Change at Week 8 (n=27,16)	Social Fn: Change at Week 16 (n=15,7)	Social Fn: Change at Week 24 (n=14,1)	Social Fn: Change at Week 32 (n=7,2)	Social Fn: Change at Week 40 (n=9,1)	Social Fn: Change at Week 48 (n=4,1)	Social Fn: Change at Week 56 (n=4,0)	Social Fn: Change at Week 64 (n=1,0)	Social Fn: Change at Week 72 (n=1,0)	QOL: Screening (n=58,31)	QOL: Change at Week 8 (n=27,16)	QOL: Change at Week 16 (n=15,7)	QOL: Change at Week 24 (n=14,1)	QOL: Change at Week 32 (n=7,2)	QOL: Change at Week 40 (n=9,1)	QOL: Change at Week 48 (n=4,1)	QOL: Change at Week 56 (n=4,0)	QOL: Change at Week 64 (n=1,0)	QOL: Change at Week 72 (n=1,0)	Fatigue: Screening (n=58,31)	Fatigue: Change at Week 8 (n=27,16)	Fatigue: Change at Week 16 (n=15,7)	Fatigue: Change at Week 24 (n=14,1)	Fatigue: Change at Week 32 (n=7,2)	Fatigue: Change at Week 40 (n=9,1)	Fatigue: Change at Week 48 (n=4,1)	Fatigue: Change at Week 56 (n=4,0)	Fatigue: Change at Week 64 (n=1,0)	Fatigue: Change at Week 72 (n=1,0)	Nausea: Screening (n=58,31)	Nausea: Change at Week 8 (n=27,16)	Nausea: Change at Week 16 (n=15,7)	Nausea: Change at Week 24 (n=14,1)	Nausea: Change at Week 32 (n=7,2)	Nausea: Change at Week 40 (n=9,1)	Nausea: Change at Week 48 (n=4,1)	Nausea: Change at Week 56 (n=4,0)	Nausea: Change at Week 64 (n=1,0)	Nausea: Change at Week 72 (n=1,0)	Pain: Screening (n=58,31)	Pain: Change at Week 8 (n=27,16)	Pain: Change at Week 16 (n=15,7)	Pain: Change at Week 24 (n=14,1)	Pain: Change at Week 32 (n=7,2)	Pain: Change at Week 40 (n=9,1)	Pain: Change at Week 48 (n=4,1)	Pain: Change at Week 56 (n=4,0)	Pain: Change at Week 64 (n=1,0)	Pain: Change at Week 72 (n=1,0)	Dyspnea: Screening (n=58,31)	Dyspnea: Change at Week 8 (n=27,16)	Dyspnea: Change at Week 16 (n=15,7)	Dyspnea: Change at Week 24 (n=14,1)	Dyspnea: Change at Week 32 (n=7,2)	Dyspnea: Change at Week 40 (n=9,1)	Dyspnea: Change at Week 48 (n=4,1)	Dyspnea: Change at Week 56 (n=4,0)	Dyspnea: Change at Week 64 (n=1,0)	Dyspnea: Change at Week 72 (n=1,0)	Insomnia: Screening (n=58,31)	Insomnia: Change at Week 8 (n=27,16)	Insomnia: Change at Week 16 (n=15,7)	Insomnia: Change at Week 24 (n=14,1)	Insomnia: Change at Week 32 (n=7,2)	Insomnia: Change at Week 40 (n=9,1)	Insomnia: Change at Week 48 (n=4,1)	Insomnia: Change at Week 56 (n=4,0)	Insomnia: Change at Week 64 (n=1,0)	Insomnia: Change at Week 72 (n=1,0)	Appetite loss: Screening (n=58,31)	Appetite loss: Change at Week 8 (n=27,16)	Appetite loss: Change at Week 16 (n=15,7)	Appetite loss: Change at Week 24 (n=14,1)	Appetite loss: Change at Week 32 (n=7,2)	Appetite loss: Change at Week 40 (n=9,1)	Appetite loss: Change at Week 48 (n=4,1)	Appetite loss: Change at Week 56 (n=4,0)	Appetite loss: Change at Week 64 (n=1,0)	Appetite loss: Change at Week 72 (n=1,0)	Constipation: Screening (n=58,31)	Constipation: Change at Week 8 (n=26,16)	Constipation: Change at Week 16 (n=15,7)	Constipation: Change at Week 24 (n=14,1)	Constipation: Change at Week 32 (n=7,2)	Constipation: Change at Week 40 (n=9,1)	Constipation: Change at Week 48 (n=4,1)	Constipation: Change at Week 56 (n=4,0)	Constipation: Change at Week 64 (n=1,0)	Constipation: Change at Week 72 (n=1,0)	Diarrhea: Screening (n=58,31)	Diarrhea: Change at Week 8 (n=27,16)	Diarrhea: Change at Week 16 (n=15,7)	Diarrhea: Change at Week 24 (n=14,1)	Diarrhea: Change at Week 32 (n=7,2)	Diarrhea: Change at Week 40 (n=9,1)	Diarrhea: Change at Week 48 (n=4,1)	Diarrhea: Change at Week 56 (n=4,0)	Diarrhea: Change at Week 64 (n=1,0)	Diarrhea: Change at Week 72 (n=1,0)	Financial Fn: Screening (n=58,31)	Financial Fn: Change at Week 8 (n=27,16)	Financial Fn: Change at Week 16 (n=15,7)	Financial Fn: Change at Week 24 (n=14,1)	Financial Fn: Change at Week 32 (n=7,2)	Financial Fn: Change at Week 40 (n=9,1)	Financial Fn: Change at Week 48 (n=4,1)	Financial Fn: Change at Week 56 (n=4,0)	Financial Fn: Change at Week 64 (n=1,0)	Financial Fn: Change at Week 72 (n=1,0)
Bevacizumab	71.95	10.37	7.56	13.81	18.10	4.44	3.33	6.67	0.00	0.00	67.82	6.17	2.22	14.29	16.67	0.00	0.00	-12.50	-50.00	-50.00	73.56	-8.02	-0.56	10.12	-2.38	-5.56	14.58	-4.17	8.33	8.33	70.40	4.94	2.22	10.71	0.00	-1.85	0.00	-4.17	16.67	16.67	72.99	1.85	1.11	13.10	-7.14	-5.56	-4.17	-12.50	-66.67	-66.67	58.05	-3.09	-4.44	4.76	3.57	-2.78	10.42	2.08	0.00	0.00	31.99	-3.29	2.22	-6.35	3.17	9.88	-8.33	2.78	0.00	0.00	2.01	1.85	0.00	-5.95	-2.38	-9.26	0.00	-4.17	-16.67	-16.67	6.90	-1.85	-10.00	-8.33	0.00	-7.41	-29.17	0.00	-16.67	-16.67	11.49	4.94	0.00	-9.52	0.00	3.70	-8.33	0.00	0.00	0.00	18.39	1.23	2.22	-9.52	28.57	14.81	25.00	33.33	0.00	0.00	7.47	0.00	-2.22	-7.14	-4.76	-7.41	-16.67	-16.67	0.00	0.00	17.82	3.85	4.44	2.38	-0.00	3.70	-16.67	0.00	-33.33	-33.33	1.15	0.00	-6.67	-7.14	-4.76	0.00	0.00	0.00	0.00	0.00	17.82	6.17	2.22	-4.76	0.00	-3.70	-16.67	-8.33	0.00	0.00
Fotemustine	78.92	7.08	8.57	0.00	13.33	6.67	6.67	NA	NA	NA	73.66	4.17	2.38	0.00	0.00	0.00	0.00	NA	NA	NA	74.19	8.33	-2.38	-33.33	16.67	8.33	8.33	NA	NA	NA	79.03	7.29	-4.76	0.00	8.33	0.00	0.00	NA	NA	NA	81.18	4.17	-2.38	0.00	8.33	16.67	16.67	NA	NA	NA	66.13	6.25	7.14	0.00	-12.50	0.00	0.00	NA	NA	NA	24.01	-13.19	-9.52	-11.11	-5.56	-11.11	-11.11	NA	NA	NA	1.08	-8.33	-14.29	0.00	0.00	0.00	-16.67	NA	NA	NA	14.52	-6.25	-2.38	0.00	-8.33	0.00	0.00	NA	NA	NA	3.23	-6.25	4.76	0.00	0.00	0.00	0.00	NA	NA	NA	18.28	-8.33	-4.76	-33.33	16.67	33.33	33.33	NA	NA	NA	5.38	-10.42	-14.29	0.00	0.00	0.00	0.00	NA	NA	NA	17.20	-4.17	-9.52	0.00	16.67	0.00	0.00	NA	NA	NA	2.15	0.00	0.00	0.00	0.00	0.00	0.00	NA	NA	NA	25.81	-4.17	9.52	0.00	-16.67	0.00	0.00	NA	NA	NA

Intervention	percentage of participants (Number)
	Week 8: Increased (n=52,28)	Week 8: Decreased (n=52,28)	Week 8: No Change (n=52,28)	Week 16: Increased (n=33,18)	Week 16: Decreased (n=33,18)	Week 16: No Change (n=33,18)	Week 24: Increased (n=21,5)	Week 24: Decreased (n=21,5)	Week 24: No Change (n=21,5)	Week 32: Increased (n=14,3)	Week 32: Decreased (n=14,3)	Week 32: No Change (n=14,3)	Week 40: Increased (n=10,2)	Week 40: Decreased (n=10,2)	Week 40: No Change (n=10,2)	Week 48: Increased (n=8,1)	Week 48: Decreased (n=8,1)	Week 48: No Change (n=8,1)	Week 56: Increased (n=6,1)	Week 56: Decreased (n=6,1)	Week 56: No Change (n=6,1)	Week 64: Increased (n=3,1)	Week 64: Decreased (n=3,1)	Week 64: No Change (n=3,1)	Week 72: Increased (n=3,0)	Week 72: Decreased (n=3,0)	Week 72: No Change (n=3,0)	Week 80: Increased (n=1,0)	Week 80: Decreased (n=1,0)	Week 80: No Change (n=1,0)	Week 88: Increased (n=1,0)	Week 88: Decreased (n=1,0)	Week 88: No Change (n=1,0)	Follow-up: Increased (n=9,3)	Follow-up: Decreased (n=9,3)	Follow-up: No Change (n=9,3)
Bevacizumab	17.31	23.08	59.62	21.21	36.36	42.42	28.57	33.33	38.10	14.29	42.86	42.86	0.00	60.00	40.00	0.00	50.00	50.00	0.00	33.33	66.67	0.00	0.00	100.00	0.00	0.00	100.00	0.00	0.00	100.00	100.00	0.00	0.00	33.33	0.00	66.67
Fotemustine	17.86	21.43	60.71	22.22	27.78	50.00	20.00	40.00	40.00	33.33	0.00	66.67	50.00	0.00	50.00	0.00	0.00	100.00	0.00	0.00	100.00	0.00	0.00	100.00	NA	NA	NA	NA	NA	NA	NA	NA	NA	0.00	33.33	66.67

Intervention	percentage of participants (Number)
	RANO Evaluation	MacDonald Evaluation
Bevacizumab	28.81	28.81
Fotemustine	9.38	6.25

fotemustine

Description

Cross-References

Synonyms (69)

Research Excerpts

Overview

Effects

Treatment

Toxicity

Pharmacokinetics

Compound-Compound Interactions

Bioavailability

Dosage Studied

Drug Classes (3)

Protein Targets (2)

Potency Measurements

Ceullar Components (1)

Bioassays (53)

Research

Studies (274)

Market Indicators

Research Demand Index: 38.68

Study Types

Clinical Trials (9)

Trial Overview

Trial Outcomes

Duration of CR - Percentage of Participants With an Event

Duration of CR - Time to Event

Duration of Overall Response of CR or PR - Percentage of Participants With an Event

Duration of Overall Response of CR or PR - Time to Event

Duration of Stable Disease - Percentage of Participants With an Event

Duration of Stable Disease - Time to Event

OS - Time to Event

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

Percentage of Participants With Clinical Benefit of CR, PR, or Stable Disease (SD)

Percentage of Participants With Complete Response (CR) or Partial Response (PR)

Time to CR - Percentage of Participants With an Event

Time to CR - Time To Event

Time to Overall Response of CR or PR - Percentage of Participants With an Event

Time to Overall Response of CR or PR - Time to Event

Time to Progression (TTP) - Percentage of Participants With an Event

Time to Treatment Failure (TTF) - Percentage of Participants With an Event

TTF - Time to Event

TTP - Time to Event

Overall Response Rate (ORR)

Overall Survival (OS)

Progression Free Survival (PFS)

Treatment Related Toxicity

Overall Survival (OS)

Percentage of Participants Alive 12 Months After Start of Treatment

Percentage of Participants Alive 30 Days After Last Dose of Study Drug

Percentage of Participants Alive 6 Months After Start of Treatment

Percentage of Participants Alive 9 Months After Start of Treatment

Percentage of Participants Who Were Alive and Progression Free 6 Months After Start of Treatment

Percentage of Participants With Corticosteroid Initiation During the Study Period

Percentage of Participants With Karnofsky Performance Status (KPS) Deterioration

Percentage of Participants With World Health Organization (WHO) Performance Status (PS) Deterioration

Progression-Free Survival (PFS)

Time to Corticosteroid Initiation

Time to Karnofsky Performance Status (KPS) Deterioration

Time to WHO PS Deterioration

Change From Screening in European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire-Core 30 (EORTC QLQ-C30) Scores at Weeks 8, 16, 24, 32, 40, 48, 56, 64, and 72

Percentage of Participants in Each Class of Corticosteroid Use

Percentage of Participants With a Best Overall Response of Complete Response (CR) or Partial Response (PR)

Related Drugs (89)

Related Conditions (160)