Page last updated: 2024-10-15

bl 4162a

Description

anagrelide: imidazoquinazoline derivative which lowers platelet count probably by inhibiting thrombopoiesis and reduces platelet aggregation; used for thrombocythemia; structure in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

anagrelide : A 1,5-dihydroimidazo[2,1-]quinazoline having an oxo substituent at the 2-position and chloro substituents at the 6- and 7-positions. [Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Cross-References

ID SourceID
PubMed CID135409400
CHEMBL ID760
CHEBI ID142290
SCHEMBL ID9411
MeSH IDM0075628

Synonyms (90)

Synonym
BIDD:GT0711
AC-3401
AB00698496-07
agrelin
xagrid
bl-4162a
6,7-dichloro-1,5-dihydroimidazo(2,1-b)quinazolin-2(3h)-one
anagrelide [inn:ban]
imidazo(2,1-b)quinazolin-2(3h)-one, 6,7-dichloro-1,5-dihydro-, monohydrochloride
imidazo(2,1-b)quinazolin-2(3h)-one, 6,7-dichloro-1,5-dihydro-
brn 0619582
anagrelida
hsdb 7325
6,7-dichlor-1,5-dihydroimidazo(2,1-b)chinazolin-2(3h)-on
anagrelida [inn-spanish]
anagrelidum [inn-latin]
bl 416201
68475-42-3
anagrelide (inn/ban)
D07455
DB00261
anagrelide
HMS2089D21
anagrelidum
CHEMBL760 ,
bdbm50000334
6,7-dichloro-1,5-dihydro-imidazo[2,1-b]quinazolin-2-one(bl-4162a)
6,7-dichloro-1,5-dihydro-imidazo[2,1-b]quinazolin-2-one(anagrelide)
6,7-dichloro-1,5-dihydro-imidazo[2,1-b]quinazolin-2-one
6,7-dichloro-5,10-dihydro-3h-imidazo[2,1-b]quinazolin-2-one
6,7-dichloro-1,5-dihydroimidazo[2,1-]quinazolin-2(3h)-one
CHEBI:142290 ,
NCGC00161408-02
NCGC00247665-01
unii-k9x45x0051
k9x45x0051 ,
6,7-dichloro-1,5-dihydroimidazo[2,1-b]quinazolin-2(3h)-one
FT-0602855
FT-0630776
BRD-K62200014-003-08-9
anagrelide [ema epar]
anagrelide [inn]
anagrelide [hsdb]
anagrelide [mi]
anagrelide [who-dd]
anagrelide [vandf]
AKOS015899342
AKOS016340524
gtpl7114
6,7-dichloro-3h,5h-imidazo[2,1-b]quinazolin-2-ol
CCG-221242
AB00698496-05
6,7-dichloro-1,5-dihydroimidazo[2,1-b]quinazolin-2[3h]-one
6,7-dichloro-1,5dihydroimidazo[2,1-b]quinazolin-2[3h]-one
OTBXOEAOVRKTNQ-UHFFFAOYSA-N
6,7-dichloro-1, 5-dihydroimidazo[2,1-b]quinazolin-2[3h]-one
6,7-dichloro-1,5-dihydroimidazo[2,1-b]-quinazolin-2(3h)-one
SCHEMBL9411
KS-5176
imidazo[2,1-b]quinazolin-2(3h)-one, 6,7-dichloro-1,5-dihydro-
6,7-dichloro-3,5-dihydroimidazo[2,1-b]quinazolin-2(1h)-one
6,7-dichloro-5,10-dihydroimidazo[2,1-b]quinazolin-2(3h)-one
AB01566808_01
AB00698496_08
6,7-dichloro-1h,2h,3h,5h-imidazolidino[2,1-b]quinazolin-2-one
mfcd00866794
6,7-dichloro-1h,5h-imidazo[2,1-b]quinazoline-2(3h)-one
SBI-0206823.P001
HMS3715J06
anagrelide(13c3)
BCP21314
Q408163
AS-14157
BRD-K62200014-003-05-5
NCGC00161408-08
HMS3742K13
A915719
6,7-di-chloro-1,5-dihydroimidazo[2,1-b]quinazolin-2[3 h ]-one base
j33 ,
6,7-bis(chloranyl)-3,5-dihydro-1h-imidazo[2,1-b]quinazolin-2-one
CS-0009495
EN300-187333
HY-B0523
6,7-dichloro-1,5-dihydroimidazo
anagrelida (inn-spanish)
l01xx35
6,7-dichloro-1,5-dihydroimidazo(2,1-)quinazolin-2(3h)-one
dtxcid6028280
anagrelidum (inn-latin)
6,7-dichloro-1,2,3,5-tetrahydroimidazo

Toxicity

ExcerptReference
"Anagrelide is efficacious and safe in ET, both for platelet and symptom control."( Efficacy, safety and tolerability of anagrelide in the treatment of essential thrombocythaemia.
Bashford, J; Brigden, MC; Bunce, I; Eliadis, P; Kelly, C; Mills, AK; Olsen, T; Rentoul, A; Seeley, G; Taylor, KM; Wright, SJ, 1999
)
"Side effects and toxic discontinuation rates were higher than in previous studies, probably because this is the first long-term prospective study of the feasibility and toxicity of anagrelide treatment."( Adverse effects and benefits of two years of anagrelide treatment for thrombocythemia in chronic myeloproliferative disorders.
Birgegård, G; Björkholm, M; Kutti, J; Lärfars, G; Löfvenberg, E; Markevärn, B; Mauritzson, N; Merup, M; Palmblad, J; Samuelsson, J; Westin, J, 2004
)
" Adverse events were documented in 46 patients (23."( Anagrelide for the treatment of thrombocythaemia in daily clinical practice: a post-marketing observational survey on efficacy and safety performed in Germany.
Schlag, R; Schmitz, S; Stauch, M, 2010
)
"6%) out of 232 ET patients experienced 88 cardiovascular adverse events (CV-AEs) during anagrelide treatment (522 pt-y)."( Low impact of cardiovascular adverse events on anagrelide treatment discontinuation in a cohort of 232 patients with essential thrombocythemia.
Cacciola, E; Cacciola, R; Candoni, A; Ciancia, R; Codeluppi, K; Crugnola, M; Grossi, A; Gugliotta, L; Iurlo, A; Liberati, AM; Lunghi, M; Martinelli, V; Mazzucconi, MG; Palmieri, F; Pierri, I; Scalzulli, PR; Specchia, G; Tieghi, A; Tortorella, G; Usala, E; Vannucchi, AM; Vianelli, N, 2011
)
" The most frequent adverse events (AEs) were headache (60 %) and palpitations (40 %)."( Cardiovascular safety of anagrelide in healthy subjects: effects of caffeine and food intake on pharmacokinetics and adverse reactions.
Datino, T; Fernández-Avilés, F; Figueiras-Graillet, L; Franklin, R; Gama, JG; Jones, C; Martínez-Sellés, M, 2013
)
" Adverse events were mild or moderate, and none led to discontinuation."( Open-label, dose-titration and continuation study to assess efficacy, safety, and pharmacokinetics of anagrelide in treatment-naïve Japanese patients with essential thrombocythemia.
Abhyankar, B; Hodgson, I; Kanakura, Y; Miyakawa, Y; Okamoto, S; Smith, J; Troy, S, 2013
)
" The most common adverse events observed during anagrelide treatment were anemia, headache, palpitations, and diarrhea."( Phase III, single-arm study investigating the efficacy, safety, and tolerability of anagrelide as a second-line treatment in high-risk Japanese patients with essential thrombocythemia.
Achenbach, H; Kanakura, Y; Miyakawa, Y; Okamoto, S; Smith, J; Wilde, P, 2014
)
" Frequency of anagrelide related adverse events was 65."( [Efficacy and safety of anagrelide in treatment of essential thrombocythemia: multicenter, randomized controlled clinical trial].
Cao, X; Fu, J; Gao, D; Ge, X; Hou, M; Jiang, B; Jin, J; Li, J; Li, K; Qian, W; Su, L; Sun, A; Wang, S; Wang, Z; Xiao, Z; Yang, L; Yang, R; Zhang, W; Zhang, X; Zhao, Y, 2015
)
" Incidence of adverse events was undifferentiated between anagrelide and hydroxyurea, but anagrelide treatment had tolerable adverse effects and no hematologic toxicity."( [Efficacy and safety of anagrelide in treatment of essential thrombocythemia: multicenter, randomized controlled clinical trial].
Cao, X; Fu, J; Gao, D; Ge, X; Hou, M; Jiang, B; Jin, J; Li, J; Li, K; Qian, W; Su, L; Sun, A; Wang, S; Wang, Z; Xiao, Z; Yang, L; Yang, R; Zhang, W; Zhang, X; Zhao, Y, 2015
)
"Data from 53 ET patients who received anagrelide as a first-line therapy were reviewed for patient characteristics, antiplatelet status, cytoreduction status, therapeutic effects, adverse events, thrombohemorrhagic event development, progression to myelofibrosis or acute leukemia, and cause of death."( Efficacy and safety of anagrelide as a first-line drug in cytoreductive treatment-naïve essential thrombocythemia patients in a real-world setting.
Fujita, S; Hashimoto, A; Hashimoto, Y; Hotta, M; Ishii, K; Ito, T; Kondo, T; Konishi, A; Nakanishi, T; Nakaya, A; Nomura, S; Omura, H; Satake, A; Shinzato, I; Tanaka, T; Tanaka, Y; Yoshimura, H, 2019
)
" The incidence of all adverse events(AEs)was higher in the ANA monotherapy(45."( Clinical Evaluation of the Efficacy and Safety of Anagrelide Used with or without Hydroxycarbamide in Japanese Patients with Essential Thrombocythemia-A Retrospective Single-Center Study of 35 Cases.
Fukuda, Y; Hamano, Y; Iizuka, H; Inano, T; Izumi, H; Nakamura, N; Noguchi, M; Okubo, M; Sakajiri, S; Sawada, T; Sekiguchi, Y; Sugimoto, K; Takizawa, H; Tomita, S; Wakabayashi, M, 2019
)
" Anaemia was the most common adverse event in patients receiving ruxolitinib (rates per 100 patient-years of exposure were 8·9 for ruxolitinib and 8·8 for the crossover population), though most anaemia events were mild to moderate in severity (grade 1 or 2 anaemia rates per 100 patient-years of exposure were 8·0 for ruxolitinib and 8·2 for the crossover population)."( Long-term efficacy and safety of ruxolitinib versus best available therapy in polycythaemia vera (RESPONSE): 5-year follow up of a phase 3 study.
Besses, C; Blau, IW; Dong, T; Durrant, S; Francillard, N; Griesshammer, M; Harrison, CN; Hino, M; Kiladjian, JJ; Kirito, K; Masszi, T; Mesa, R; Miller, CB; Moiraghi, B; Pane, F; Passamonti, F; Rosti, V; Rumi, E; Vannucchi, AM; Verstovsek, S; Wroclawska, M; Zachee, P, 2020
)
"We showed that ruxolitinib is a safe and effective long-term treatment option for patients with polycythaemia vera who are resistant to or intolerant of hydroxyurea."( Long-term efficacy and safety of ruxolitinib versus best available therapy in polycythaemia vera (RESPONSE): 5-year follow up of a phase 3 study.
Besses, C; Blau, IW; Dong, T; Durrant, S; Francillard, N; Griesshammer, M; Harrison, CN; Hino, M; Kiladjian, JJ; Kirito, K; Masszi, T; Mesa, R; Miller, CB; Moiraghi, B; Pane, F; Passamonti, F; Rosti, V; Rumi, E; Vannucchi, AM; Verstovsek, S; Wroclawska, M; Zachee, P, 2020
)
" There were no significant differences in adverse events between treatment groups, and no reports of malignant transformation."( Cardiovascular Safety of Anagrelide Hydrochloride versus Hydroxyurea in Essential Thrombocythaemia.
Achenbach, H; Egyed, M; Gercheva, L; Gotic, M; Kvasnicka, HM; Warzocha, K; Wu, J, 2021
)
"3% experienced adverse drug reactions (ADRs)."( Safety and efficacy of anagrelide in Japanese post-marketing surveillance, with subgroup analyses on the effect of previous cytoreductive therapies, age, and starting dose.
Akimoto, T; Baba, T; Fernandez, J; Hashimoto, Y; Komatsu, N; Otsuka, M, 2022
)
" Treatment-emergent adverse events-including headaches, cardiac palpitations and arrhythmias, nausea, vomiting and/or diarrhea-led to ANA discontinuation in 76."( Anagrelide for platelet-directed cytoreduction in polycythemia vera: Insights into utility and safety outcomes from a large multi-center database.
Fleischman, A; Gotlib, J; Heaney, M; Hoffman, R; Kremyanskaya, M; Kuykendall, A; Mascarenhas, J; Mesa, R; O'Connell, C; Podoltsev, N; Rippel, N; Shammo, JM; Tremblay, D; Yacoub, A; Zubizarreta, N, 2022
)

Pharmacokinetics

ExcerptReference
" Because the formulations and manufacturers differed, the differences in tolerability, as well as platelet counts, might have been related to differences in pharmacokinetic properties between the 2 formulations."( Pharmacokinetics, bioequivalence, tolerability, and effects on platelet counts of two formulations of anagrelide in healthy volunteers and patients with thrombocythemia associated with chronic myeloproliferation.
Gisslinger, H; Krumpl, G; Linkesch, W; Petrides, PE; Schüller, A; Steurer, M; Widmann, R, 2009
)
"The present series of investigations (1) determined the pharmacokinetic profile of anagrelide and its metabolites; (2) compared the pharmacokinetic profiles of the test and reference formulations of anagrelide; (3) investigated the in vitro release of anagrelide as a marker of intragastric anagrelide release of the test and reference formulations; and (4) compared the platelet-reducing effects of the test and reference formulations in patients with thrombocythemia in 2 longitudinal studies over 4 weeks."( Pharmacokinetics, bioequivalence, tolerability, and effects on platelet counts of two formulations of anagrelide in healthy volunteers and patients with thrombocythemia associated with chronic myeloproliferation.
Gisslinger, H; Krumpl, G; Linkesch, W; Petrides, PE; Schüller, A; Steurer, M; Widmann, R, 2009
)
" In a pilot, prospective, singledose study in healthy volunteers, the pharmacokinetic properties (C(max), T(max), and AUC(0-infinity)) of a test formulation of anagrelide were assessed using high-performance liquid chromatography analysis of plasma samples."( Pharmacokinetics, bioequivalence, tolerability, and effects on platelet counts of two formulations of anagrelide in healthy volunteers and patients with thrombocythemia associated with chronic myeloproliferation.
Gisslinger, H; Krumpl, G; Linkesch, W; Petrides, PE; Schüller, A; Steurer, M; Widmann, R, 2009
)
"The pilot pharmacokinetic study of the test formulation in 16 volunteers (10 women, 6 men; mean [SD] age, 20."( Pharmacokinetics, bioequivalence, tolerability, and effects on platelet counts of two formulations of anagrelide in healthy volunteers and patients with thrombocythemia associated with chronic myeloproliferation.
Gisslinger, H; Krumpl, G; Linkesch, W; Petrides, PE; Schüller, A; Steurer, M; Widmann, R, 2009
)
"The pharmacokinetic properties, adverse event rates, and in vitro dissolution profile differed between the test and reference anagrelide formulations in these healthy volunteers."( Pharmacokinetics, bioequivalence, tolerability, and effects on platelet counts of two formulations of anagrelide in healthy volunteers and patients with thrombocythemia associated with chronic myeloproliferation.
Gisslinger, H; Krumpl, G; Linkesch, W; Petrides, PE; Schüller, A; Steurer, M; Widmann, R, 2009
)
" Three days prior to pharmacokinetic assessment, patients divided their normal daily anagrelide into a structured twice-daily dosing (BID) schedule."( Pharmacokinetics and tolerability of anagrelide hydrochloride in young (18 - 50 years) and elderly (≥ 65 years) patients with essential thrombocythemia.
Alvarez-Larrán, A; Besses, C; Coll, R; Freitag, C; Martin, P; Purkayastha, J; Troy, S; Zeller, W, 2012
)
" This cohort of Japanese patients exhibited higher pharmacokinetic exposures of anagrelide and its active metabolite than those previously documented in non-Japanese patients."( Open-label, dose-titration and continuation study to assess efficacy, safety, and pharmacokinetics of anagrelide in treatment-naïve Japanese patients with essential thrombocythemia.
Abhyankar, B; Hodgson, I; Kanakura, Y; Miyakawa, Y; Okamoto, S; Smith, J; Troy, S, 2013
)

Bioavailability

ExcerptReference
"4 microM) inhibitory activities, was found to be orally bioavailable with a long duration of action and offered effective protection against mortality in a collagen-epinephrine-induced pulmonary thromboembolism model in mice."( 3,4-Dihydroquinolin-2(1H)-ones as combined inhibitors of thromboxane A2 synthase and cAMP phosphodiesterase.
Bruno, JJ; Hirschfeld, DR; Maloney, PJ; Martinez, GR; Walker, KA; Yang, DS, 1992
)
" Anagrelide is metabolized by cytochrome P450 (CYP) 1A2, and previous studies of the effect of food on the bioavailability and pharmacokinetics of anagrelide were conducted prior to the identification of the active metabolite, 3-hydroxyanagrelide."( Cardiovascular safety of anagrelide in healthy subjects: effects of caffeine and food intake on pharmacokinetics and adverse reactions.
Datino, T; Fernández-Avilés, F; Figueiras-Graillet, L; Franklin, R; Gama, JG; Jones, C; Martínez-Sellés, M, 2013
)
" Bioavailability of AER was 55% of the CARP under fasting conditions and 60% under fed conditions."( Pharmacokinetics of a Novel Anagrelide Extended-Release Formulation in Healthy Subjects: Food Intake and Comparison With a Reference Product.
Jilma, B; Klade, CS; Petrides, PE; Schoergenhofer, C; Widmann, R, 2018
)
"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
)

Dosage Studied

ExcerptReference
" 7e, 9e, 13a, 13d, 18, 20, 21, and 23, when dosed orally in conscious spontaneously hypertensive rats."( 3,4-Dihydroquinolin-2(1H)-ones as combined inhibitors of thromboxane A2 synthase and cAMP phosphodiesterase.
Bruno, JJ; Hirschfeld, DR; Maloney, PJ; Martinez, GR; Walker, KA; Yang, DS, 1992
)
" Ester 11b, acid 12b, amide 13d, and sulfone 29c protected against thrombus formation in two different animal models following oral dosing and were found to be superior to anagrelide (2) and BMY 20844 (5)."( Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
Baryla, UM; Buchanan, JO; Gamberdella, M; Gillespie, E; Meanwell, NA; Pearce, BC; Roth, HR; Smith, EC; Wedding, DL; Wright, JJ, 1992
)
" Because current dosing guidelines for anagrelide are scarce, the dosing method of the Anagrelide Study Group that published the largest study to date on the drug's efficacy in thrombocytosis was followed."( Precipitous fall in platelet count with anagrelide: case report and critique of dosing recommendations.
Liles, D; Lindley, C; McCune, JS,
)
"The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of anagrelide are reviewed."( Anagrelide, a selective thrombocytopenic agent.
Oertel, MD, 1998
)
" Anticipatory changes in hydroxyurea dosage or the maintenance of a constant dose did not abolish periodicity, but a change in therapy to the non-cycle-specific drug anagrelide dampened and abolished the cycling."( Hydroxyurea and periodicity in myeloproliferative disease.
Bennett, M; Grunwald, AJ, 2001
)
"Anagrelide was introduced with gradually higher dosage, while the dosage of hydroxyurea was gradually reduced."( [Anagrelide in primary thrombocythemia].
Hysing, J; Knutsen, H, 2001
)
" Anagrelide offers the advantage of oral dosing and long-term effectiveness at managing platelet counts."( Indications for lowering platelet numbers in essential thrombocythemia.
Barbui, T, 2003
)
" Dosage was titrated to achieve a platelet count < 600 x 10(9) L(-1) and ideally between 130 and 450 x 10(9) L(-1)."( Anagrelide: analysis of long-term efficacy, safety and leukemogenic potential in myeloproliferative disorders.
Fiddler, G; Fruchtman, SM; Gilbert, HS; Lyne, A; Petitt, RM, 2005
)
"Parallel dose-response effects were found in both CD41(+) number and TPO-specific pTyr activity."( A preliminary investigation into the action of anagrelide: thrombopoietin-c-Mpl receptor interactions.
Dessypris, EN; Kanamori, D; McCarty, JM; Melone, PD; Simanis, JP; Warshamana-Greene, GS, 2006
)
" However, the response rates of IFN-alpha therapy frequently have been hampered by high dropout rates due to side effects and inconvenient dosing schedules."( Pegylated interferon therapy for patients with Philadelphia chromosome-negative myeloproliferative disorders.
Giles, F; Kantarjian, HM; Quintás-Cardama, A; Verstovsek, S, 2006
)
" This is likely to be due to lack of radical corrections in the dosage of the drug for different reasons."( [What is the current treatment of patients with essential thrombocytopenia and other myeloproliferations accompanied with thrombocythemia [corrected] and what can be the predictive sign of the risk of thrombosis in such patients--a report from the registr
Brychtová, Y; Cerná, O; Doubek, M; Dulícek, P; Dusek, L; Hadacová, I; Hlusi, A; Hochová, I; Kissová, J; Pavlík, T; Penka, M; Pytiĺk, R; Schutzová, M; Schwarz, J; Seghetová, J; Szotkowski, T; Voglová, J; Volková, Z; Vozobulová, V,
)
" We think that in our case, the adverse response of anagrelide therapy was determined, by accumulated dosage of the drug, through an intensive inotropic stimulation and a sympathetic hyperactivation in a vulnerable myocardium."( Atypical Takotsubo syndrome during anagrelide therapy.
Ardizzone, F; Maccio, S; Proietti, R; Rognoni, A; Rognoni, G; Santagostino, A, 2009
)
" The current analysis focused mainly on evaluation of anagrelide dosage needed to achieve a complete response in high-risk patients: reduction in platelet count to below 400 x 10(9)/l, which was also considered as reaching the therapeutic goal."( [The results of patients with essentials thrombocythemia and other myeloproliferation-related thrombocythemia--a report of patients treated with Thromboreductin].
Bodzásová, C; Brychtová, Y; Cerná, O; Doubek, M; Dulícek, P; Dusek, L; Hadacová, I; Hlusí, A; Hochová, I; Indrák, K; Jelínková, P; Jonásová, A; Kissová, J; Korístek, Z; Nováková, L; Pavlík, T; Penka, M; Pospísilová, D; Schutzová, M; Schwarz, J; Segethová, J; Voglová, J; Vozobulová, V; Walterová, L, 2009
)
" All other treatments were continued with some dosage adjustments."( Management of refractory essential thrombocythemia with anagrelide in a patient undergoing hemodialysis.
Demulder, AC; Malarme, M; Mesquita, Mdo C; Noubouossie, D; Sol, EB, 2009
)
"To ascertain the role of patient age as an influencing factor in the pharmacokinetics of anagrelide and to clarify whether different dosing is required in young (18 - 50 years) vs."( Pharmacokinetics and tolerability of anagrelide hydrochloride in young (18 - 50 years) and elderly (≥ 65 years) patients with essential thrombocythemia.
Alvarez-Larrán, A; Besses, C; Coll, R; Freitag, C; Martin, P; Purkayastha, J; Troy, S; Zeller, W, 2012
)
" Three days prior to pharmacokinetic assessment, patients divided their normal daily anagrelide into a structured twice-daily dosing (BID) schedule."( Pharmacokinetics and tolerability of anagrelide hydrochloride in young (18 - 50 years) and elderly (≥ 65 years) patients with essential thrombocythemia.
Alvarez-Larrán, A; Besses, C; Coll, R; Freitag, C; Martin, P; Purkayastha, J; Troy, S; Zeller, W, 2012
)
"To conclude, the differences observed in anagrelide and 3-hydroxy-anagrelide pharmacokinetics do not justify using a different dosing regimen in young vs."( Pharmacokinetics and tolerability of anagrelide hydrochloride in young (18 - 50 years) and elderly (≥ 65 years) patients with essential thrombocythemia.
Alvarez-Larrán, A; Besses, C; Coll, R; Freitag, C; Martin, P; Purkayastha, J; Troy, S; Zeller, W, 2012
)
" We intended to identify the optimum dosage of anagrelide in treatment-naïve Japanese patients with ET and assess its long-term safety and efficacy."( Open-label, dose-titration and continuation study to assess efficacy, safety, and pharmacokinetics of anagrelide in treatment-naïve Japanese patients with essential thrombocythemia.
Abhyankar, B; Hodgson, I; Kanakura, Y; Miyakawa, Y; Okamoto, S; Smith, J; Troy, S, 2013
)
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
anticoagulantAn agent that prevents blood clotting.
platelet aggregation inhibitorA drug or agent which antagonizes or impairs any mechanism leading to blood platelet aggregation, whether during the phases of activation and shape change or following the dense-granule release reaction and stimulation of the prostaglandin-thromboxane system.
antifibrinolytic drugA drug that prevent fibrinolysis or lysis of a blood clot or thrombus.
cardiovascular drugA drug that affects the rate or intensity of cardiac contraction, blood vessel diameter or blood volume.
[role information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Drug Classes (1)

ClassDescription
imidazoquinazoline
[compound class information is derived from Chemical Entities of Biological Interest (ChEBI), Hastings J, Owen G, Dekker A, Ennis M, Kale N, Muthukrishnan V, Turner S, Swainston N, Mendes P, Steinbeck C. (2016). ChEBI in 2016: Improved services and an expanding collection of metabolites. Nucleic Acids Res]

Protein Targets (7)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
PPM1D proteinHomo sapiens (human)Potency0.08290.00529.466132.9993AID1347411
EWS/FLI fusion proteinHomo sapiens (human)Potency22.84650.001310.157742.8575AID1259252; AID1259253; AID1259255; AID1259256
euchromatic histone-lysine N-methyltransferase 2Homo sapiens (human)Potency19.95260.035520.977089.1251AID504332
Interferon betaHomo sapiens (human)Potency0.08290.00339.158239.8107AID1347411
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
cGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)IC50 (µMol)34.00000.00001.77679.2000AID158577; AID219326
cGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)IC50 (µMol)0.23270.00002.072410.0000AID158576; AID219160; AID219175; AID219178; AID219853; AID219979
cGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)IC50 (µMol)0.23270.00031.990110.0000AID158576; AID219160; AID219175; AID219178; AID219853; AID219979
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (71)

Processvia Protein(s)Taxonomy
heart valve developmentcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
ventricular septum developmentcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
aorta developmentcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
negative regulation of transcription by RNA polymerase IIcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
adenylate cyclase-inhibiting G protein-coupled receptor signaling pathwaycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
regulation of cGMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cAMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cGMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to macrophage colony-stimulating factor stimuluscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
negative regulation of vascular permeabilitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
positive regulation of vascular permeabilitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
regulation of cAMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cGMP catabolic processcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
positive regulation of inflammatory responsecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
establishment of endothelial barriercGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to mechanical stimuluscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to cAMPcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to cGMPcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to transforming growth factor beta stimuluscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
negative regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathwaycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cellular response to 2,3,7,8-tetrachlorodibenzodioxinecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
positive regulation of gene expressioncGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
negative regulation of cGMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
negative regulation of cAMP-mediated signalingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
regulation of mitochondrion organizationcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
angiogenesiscGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
negative regulation of cell adhesioncGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
G protein-coupled receptor signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
negative regulation of angiogenesiscGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
cellular response to insulin stimuluscGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
negative regulation of cell adhesion mediated by integrincGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
negative regulation of lipid catabolic processcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
negative regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
cAMP-mediated signalingcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
oocyte maturationcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
lipid metabolic processcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
G protein-coupled receptor signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
response to xenobiotic stimuluscGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cAMP-mediated signalingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cGMP-mediated signalingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
regulation of meiotic nuclear divisioncGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
negative regulation of apoptotic processcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
negative regulation of vascular permeabilitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
positive regulation of vascular permeabilitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
steroid hormone mediated signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
negative regulation of cAMP-mediated signalingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
positive regulation of oocyte developmentcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
regulation of ribonuclease activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cellular response to cGMPcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cellular response to transforming growth factor beta stimuluscGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
apoptotic signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
negative regulation of adenylate cyclase-activating G protein-coupled receptor signaling pathwaycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (21)

Processvia Protein(s)Taxonomy
magnesium ion bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cGMP-stimulated cyclic-nucleotide phosphodiesterase activitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
protein bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
zinc ion bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cAMP bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cGMP bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
TPR domain bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
phosphate ion bindingcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
protein homodimerization activitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
3',5'-cyclic-nucleotide phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
cGMP-inhibited cyclic-nucleotide phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
protein bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
protein kinase B bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
metal ion bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
3',5'-cyclic-nucleotide phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
3',5'-cyclic-AMP phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cGMP-inhibited cyclic-nucleotide phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
protein bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
nuclear estrogen receptor activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
metal ion bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
3',5'-cyclic-GMP phosphodiesterase activitycGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
estrogen bindingcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (16)

Processvia Protein(s)Taxonomy
plasma membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
nucleuscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cytoplasmcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
mitochondrial outer membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
mitochondrial inner membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
endoplasmic reticulumcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
Golgi apparatuscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cytosolcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
plasma membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
presynaptic membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
perinuclear region of cytoplasmcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
nucleuscGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
mitochondrial inner membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
perinuclear region of cytoplasmcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
mitochondrial outer membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
synaptic membranecGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
cytosolcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
mitochondrial matrixcGMP-dependent 3',5'-cyclic phosphodiesteraseHomo sapiens (human)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
endoplasmic reticulumcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
Golgi apparatuscGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
cytosolcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
membranecGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
guanyl-nucleotide exchange factor complexcGMP-inhibited 3',5'-cyclic phosphodiesterase BHomo sapiens (human)
cytosolcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
membranecGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
cytosolcGMP-inhibited 3',5'-cyclic phosphodiesterase AHomo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (121)

Assay IDTitleYearJournalArticle
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID174235Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg (6h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID225749Inhibition of adp-induced platelet aggregation in human platelet rich plasma.1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID165601Inhibition of platelet aggregation using Adenosine diphosphate (ADP) as activating agent in rabbit platelet rich plasma (PRP)1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID194038Effect on heart rate in rat after an oral dose at 50 mg/kg (3h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID161780In vitro inhibition of ADP-induced blood platelet aggregation1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID61948Inhibition of coronary artery occlusion (mean area under flow time curve) in anesthetized dog at 0.3 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID165602Inhibition of platelet aggregation using collagen as activating agent in rabbit platelet rich plasma (PRP)1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID166514Inhibition of thrombus formation (mean thrombus area) in conscious rabbits at 1.0 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID161781In vitro inhibition of collagen-induced blood platelet aggregation1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID219979Inhibition of platelet cAMP phosphodiesterase1988Journal of medicinal chemistry, Nov, Volume: 31, Issue:11
Inhibitors of cyclic AMP phosphodiesterase. 3. Synthesis and biological evaluation of pyrido and imidazolyl analogues of 1,2,3,5-tetrahydro-2-oxoimidazo[2,1-b]quinazoline.
AID225752Inhibition of platelet aggregation induced by collagen in rabbit platelet rich plasma1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID158577Inhibition of human platelet PDE by inhibiting cyclic Guanosine monophosphate (cGMP) hydrolysis1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID174232Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg (3h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID61946Inhibition of coronary artery occlusion (mean area under flow time curve) in anesthetized dog at 0.03 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID193724Ex vivo inhibition of collagen-induced blood platelet aggregation in rat was measured 2 hr after oral administration of 50 mg/kg1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID175857In vitro inhibition of blood platelet aggregation (collagen) in rats1985Journal of medicinal chemistry, Oct, Volume: 28, Issue:10
Cyclic guanidines. 17. Novel (N-substituted amino)imidazo[2,1-b]quinazolin-2 ones: water-soluble platelet aggregation inhibitors.
AID194039Effect on heart rate in rat after an oral dose at 50 mg/kg (4h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID166519Inhibition of thrombus formation (mean thrombus area) in conscious rabbits at 3.0 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID158576Inhibition of human platelet PDE by inhibiting cyclic Adenosine monophosphate (cAMP) hydrolysis1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID166517Inhibition of thrombus formation (mean thrombus area) in conscious rabbits at 10.0 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID225751Inhibition of platelet aggregation induced by ADP in rabbit platelet rich plasma1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID193277Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID477295Octanol-water partition coefficient, log P of the compound2010European journal of medicinal chemistry, Apr, Volume: 45, Issue:4
QSPR modeling of octanol/water partition coefficient of antineoplastic agents by balance of correlations.
AID193721Ex vivo inhibition of ADP-induced blood platelet aggregation in rat was measured 2 hr after administration of vehical alone (delta A/min *10e 3)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID219326Inhibition of cGMP hydrolysis by human platelet phosphodiesterase1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID92528Inhibition of platelet aggregation using adenosine diphosphate (ADP) as activating agent in human platelet rich plasma (PRP)1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID174227Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg (1h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID174229Effect of compound on systolic blood pressure in rat after an oral dose at 50 mg/kg (24h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID219995Inhibition of rat heart cAMP phosphodiesterase (weak partial inhibition)1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Inhibitors of cyclic AMP phosphodiesterase. 1. Analogues of cilostamide and anagrelide.
AID92096Inhibition of ADP-induced platelet aggregation1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Inhibitors of cyclic AMP phosphodiesterase. 1. Analogues of cilostamide and anagrelide.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID567091Drug absorption in human assessed as human intestinal absorption rate2011European journal of medicinal chemistry, Jan, Volume: 46, Issue:1
Prediction of drug intestinal absorption by new linear and non-linear QSPR.
AID1915712Inhibition of PDE2 (unknown origin)2021European journal of medicinal chemistry, Feb-05, Volume: 211Therapeutic progression of quinazolines as targeted chemotherapeutic agents.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID193723Ex vivo inhibition of collagen-induced blood platelet aggregation in rat was measured 2 hr after administration of vehical alone1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID194040Effect of compound on heart rate in rat after an oral dose at 50 mg/kg (5h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID194042Effect of compound on heart rate in rat after an oral dose at 50 mg/kg (6h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID194033Effect on heart rate in rat after an oral dose at 50 mg/kg (1h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID61947Inhibition of coronary artery occlusion (mean area under flow time curve) in anesthetized dog at 0.1 mg/kg1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID219160Inhibition of human platelet c-AMP phosphodiesterase PDE 31992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 3. 1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-one derivatives with enhanced aqueous solubility.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID174233Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg (4h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID219175Inhibition of human blood platelet c-AMP phosphodiesterase1992Journal of medicinal chemistry, Feb-21, Volume: 35, Issue:4
3,4-Dihydroquinolin-2(1H)-ones as combined inhibitors of thromboxane A2 synthase and cAMP phosphodiesterase.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID193720Ex vivo inhibition of ADP-induced blood platelet aggregation in rat was measured 2 hr after administration of vehical alone1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID185811Effect on heart rate in rat after an oral dose at 50 mg/kg1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID174234Effect on systolic blood pressure in rat after an oral dose at 50 mg/kg (5h after dose)1981Journal of medicinal chemistry, Apr, Volume: 24, Issue:4
Cyclic guanidines. 14. Imidazo[1,2-a]thienopyrimidin-2-one derivatives as blood platelet aggregation inhibitors.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID225747Ex vivo inhibition of rat platelet aggregation induced by ADP.1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID175856In vitro inhibition of blood platelet aggregation (ADP) in rats1985Journal of medicinal chemistry, Oct, Volume: 28, Issue:10
Cyclic guanidines. 17. Novel (N-substituted amino)imidazo[2,1-b]quinazolin-2 ones: water-soluble platelet aggregation inhibitors.
AID219853In vitro inhibition of cyclic AMP phosphodiesterase from human platelets.1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Inhibitors of cyclic AMP phosphodiesterase. 1. Analogues of cilostamide and anagrelide.
AID219178Inhibition of hydrolysis of c-AMP phosphodiesterase in human platelets1991Journal of medicinal chemistry, Sep, Volume: 34, Issue:9
1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-ones--inhibitors of blood platelet cAMP phosphodiesterase and induced aggregation.
AID183710Ex vivo inhibition of blood platelet aggregation (collagen) in rats at oral dose 10 mg/kg 1 hour before the test1985Journal of medicinal chemistry, Oct, Volume: 28, Issue:10
Cyclic guanidines. 17. Novel (N-substituted amino)imidazo[2,1-b]quinazolin-2 ones: water-soluble platelet aggregation inhibitors.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID183707Ex vivo in vitro inhibition of blood platelet aggregation (ADP) in rats at oral dose 10 mg/kg 1 hour before the tes1985Journal of medicinal chemistry, Oct, Volume: 28, Issue:10
Cyclic guanidines. 17. Novel (N-substituted amino)imidazo[2,1-b]quinazolin-2 ones: water-soluble platelet aggregation inhibitors.
AID92673Compound was evaluated for the inhibition of ADP-induced aggregation of human platelets1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 3. 1,3-Dihydro-2H-imidazo[4,5-b]quinolin-2-one derivatives with enhanced aqueous solubility.
AID1296008Cytotoxic Profiling of Annotated Libraries Using Quantitative High-Throughput Screening2020SLAS discovery : advancing life sciences R & D, 01, Volume: 25, Issue:1
Cytotoxic Profiling of Annotated and Diverse Chemical Libraries Using Quantitative High-Throughput Screening.
AID1347083qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: Viability assay - alamar blue signal for LASV Primary Screen2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347101qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-12 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347107qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh30 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1508630Primary qHTS for small molecule stabilizers of the endoplasmic reticulum resident proteome: Secreted ER Calcium Modulated Protein (SERCaMP) assay2021Cell reports, 04-27, Volume: 35, Issue:4
A target-agnostic screen identifies approved drugs to stabilize the endoplasmic reticulum-resident proteome.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347094qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for BT-37 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347104qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for RD cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347098qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-SH cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
AID1347102qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh18 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347099qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB1643 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347108qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Rh41 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347106qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for control Hh wild type fibroblast cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347090qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for DAOY cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1347095qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for NB-EBc1 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347105qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for MG 63 (6-TG R) cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347091qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SJ-GBM2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347089qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for TC32 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347093qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for SK-N-MC cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347082qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lassa (LASV) Arenavirus: LASV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347096qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for U-2 OS cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347092qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for A673 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1345205Human phosphodiesterase 3A (Phosphodiesterases, 3',5'-cyclic nucleotide (PDEs))1992Journal of medicinal chemistry, Feb-21, Volume: 35, Issue:4
3,4-Dihydroquinolin-2(1H)-ones as combined inhibitors of thromboxane A2 synthase and cAMP phosphodiesterase.
AID1345205Human phosphodiesterase 3A (Phosphodiesterases, 3',5'-cyclic nucleotide (PDEs))1987Journal of medicinal chemistry, Feb, Volume: 30, Issue:2
Inhibitors of cyclic AMP phosphodiesterase. 1. Analogues of cilostamide and anagrelide.
AID1345205Human phosphodiesterase 3A (Phosphodiesterases, 3',5'-cyclic nucleotide (PDEs))1992Journal of medicinal chemistry, Jul-10, Volume: 35, Issue:14
Inhibitors of blood platelet cAMP phosphodiesterase. 2. Structure-activity relationships associated with 1,3-dihydro-2H-imidazo[4,5-b]quinolin-2-ones substituted with functionalized side chains.
AID1347411qHTS 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) Libary2020ACS 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.
AID1347414qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Secondary screen by immunofluorescence2020ACS 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.
AID1347412qHTS assay to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: Counter screen cell viability and HiBit confirmation2020ACS 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.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (313)

TimeframeStudies, This Drug (%)All Drugs %
pre-199021 (6.71)18.7374
1990's40 (12.78)18.2507
2000's127 (40.58)29.6817
2010's96 (30.67)24.3611
2020's29 (9.27)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials41 (12.35%)5.53%
Reviews83 (25.00%)6.00%
Case Studies69 (20.78%)4.05%
Observational5 (1.51%)0.25%
Other134 (40.36%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]