Compounds > imatinib mesylate
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imatinib mesylate

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Description

imatinib methanesulfonate : A methanesulfonate (mesylate) salt that is the monomesylate salt of imatinib. Used for treatment of chronic myelogenous leukemia and gastrointestinal stromal tumours. [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 CID123596
CHEMBL ID1642
CHEBI ID31690
SCHEMBL ID8217
MeSH IDM0391958

Synonyms (133)

Synonym
AC-525
HY-50946
imatinib (mesylate)
HMS3394B09
gleevec
glivec
cgp 57148b
220127-57-1
nsc716051
4-(4-methyl-piperazin-1-ylmethyl)-n-[4-methyl-3-(4-pyridin- 3-yl)-pyrimidin-2-ylamino)-phenyl]-benzamidemethanesulfonic acid salt
ggp-57148b
qti-571
cgp-57148
hsdb 7142
benzamide, 4-((4-methyl-1-piperazinyl)methyl)-n-(4-methyl-3-((4-(3-pyridinyl)-2-pyrimidinyl)amino)phenyl)-, monomethanesulfonate
sti-571
smr000469175
MLS001401456
NCGC00159456-02
imatinib mesylate ,
sti 571
benzamide,monomethanesulfonate
imatinib mesilate
nsc-716051
gleevac
imatinib, methanesulfonate salt
D01441
gleevec (tn)
glivec (tn)
imatinib mesilate (jan)
imatinib mesylate (usan)
cgp57148b
imatinib methanesulfonate
imatinib methansulfonate
4-[(4-methylpiperazin-1-yl)methyl]-n-{4-methyl-3-[(4-pyridin-3-ylpyrimidin-2-yl)amino]phenyl}benzamide methanesulfonate
imatinib monomesylate
CHEBI:31690 ,
4-[(4-methylpiperazin-1-yl)methyl]-n-(4-methyl-3-{[4-(pyridin-3-yl)pyrimidin-2-yl]amino}phenyl)benzamide methanesulfonate
HMS2052B09
111GE005
methanesulfonic acid; 4-[(4-methylpiperazin-1-yl)methyl]-n-[4-methyl-3-[(4-pyridin-3-ylpyrimidin-2-yl)amino]phenyl]benzamide
EC-000.2338
imatinib (as mesilate)
qti571
imatinib accord
imatinib methane sulfonate
CHEMBL1642
imatinib medac
cas-220127-57-1
tox21_111684
dtxcid7020502
dtxsid9040502 ,
A815828
methanesulfonic acid; 4-[(4-methyl-1-piperazinyl)methyl]-n-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]benzamide
4-[(4-methyl-1-piperazinyl)methyl]-n-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-benzamide monomethanesulfonate
cgp-57148b
HMS2233D16
CCG-101175
BCP9000776
imatinib monomethanesulfonate
8a1o1m485b ,
unii-8a1o1m485b
imatinib mesylate [usan]
nsc 716051
shantinib
HMS3265F02
HMS3265F01
HMS3265E01
HMS3265E02
BCPP000204
imatinib mesylate,gleevec,glivec,cgp-57148b,sti-571
FT-0601612
imatinib mesylate [hsdb]
imatinib mesilate [who-dd]
imatinib mesylate [orange book]
imatinib mesylate [vandf]
imatinib mesilate [jan]
imatinib methanesulfonate [mi]
imatinib mesilate [mart.]
benzamide, 4-((4-methyl-1-piperazinyl)methyl)-n-(4-methyl-3-((4-(3-pyridinyl)-2-pyrimidinyl)aminophenyl)-, methanesulphonate salt
benzamide, 4-((4-methyl-1-piperazinyl)methyl)-n-(4-methyl-3-((4-(3-pyridinyl)-2-pyrimidinyl)aminophenyl)-, methanesulfonate salt
imatinib mesilate [ep monograph]
n-(4-methyl-3-(4-(pyridin-3-yl)pyrimidin-2-ylamino)phenyl)-4-((4-methylpiperazin-1-yl)methyl)benzamide methanesulfonate
;4-[(4-methylpiperazin-1-yl)methyl]-n-[4-methyl-3-[(4-pyridin-3-ylpyrimidin-2-yl)amino]phenyl]benzamide methanesulfonate
S1026
AKOS015852497
benzamide, 4-[(4-methyl-1-piperazinyl)methyl]-n-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]-, methanesulfonate (1:1)
AM20080900
HMS3372O12
YLMAHDNUQAMNNX-UHFFFAOYSA-N
4-[(4-methyl-1-piperazinyl)-methyl]-n-{4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]-amino]-phenyl}-benzamide monomethanesulphonate
NC00425
SCHEMBL8217
tox21_111684_1
NCGC00159456-11
KS-1236
mfcd04307699
4-[(4-methyl-1-piperazinyl)methyl]-n-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]-phenyl]benzamide methanesulfonate
Q-201232
gleevec (imatinib mesylate)
n-(4-methyl-3-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)phenyl)-4-((4-methylpiperazin-1-yl)methyl)benzamide methanesulfonate
I0936
imatinib mesylate (sti571)
imatinibmesylate
J-523068
methanesulfonate, imatinib
mesylate, imatinib
EX-A954
st-1571 mesylate
HMS3654C07
4-[(4-methyl-1-piperazinyl)methyl]-n-[4-methyl-3-[[4-(3-pyridinyl)-2-pyrimidinyl]amino]phenyl]benzamide methanesulfonate
SY013513
SW197805-4
imatinib(free base)
220127-57-1 (mesylate)
Q27114666
BCP01255
4-(4-methylpiperazin-1-ylmethyl)-n-[4-methyl-3-(4-pyridin-3-yl-pyrimidin-2-ylamino)phenyl]benzamide methanesulfonic acid salt
A846640
imatinib methanesulfonate salt
M06311
genfatinib
n-(4-methyl-3-((4-(pyridin-3-yl)pyrimidin-2-yl)amino)phenyl)-4-((4-methylpiperazin-1-yl)methyl)benzamidemethanesulfonate
hydron;methanesulfonate;4-[(4-methylpiperazin-1-yl)methyl]-n-[4-methyl-3-[(4-pyridin-3-ylpyrimidin-2-yl)amino]phenyl]benzamide
imatinib mesylate (cgp-57148b, sti-571)
BI164678
c29h31n7o.ch4o3s
HB1943
4-((4-methylpiperazin-1-yl)methyl)-n-(4-methyl-3-((4-pyridin-3-ylpyrimidin-2-yl)amino)phenyl)benzamide methanesulfonate
4-((4-methyl-1-piperazinyl)methyl)-n-(4-methyl-3-((4-(3-pyridinyl)-2-pyrimidinyl)amino)phenyl)benzamide monomethanesulfonate
imatinib mesilate (ep monograph)
imatinib mesylate400 mg
imatinib mesilate (mart.)

Research Excerpts

Overview

Imatinib mesylate (IM) is a first-line treatment option for patients with chronic myeloid leukemia (CML) IM is expected to alleviate inflammation by inhibiting discoidin domain receptor 1 activity. Imatinib Mesylate is a molecularly targeted tyrosine kinase inhibitor drug.

ExcerptReferenceRelevance
"Imatinib mesylate is a potent tyrosine kinase inhibitor that may induce immunological effects, such as inhibition of immune suppressive cells; but, how it modulates the immune system remains to be completely elucidated. "( Imatinib Mesylate Exerted Antitumor Effect by Promoting Infiltration of Effector T Cells in Tumor.
Aoki, K; Henmi, M; Hirata, A; Mizoguchi, Y; Narumi, K; Sawai, E; Shibasaki, C, 2022)		3.61
"Imatinib mesylate is a novel ophthalmic formulation of imatinib mesylate, which is expected to alleviate inflammation by inhibiting the discoidin domain receptor 1 activity."( Safety, tolerability, and pharmacokinetics of single and multiple topical ophthalmic administration of imatinib mesylate in healthy subjects.
Chung, JY; Huh, KY; Hyon, JY; Koo, HC; Lee, JH; Na, JY; You, JC; Yu, KS, 2022)		1.66
"Imatinib mesylate is a first-generation tyrosine kinase inhibitor. "( Occupational allergic contact dermatitis to Piperamido Nitrotoluene in pharmaceutical workers: A case series.
Bourke, JF; Hollywood, A, 2022)		2.16
"Imatinib mesylate (IM) is a reliable first line treatment for chronic myeloid leukaemia (CML). "( Association of
Alimirzoyeva, Z; Asadov, C; Bayramov, B; Hasanova, A; Karimova, N; Shirinova, A, 2023)		2.35
"Imatinib mesylate (IM) is a first-line treatment option for patients with chronic myeloid leukemia (CML). "( Cost effectiveness of therapeutic drug monitoring for imatinib administration in chronic myeloid leukemia.
Bernard, PS; Kim, K; McMillin, GA; Schmidt, RL; Tantravahi, S; Walker, BS, 2019)		1.96
"Imatinib mesylate is a well-known tyrosine kinase inhibitor used to treat chronic myeloid leukemia, gastrointestinal stromal tumor, as well as a variety of other malignancies."( Hyperpigmentation due to imatinib: A rare case of cutaneous involvement.
Hakim, N; Rehman, H; Saif, MW; Seetharamu, N; Sugarman, R, 2020)		2
"Imatinib mesylate is a molecularly targeted tyrosine kinase inhibitor drug. "( Aberrant DNA methylation at HOXA4 and HOXA5 genes are associated with resistance to imatinib mesylate among chronic myeloid leukemia patients.
Ankathil, R; Azlan, H; Baba, AA; Elias, MH; Sulong, S, 2018)		2.15
"Imatinib mesylate is a tyrosine kinase inhibitor used as a first-line medication in the management of oncohematological conditions such as chronic myeloid leukemia and gastrointestinal stromal tumors."( The blue palate-A case series of imatinib-related oral pigmentation and literature review.
Carrozzo, M; Donnell, CC; Walton, RL, 2021)		1.34
"Imatinib mesylate (IM) is an anticancer drug that belongs to tyrosine kinase inhibitors. "( Deregulation of whole-transcriptome gene expression in zebrafish (Danio rerio) after chronic exposure to low doses of imatinib mesylate in a complete life cycle study.
Baebler, Š; Bakos, K; Csenki, Z; Filipič, M; Gajski, G; Garaj-Vrhovac, V; Gazsi, G; Gerić, M; Horváth, Á; Kovács, R; Novak, M; Rotter, A; Žegura, B, 2021)		2.27
"Imatinib mesylate is a tyrosine-kinase inhibitor mainly used in the treatment of blood cancers, frequently in multidrug therapy with cyclophosphamide."( Spectroscopic studies of simultaneous binding of cyclophosphamide and imatinib mesylate to human holo-transferrin.
Śliwińska-Hill, U, 2021)		1.58
"Imatinib mesylate is a tyrosine kinase inhibitor used in the treatment of a variety of oncological conditions. "( Imatinib-induced eruptive nevi.
Abbas, O; Hamie, L; Sawaya, RT, 2021)		2.06
"Imatinib mesylate is an effective treatment for chronic myelogenous leukemia and gastrointestinal stromal tumors. "( Sab mediates mitochondrial dysfunction involved in imatinib mesylate-induced cardiotoxicity.
Chambers, JW; Chambers, TP; Gomez, D; Santiesteban, L, 2017)		2.15
"Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor initially approved by the US Food and Drug Administration in 2001 for chronic myeloid leukemia (CML). "( Imatinib mesylate-induced lichenoid drug eruption.
Chung, HJ; Keller, M; Penn, EH, 2017)		3.34
"Imatinib mesylate is a tyrosine kinase inhibitor used in the treatment of oncological conditions, including chronic myeloid leukemia and gastrointestinal stromal tumors. "( A case series of imatinib-induced generalized hypopigmentation and progression of existing acquired dermal melanocytosis.
Chen, Q; Chua, SH; Kok, WL; Lee, SSJ; Ng, SK, 2017)		1.9
"Imatinib mesylate is a tyrosine-kinase inhibitor used as the first-line treatment in chronic myeloid leukemia patients, but it is also indicated for other hematological diseases and solid tumors. "( Imatinib-induced diffuse hyperpigmentation of the oral mucosa, the skin, and the nails in a patient affected by chronic myeloid leukemia: report of a case and review of the literature.
Di Tullio, F; Mandel, VD; Padalino, C; Pellacani, G; Scotti, R, 2018)		1.92
"Imatinib mesylate (IM) is an anti-neoplasic drug used for the treatment of cancer. "( Characterization of imatinib mesylate formulations distributed in South American countries: Determination of genotoxic impurities by UHPLC-MS/MS and dissolution profile.
Comparsi Wagner, S; Dillenburg, TL; Linden, R; Venzon Antunes, M; Verza, SG; Wolff, FC, 2018)		2.25
"Imatinib mesylate is a tyrosine kinase inhibitor used in the treatment of several malignancies. "( Cystic acne due to imatinib therapy for chronic myelocytic leukemia.
Dasanu, CA; Del Rosario, M; Hwang, A; Iskandar, A, 2019)		1.96
"Imatinib mesylate is an anti‑neoplastic targeted chemotherapeutic agent, which can inhibit tyrosine kinase receptors, including BCR‑ABL, platelet‑derived growth factor receptors (PDGFRs) and c‑Kit. "( Antiproliferative effects of imatinib mesylate on ZR‑75‑1 and MDA‑MB‑231 cell lines via PDGFR‑β, PDGF‑BB, c‑Kit and SCF expression.
Aditya, A; Akbari Javar, H; Davoudi, ET; Ibrahim Noordin, M; Kadivar, A; Kamalidehghan, B; Sedghi, R, 2018)		2.21
"Imatinib mesylate is a tyrosine kinase inhibitor that binds to the Abelson tyrosine kinase and related proteins."( Effect of imatinib on plasma glucose concentration in subjects with chronic myeloid leukemia and gastrointestinal stromal tumor.
Aguayo-González, Á; Avila-Rojo, JA; Baquerizo-Burgos, JE; Coronel, MFC; Cuevas-Ramos, D; Gomez-Perez, FJ; Gómez-Sámano, MÁ; Gulias-Herrero, A; Molina-Botello, D; Palacios-Báez, L; Villanueva-Martinez, F; Wong-Campoverde, BD; Zentella-Dehesa, A, 2018)		1.2
"Imatinib mesylate (imatinib) is a classic tyrosine kinase inhibitor used to treat chronic myeloid leukemia. "( Imatinib-induced irreversible interstitial lung disease: A case report.
Huang, J; Jin, F; Ouyang, G; Pan, J; Zhang, P, 2019)		1.96
"Imatinib mesylate is an anticancer agent that inhibits competitively several receptor tyrosine kinases (RTKs)."( Imatinib mesylate does not counteract ovarian tissue fibrosis in postnatal rat ovary.
Asadi-Azarbaijani, B; Braber, S; Jahnukainen, K; Oskam, I; Santos, R; van Duursen, M, 2019)		2.68
"Imatinib mesylate is a selective inhibitor of this tyrosine kinase."( Mutations Associated with Imatinib Mesylate Resistance - Review.
Goranova-Marinova, VS; Ivanov, HJ; Ivanova, H; Linev, AJ; Stoyanova, VK; Zhelyazkov, IG, 2018)		1.5
"Imatinib mesylate is a potent inhibitor of the platelet-derived growth factor receptor (PDGFR) and its activity has been tested in preclinical models and in Phase I and II clinical trials."( Imatinib and prostate cancer: lessons learned from targeting the platelet-derived growth factor receptor.
Mathew, P; Rosenberg, A, 2013)		1.11
"Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL, c-kit, and PDGF (platelet-derived growth factor) receptors. "( Adverse skin effects of imatinib, a tyrosine kinase inhibitor.
Ormaechea-Pérez, N; Pretel-Irazabal, M; Tuneu-Valls, A, 2014)		1.85
"Imatinib mesylate is a selective protein tyrosine kinase inhibitor, which can inhibit BCR/Abl, PDGF-R, c-KIT, c-fms, TCR/Abl, Lck, FLT-3 and MAPKs activities on various cell types. "( Imatinib mesylate: an innovation in treatment of autoimmune diseases.
Azizi, G; Mirshafiey, A, 2013)		3.28
"Imatinib mesylate (IM) is a potent and specific tyrosine inhibitor and has been reported to inhibit mesenchymal cell proliferation in pulmonary fibrosis. "( Effects of imatinib mesylate on pulmonary allergic vasculitis in a murine model.
Nagashima, H; Nakamura, Y; Sasaki, N; Sawai, T; Suzuki, N; Utsumi, Y; Yamashita, M; Yamauchi, K, 2013)		2.22
"Imatinib mesylate is a selective tyrosine kinase inhibitor used in the treatment of chronic myelogenous leukemia. "( Imatinib-induced postoperative periorbital purpura: GASP (Gleevec-Associated Surgical Purpura) in a woman with imatinib-treated chronic myelogenous leukemia.
Anzalone, CL; Cohen, PR; Cortes, JE; Kurzrock, R, 2014)		1.85
"Imatinib mesylate is a specific tyrosine kinase inhibitor that may block the platelet-derived growth factor and transforming growth factor pathways. "( Imatinib mesylate attenuates myocardial remodeling through inhibition of platelet-derived growth factor and transforming growth factor activation in a rat model of hypertension.
Chang, K; Choo, EH; Ihm, SH; Jang, SW; Kim, HY; Kim, OR; Park, CS; Seung, KB, 2014)		3.29
"Imatinib mesylate is a selective protein tyrosine kinase inhibitor with immunomodulatory properties that abrogates multiple signal transduction pathways in immune cells."( Effects of imatinib mesylate in mouse models of multiple sclerosis and in vitro determinants.
Azizi, G; Haidari, MR; Javanbakht, MH; Khorramizadeh, M; Mirshafiey, A; Naddafi, F; Sadria, R; Sedaghat, R; Tofighi Zavareh, F, 2014)		1.51
"Imatinib mesylate is an inhibitor of kinase tyrosine that has proved to be useful in patients with chronic myeloid leukemia."( [Molecular response with triple therapy in patients with chronic myeloid leukemia].
López-Arroyo, JL; Portillo-García, ML; Rico-Ramos, HJ, )		0.85
"Imatinib mesylate is a selective tyrosine-kinase inhibitor used in the treatment of multiple cancers, most notably chronic myelogenous leukemia. "( Imatinib activates pathological hypertrophy by altering myocyte calcium regulation.
Barr, LA; Berretta, RM; Force, T; Gao, H; Houser, SR; Kubo, H; Makarewich, CA; Recchia, F; Troupes, CD; Woitek, F, 2014)		1.85
"Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets the BCR-ABL protein and induces hematological remission in patients with chronic myeloid leukemia (CML)."( Silencing of suppressor of cytokine signaling-3 due to methylation results in phosphorylation of STAT3 in imatinib resistant BCR-ABL positive chronic myeloid leukemia cells.
Al-Jamal, HA; Asan, JM; Hassan, R; Johan, MF; Jusoh, SA; Yong, AC, 2014)		1.12
"Imatinib mesylate is a tyrosine kinase inhibitor with selectivity for abelson tyrosine-protein kinase 1 (c-Abl), breakpoint cluster region (Bcr)-Abl fusion protein (Bcr-Abl), mast/stem cell growth factor receptor Kit (c-Kit), and platelet-derived growth factor receptor (PDGFR). "( Exposure of neuroblastoma cell lines to imatinib results in the upregulation of the CDK inhibitor p27(KIP1) as a consequence of c-Abl inhibition.
Buccinnà, B; Lupino, E; Piccinini, M; Ramondetti, C, 2014)		1.85
"Imatinib mesylate is a multikinase inhibitor of several signaling pathways implicated in skin fibrosis with in vitro antifibrotic activity."( Imatinib mesylate for the treatment of steroid-refractory sclerotic-type cutaneous chronic graft-versus-host disease.
Baird, K; Booher, S; Comis, LE; Cowen, EW; Figg, WD; Flanders, KC; Hakim, FT; Joe, GO; Mitchell, SA; Pavletic, SZ; Rose, JJ; Sarantopoulos, S; Steinberg, SM; Takebe, N; Yao, L, 2015)		2.58
"Imatinib mesylate is a chemotherapeutic drug that inhibits the tyrosine kinase activity of c-KIT and has been successfully used to treat leukemias and some solid tumors. "( Paradoxical and contradictory effects of imatinib in two cell line models of hormone-refractory prostate cancer.
Cardoso, HJ; Correia, S; Figueira, MI; Maia, CJ; Marques, R; Socorro, S; Vaz, CV, 2015)		1.86
"Imatinib mesylate (IM) is a selective tyrosine kinase inhibitor for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors. "( Bioequivalence of a single 400-mg dose of imatinib 100-mg oral tablets and a 400-mg tablet in healthy adult Korean volunteers.
Gwon, MR; Kim, HJ; Kim, W; Lee, HW; Lee, J; Lim, MS; Lim, SM; Park, SM; Seong, SJ; Yang, DH; Yoon, YR, 2015)		1.86
"Imatinib mesylate is a competitive inhibitor of BCR/ ABL tyrosine kinase and inhibits also several receptor tyrosin kinases. "( [Potential clinical benefit of therapeutic drug monitoring of imatinib in oncology].
Demlová, R; Juřica, J; Turjap, M, 2015)		1.86
"Imatinib mesylate is an antineoplastic agent which has high absorption in the upper part of the gastrointestinal tract (GIT). "( Formulation and in vitro, in vivo evaluation of effervescent floating sustained-release imatinib mesylate tablet.
Chung, LY; Davoudi, ET; Javar, HA; Kadivar, A; Kamalidehghan, B; Noordin, MI; Sabeti, B; Zaharuddin, ND, 2015)		2.08
"Imatinib mesylate is a small-molecule tyrosine kinase inhibitor (TKi) designed to target c-ABL and BCR-ABL, approved for the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors. "( Possible Role of Interleukin-31/33 Axis in Imatinib Mesylate-Associated Skin Toxicity.
Allegra, A; Alonci, A; Calapai, G; Gangemi, S; Maisano, V; Mannucci, C; Musolino, C; Russo, S, 2015)		2.12
"Imatinib mesylate (IM) is a frontline treatment in the early chronic phase of chronic myeloid leukemia (CML). "( miR-101 sensitizes K562 cell line to imatinib through Jak2 downregulation and inhibition of NF-κB target genes.
Farhadi, E; Rezvani, MR; Safa, M; Zaker, F, 2016)		1.88
"Imatinib mesylate (IM) is a selective tyrosine kinase inhibitor and is approved for indefinite treatment of pediatric chronic myelogenous leukemia (CML). "( Adverse effects of imatinib in children with chronic myelogenous leukemia.
Charoenkwan, P; Choeyprasert, W; Natesirinilkul, R; Wejaphikul, K; Yansomdet, T, 2017)		1.9
"Imatinib mesylate (Imt) is a tyrosine kinase inhibitor mainly used in the treatment of Philadelphia chromosome-positive chronic myelogenous leukemia (Ph+CML). "( Interaction of imatinib mesylate with human serum transferrin: The comparative spectroscopic studies.
Śliwińska-Hill, U, 2017)		2.25
"Imatinib mesylate is an anti-cancer agent that competitively inhibits several receptor tyrosine kinases (RTKs). "( Developmental effects of imatinib mesylate on follicle assembly and early activation of primordial follicle pool in postnatal rat ovary.
Asadi-Azarbaijani, B; Braber, S; Jahnukainen, K; Nurmio, M; Oskam, IC; Santos, RR; Saugstad, OD; Toppari, J; van Duursen, MBM, 2017)		2.2
"Imatinib mesylate (IM) is a first-line treatment for chronic myeloid leukaemia (CML) as a specific inhibitor of BCR-ABL tyrosine kinase. "( Suppression of carboxylesterases by imatinib mediated by the down-regulation of pregnane X receptor.
Fan, H; Liu, C; Luo, W; Xi, T; Xin, Y; Xiong, J; Zhang, F; Zhao, X, 2017)		1.9
"Imatinib mesylate is a selective inhibitor of receptor tyrosine kinase, including PDGFR-β and c-Kit."( Antiproliferation effect of imatinib mesylate on MCF7, T-47D tumorigenic and MCF 10A nontumorigenic breast cell lines via PDGFR-β, PDGF-BB, c-Kit and SCF genes.
Akbari Javar, H; Kadivar, A; Kamalidehghan, B; Karimi, B; Noordin, MI; Sedghi, R, 2017)		1.47
"Imatinib mesylate is a tyrosine kinase inhibitor used as first line treatment in chronic myeloid leukemia and gastrointestinal stromal tumor patients. "( Development of hypogammaglobulinemia in patients treated with imatinib for chronic myeloid leukemia or gastrointestinal stromal tumor.
Alfieri, P; Arcari, A; Ferrari, A; Leonardi, G; Longo, G; Luppi, G; Maffei, R; Marasca, R; Martinelli, S; Piacentini, F; Santachiara, R; Torelli, G; Trabacchi, E; Vallisa, D, 2008)		1.79
"Imatinib mesylate is a small molecule targeted at dysregulated protein-tyrosine kinase. "( Effect of tyrosine kinase inhibition by imatinib mesylate on mast cell tumors in dogs.
Bonkobara, M; Fujino, Y; Fujita, M; Ishida, N; Isotani, M; Kato, R; Kobayashi, T; Ochi, S; Ono, K; Setoguchi, A; Tamura, K; Tominaga, M; Washizu, T; Yagihara, H, )		1.84
"Imatinib mesylate (IM) is a new drug which has been shown to induce complete hematological remission in 55% and complete cytogenetic response in 22% of the patients with CML in blast crisis."( Prophylaxis of central nervous system leukemia: a case of chronic myeloid leukemia with lymphoid blast crisis treated with imatinib mesylate.
Seth, R; Thavaraj, V, 2008)		1.27
"Imatinib mesylate is a tyrosine kinase inhibitor targeting the platelet-derived growth factor (PDGFR-alpha and PDGFR-beta), the BCR-ABL, and c-KIT receptors."( Brief report: activity of imatinib in a patient with platelet-derived-growth-factor receptor positive malignant solitary fibrous tumor of the pleura.
Agostini, M; Colombo, P; de Braud, F; De Pas, T; Manzotti, M; Pelosi, G; Toffalorio, F; Trifirò, G; Vigna, PD, 2008)		1.07
"Imatinib mesylate is a tyrosine kinase receptor inhibitor targeted against PDGFR alpha and beta, c-kit and bcr-abl. "( Combination of imatinib and vinorelbine enhances cell growth inhibition in breast cancer cells via PDGFR beta signalling.
Bauer, M; Bauerschlag, DO; Jonat, W; Maass, N; Meinhold-Heerlein, I; Mundhenke, C; Schem, C; Weigel, MT, 2009)		1.8
"Imatinib mesylate (imatinib) is a potent and selective inhibitor of the tyrosine kinases, Bcr-Abl, c-Kit and platelet-derived growth factor receptors (PDGFRs). "( Imatinib mesylate suppresses bone metastases of breast cancer by inhibiting osteoclasts through the blockade of c-Fms signals.
Hiraga, T; Nakamura, H, 2009)		3.24
"Imatinib mesylate is a recently developed oral anticancer agent designed to selectively inhibit tyrosine kinases implicated in oncogenesis and it seems to represent a promising opportunity (also in first line) in the treatment of patients with advanced disease not candidate to prior surgery."( Control of aggressive fibromatosis by treatment with imatinib mesylate: a step forward?
Nicoletti, S; Papi, M; Ravaioli, A; Tamburini, E, 2009)		1.32
"Imatinib mesylate is a potent, molecularly targeted therapy against the oncogenic tyrosine kinase BCR-ABL. "( Stat3 contributes to resistance toward BCR-ABL inhibitors in a bone marrow microenvironment model of drug resistance.
Bewry, NN; Boulware, D; Emmons, MF; Hazlehurst, LA; Nair, RR; Pinilla-Ibarz, J, 2008)		1.79
"Imatinib mesylate is a tyrosine kinase inhibitor used to treat chronic myeloid leukemia (CML) throughout all the phases of the disease. "( Skin and oral lesions associated to imatinib mesylate therapy.
Basso, FG; Boer, CC; Cintra, ML; Corrêa, ME; da Silva Santos, P; de Magalhães, MH; de Souza, CA; Torrezan, M, 2009)		2.07
"Imatinib mesylate (Gleevec(R)) is a small molecule with tyrosine kinase activity that has shown marked effects in some individuals with HES."( Atypical cardiac manifestation of hypereosinophilic syndrome and reversible cardiotoxicity to imatinib.
Bosch, X; Garcia-Albeniz, X; Garcia-Alvarez, A; Loma-Osorio, P; Sionis, A; Sitges, M, 2010)		1.08
"Imatinib mesylate is a potent inhibitor of the Bcr-Abl, c-Kit, and platelet-derived growth factor receptor (PDGFR) tyrosine kinases. "( A phase II study of imatinib mesylate and capecitabine in metastatic breast cancer: Southwest Oncology Group Study 0338.
Albain, K; Barlow, WE; Chew, HK; Gown, A; Gralow, J; Hayes, DF; Hortobagyi, GN; Lew, D; Livingston, R, 2008)		2.11
"Imatinib mesylate is a specific inhibitor of three tyrosine kinase receptors, two of which, PDGF-R and c-Kit, are implicated in the pathogenesis of intimal hyperplasia."( On the ability of imatinib mesylate to inhibit smooth muscle cell proliferation without delaying endothelialization: an in vitro study.
Laroche, G; Petitclerc, E; Vallières, K, 2009)		1.41
"Imatinib mesylate is an inhibitor of tyrosine kinases and is used for the therapy of patients with tumors including leukemias, but is not effective as a monotherapy for malignant glioma."( Stage-specific effect of inhibition of autophagy on chemotherapy-induced cytotoxicity.
Akiyama, Y; Bögler, O; Fujiwara, K; Kondo, S; Moritake, K; Shingu, T; Shinojima, N; Tamada, Y; Yokoyama, T, 2009)		1.07
"Imatinib mesylate is a small molecule that inhibits activation of the KIT and platelet-derived growth factor receptor alpha proteins, and is effective in first-line treatment of metastatic gastrointestinal stromal tumour."( Adjuvant imatinib mesylate after resection of localised, primary gastrointestinal stromal tumour: a randomised, double-blind, placebo-controlled trial.
Antonescu, CR; Ballman, KV; Blackstein, ME; Blanke, CD; Brennan, MF; Dematteo, RP; Demetri, GD; Maki, RG; McCarter, MD; Owzar, K; Patel, S; Pisters, PW; Polikoff, JA; Tan, BR; von Mehren, M, 2009)		1.49
"Imatinib mesylate (IM) is a very important drug in the treatment of gastrointestinal stromal tumors (GISTs) and chronic myeloid leukaemia (CML). "( Congestive heart failure during imatinib mesylate treatment.
Bolognese, L; Fiorentini, G; Grotti, S; Marinozzi, C; Montagnani, F; Turrisi, G, 2010)		2.09
"Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia, Philadelphia-positive acute lymphoblastic leukemia, and advanced gastrointestinal stromal tumors. "( Imatinib mesylate-induced acute liver failure in a patient with gastrointestinal stromal tumors.
Akyurek, N; Benekli, M; Buyukberber, S; Coskun, U; Demirci, U; Karakan, T; Tonyali, O; Yildiz, R, 2010)		3.25
"Imatinib mesylate (Gleevec) is a selective Bcr-Abl protein tyrosine-kinase inhibitor, and it also inhibits the receptor tyrosine kinases for stem cell factor (c-kit) and platelet-derived growth factor (PDGFR). "( Development of lichen sclerosus et atrophicus while receiving a therapeutic dose of imatinib mesylate for chronic myelogenous leukemia.
Abuav, R; Goldenberg, G; High, W; Pass, C; Skupsky, H, 2010)		2.03
"Imatinib mesylate is a targeted agent that may be used against Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL), one of the highest risk pediatric ALL groups."( Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a children's oncology group study.
Aledo, A; Borowitz, MJ; Bowman, WP; Burden, L; Camitta, B; Carroll, A; Carroll, WL; Davies, SM; Devidas, M; Gaynon, PS; Heerema, NA; Hunger, SP; Jorstad, D; Rutledge, R; Sather, H; Schultz, KR; Slayton, WB; Trigg, M; Wang, C; Winick, N, 2009)		1.8
"Imatinib mesylate (IM) is a tyrosine kinase inhibitor selective for BCR-ABL and indicated for the treatment of chronic myeloid leukemia. "( Effect of imatinib on the signal transduction cascade regulating telomerase activity in K562 (BCR-ABL-positive) cells sensitive and resistant to imatinib.
Bakhanashvili, M; Granot, G; Lahav, J; Lahav, M; Mor-Tzuntz, R; Raanani, P; Rabizadeh, E; Shpilberg, O; Uziel, O; Zimra, Y, 2010)		1.8
"Imatinib mesylate is a rationally designed tyrosine kinase inhibitor that has revolutionized the treatment of chronic myeloid leukemia and gastrointestinal stromal tumors. "( Dysregulation of bone remodeling by imatinib mesylate.
Dewar, AL; Fitter, S; Hughes, TP; Vandyke, K; Zannettino, AC, 2010)		2.08
"Imatinib mesylate is an inhibitor of c-kit and is indicated in the treatment of chronic myeloid leukemia and GISTs."( Disappearance of lentigines in a patient receiving imatinib treatment for familial gastrointestinal stromal tumor syndrome.
Campbell, T; Felsten, L; Moore, J, 2009)		1.07
"Imatinib mesylate is a small molecule inhibitor that selectively inhibits the PDGF receptor kinase as well the cKIT and Abl kinases, among other targets. "( Evaluation of imatinib mesylate in the treatment of pulmonary arterial hypertension.
Chhina, MK; Grant, GM; Nargues, W; Nathan, SD, 2010)		2.16
"Imatinib mesylate has proven to be an extremely effective and generally well tolerated drug, producing durable responses in most patients with chronic phase chronic myeloid leukaemia. "( Managing imatinib resistance in chronic myeloid leukaemia.
Hughes, T; Osborn, M, 2010)		1.8
"Imatinib mesylate is a potent inhibitor of Bcr-Abl tyrosine kinase, an oncoprotein that plays a key role in the development of chronic myeloid leukemia. "( Gaining insights into the Bcr-Abl activity-independent mechanisms of resistance to imatinib mesylate in KCL22 cells: a comparative proteomic approach.
Catanzano, F; Colavita, I; Esposito, N; Martinelli, R; Melo, JV; Pane, F; Ruoppolo, M; Salvatore, F, 2010)		2.03
"Imatinib mesylate is a highly selective inhibitor of this kinase, producing normal blood-counts in 98% of patients in chronic phase CML and disappearance of the Philadelphia chromosome in 86%."( Second-generation tyrosine kinase inhibitors as therapy for chronic myeloid leukemia.
Alvarado, Y; Cortes, J; Giles, FJ; Swords, R, 2007)		1.06
"Imatinib mesylate is a selective inhibitor of bcr-abl, PRGFR alpha, beta and c-kit."( In vitro effects of imatinib mesylate on radiosensitivity and chemosensitivity of breast cancer cells.
Bauer, M; Bauerschlag, DO; Dahmke, L; Jonat, W; Maass, N; Mundhenke, C; Niehoff, P; Schem, C; Strauss, A; Weber, K; Weigel, MT, 2010)		1.41
"Imatinib mesylate is a tyrosine kinase inhibitor used in the management of disorders in which activation of c-Abl, PDGFR, or c-Kit signaling plays a critical role. "( Imatinib mesylate does not increase bone volume in vivo.
Browett, P; Callon, KE; Cornish, J; Gamble, GD; Grey, A; Karsdal, MA; Ladefoged, M; Naot, D; O'Sullivan, S; Watson, M, 2011)		3.25
"Imatinib mesylate (Imatinib) is a potent inhibitor of defined tyrosine kinases and is effectively used for the treatment of malignancies characterized by the constitutive activation of these tyrosine kinases, such as Philadelphia chromosome-positive (Ph(+)) leukemias and gastrointestinal stromal tumors. "( Immunocompetent cell functions in Ph+ acute lymphoblastic leukemia patients on prolonged Imatinib maintenance treatment.
Calabrese, E; De Propris, MS; Della Starza, I; Elia, L; Foà, R; Guarini, A; Intoppa, S; Maggio, R; Milani, ML; Peragine, N; Vitale, A, 2011)		1.81
"Imatinib mesylate is a tyrosine kinase inhibitor which targets Bcr-Abl-protein, c-Kit, and platelet-derived growth factor receptor. "( Oral pigmentation in the hard palate associated with imatinib mesylate therapy: a report of three cases.
Christerson, L; Halbritter, S; Mattsson, U; Mörner Serikoff, E; Warfvinge, G, 2011)		2.06
"Imatinib mesylate is an effective treatment for recurrent or metastatic gastrointestinal stromal tumors (GISTs), but secondary resistance has been reported. "( Surgical intervention for imatinib and sunitinib-resistant gastrointestinal stromal tumors.
Kamiya, K; Kikuchi, H; Konno, H; Miyazaki, S; Ohta, M; Sakaguchi, T; Setoguchi, T; Yamamoto, M, 2011)		1.81
"Imatinib mesylate is a small molecule tyrosine kinase inhibitor that has been shown to selectively inhibit both the platelet-derived growth factor receptor and transforming growth factor-β signaling pathways."( A case of sclerodermatous graft-versus-host disease responsive to imatinib therapy.
Lazar, J; Poonawalla, T; Teng, JM, )		0.85
"Imatinib mesylate is a first line treatment of Chronic Myelogenous Leukemia and of a rare form of gastrointestinal stromal cancer, where the response to the drug is also linked to the immune system activation with production of antineoplastic cytokines. "( Imatinib treatment induces CD5+ B lymphocytes and IgM natural antibodies with anti-leukemic reactivity in patients with chronic myelogenous leukemia.
Catellani, S; Gobbi, M; Pierri, I; Poggi, A; Zocchi, MR, 2011)		1.81
"Imatinib mesylate (IM) is a first-line treatment of chronic phase-chronic myeloid leukemia (CP-CML). "( Assessment of quality of life with imatinib mesylate as first-line treatment in chronic phase-chronic myeloid leukemia.
Aaqib, M; Akram, M; Aziz, Z; Iqbal, J; Saeed, A, 2011)		2.09
"Imatinib mesylate (IM) is a compound that inhibits both BCR-ABL tyrosine kinase and c-kit receptors. "( Imatinib mesylate alters the expression of genes related to disease progression in an animal model of uveal melanoma.
Abourbih, D; Antecka, E; Burnier, MN; Castiglione, E; Di Cesare, S; Fernandes, BF; Isenberg, J; Maloney, S; Martins, C; Neto Belfort, R, 2011)		3.25
"Imatinib mesylate is a tyrosine kinase inhibitor used as first line treatment in chronic myeloid leukaemia. "( α-defensin 1-3 and α-defensin 4 as predictive markers of imatinib resistance and relapse in CML patients.
Chollet, C; Costaglioli, P; Dupouy, M; Etienne, G; Garbay, B; Lagarde, V; Mahon, FX; Pasquet, JM; Reiffers, J; Turcq, B, 2011)		1.81
"Imatinib mesylate is a tyrosine kinase inhibitor that was approved by the U.S. "( In vivo imaging of Bcr-Abl overexpressing tumors with a radiolabeled imatinib analog as an imaging surrogate for imatinib.
Glekas, AP; Khan, N; Larson, SM; Pillarsetty, NK; Punzalan, B; Smith-Jones, P, 2011)		1.81
"Imatinib mesylate (Gleevec(®)) is a protein inhibitor used in the management of several hematological malignancies associated with dermatological side effects, like hyperpigmentation."( Imatinib-associated hyperpigmentation of the palate in post-HSCT patient.
Abreu, MH; Gomez, RS; Resende, RG; Silva, ME; Teixeira, RG; Vasconcelos, Fde O, 2012)		1.1
"Imatinib Mesylate (Gleevec) is a drug that potently counteracts diabetes both in humans and in animal models for human diabetes. "( Effects of Imatinib Mesylate (Gleevec) on human islet NF-kappaB activation and chemokine production in vitro.
Li, T; Lu, T; Mokhtari, D; Welsh, N, 2011)		2.2
"Imatinib mesylate is a drug that has been approved for treatment of advanced gastrointestinal stromal tumors (GISTs) and patients with leukemia such as chronic myeloid or Philadelphia chromosome-positive acute lymphoblastic. "( Imatinib-associated bilateral gynecomastia and unilateral testicular hydrocele in male patient with metastatic gastrointestinal stromal tumor: a literature review.
Barutca, S; Guney, E; Meydan, N; Sargin, G; Tanriverdi, O; Taskin, F; Unubol, M, 2012)		1.82
"Imatinib mesylate (IM) is a selective tyrosine kinase inhibitor used for treating chronic myeloid leukemia (CML). "( ABCB1 haplotype is associated with major molecular response in chronic myeloid leukemia patients treated with standard-dose of imatinib.
Bueno, CT; Chiattone, CS; Guerra-Shinohara, EM; Hirata, MH; Hirata, RD; Lima, LT; Luchessi, AD; Vivona, D; Zanichelli, MA, 2012)		1.82
"Imatinib mesylate (IM) is a phenylaminopyrimidine that represents the first-line treatment for chronic myeloid leukemia (CML), Philadelphia chromosome-positive. "( Photoinduced dermatitis and oral lichenoid reaction in a chronic myeloid leukemia patient treated with imatinib mesylate.
Borroni, G; Brazzelli, V; Fiandrino, G; Lucioni, M; Manna, G; Moggio, E; Muzio, F; Orlandi, E; Vassallo, C, 2012)		2.04
"Imatinib mesylate is a tyrosine kinase inhibitor used as first-line treatment in Philadelphia chromosome-positive chronic myeloid leukemia (Ph+ CML) and metastatic or unresectable gastrointestinal stromal tumors (GIST). "( The role of therapeutic drug monitoring of imatinib in patients with chronic myeloid leukemia and metastatic or unresectable gastrointestinal stromal tumors.
Ensom, MH; Mabasa, VH; Teng, JF, 2012)		1.82
"Imatinib mesylate is a receptor kinase inhibitor approved by the Food and Drug Administration for the treatment of malignant metastatic and/or unresectable gastrointestinal stromal tumors and chronic myelogenous leukemia. "( Gastric antral vascular ectasia in a patient with GIST after treatment with imatinib: case report and literature review.
Mourad, F; Saad Aldin, E; Tfayli, A, 2012)		1.82
"Imatinib mesylate is a small molecule receptor tyrosine kinase inhibitor indicated for treatment of chronic myelogenous leukaemia and GI stromal tumours."( Anti-fibrotic activity and enhanced interleukin-6 production by hepatic stellate cells in response to imatinib mesylate.
Albanis, E; Chou, HI; Fiel, MI; Friedman, SL; Khitrov, G; Kim, Y; Zhang, W, 2012)		1.32
"Imatinib mesylate (IM) is a potent tyrosine kinase inhibitor used as front-line therapy in chronic myeloid leukemia, a disease caused by the oncogenic kinase Bcr-Abl. "( Quantitative- and phospho-proteomic analysis of the yeast response to the tyrosine kinase inhibitor imatinib to pharmacoproteomics-guided drug line extension.
Dos Santos, SC; Mira, NP; Moreira, AS; Sá-Correia, I, 2012)		1.82
"Imatinib mesylate is a molecular targeted agent for treating chronic myeloid leukemia (CML) and gastrointestinal stromal tumor. "( Hepatitis B virus reactivation in a chronic myeloid leukemia patient treated with imatinib mesylate.
Cui, GH; Gowrea, B; Hu, Y; Li, M; Wang, YD; Xia, J, 2012)		2.05
"Imatinib mesylate (Gleevec) is a chemotherapy medication developed to treat chronic myelogenous leukemia as well as gastrointestinal stromal tumors (Savage, N Engl J Med 2002;346:683-93). "( Imatinib mesylate (Gleevec) induced unilateral optic disc edema.
DeLuca, C; Haskes, C; Shenouda-Awad, N; Wrzesinski, S, 2012)		3.26
"Imatinib mesylate is a potent inhibitor of platelet-derived growth factor and transforming growth factor-β signalling pathways which may play a role in systemic sclerosis (SSc)-associated skin changes."( Imatinib mesylate in scleroderma-associated diffuse skin fibrosis: a phase II multicentre randomized double-blinded controlled trial.
Barcat, D; Bouchet, S; Chatelus, E; Chene, G; de Korwin-Krokowski, JD; Diot, E; Doussau, A; Durant, C; Ezzedine, K; Grandoulier, AS; Hachulla, E; Kostrzewa, E; Lepreux, S; Mahon, FX; Paul, C; Prey, S; Quemeneur, T; Schaeverbeke, T; Seneschal, J; Solanilla, A; Sparsa, A; Taïeb, A, 2012)		3.26
"Imatinib mesylate is an oral agent that is a selective protein tyrosine kinase inhibitor of the KIT protein tyrosine kinase, and it has demonstrated clinical benefit and objective tumor responses in most GIST patients in phase II and III trials."( Is exon mutation analysis needed for adjuvant treatment of gastrointestinal stromal tumor?
Akinci, MB; Aksoy, S; Ozdemir, NY; Sendur, MA; Uncu, D; Zengin, N, 2013)		1.11
"Imatinib mesylate is a tyrosine kinase inhibitor used widely as the first-line treatment for chronic myeloid leukaemia (CML). "( Imatinib-induced Stevens-Johnsons syndrome.
Himanshu, D; Jain, N; Jha, P; Singh, AK, 2013)		1.83
"Imatinib mesylate is an orally administered selective inhibitor of certain tyrosine kinases including KIT."( Management of malignant gastrointestinal stromal tumours.
Demetri, G; Dimitrijevic, S; Fletcher, C; Joensuu, H; Roberts, P; Silberman, S, 2002)		1.04
"Imatinib mesylate is a selective Bcr-Abl kinase inhibitor, effective in the treatment of chronic myelogenous leukemia. "( Several Bcr-Abl kinase domain mutants associated with imatinib mesylate resistance remain sensitive to imatinib.
Corbin, AS; Deininger, MW; Druker, BJ; La Rosée, P; Stoffregen, EP, 2003)		2.01
"Imatinib mesylate (STI571) is a highly effective and well-tolerated treatment for patients with chronic-phase chronic myeloid leukaemia (CML), but information on its efficacy and tolerance in intensively pretreated patients is scarce. "( Imatinib mesylate (STI571) treatment in patients with chronic-phase chronic myelogenous leukaemia previously submitted to autologous stem cell transplantation.
Camós, M; Cervantes, F; del Campo, R; García-Conde, J; Hernández-Boluda, JC; Martínez-Climent, JA; Montserrat, E; Odriozola, J; Villalón, L, 2003)		3.2
"Imatinib mesylate (imatinib) is an orally administered competitive inhibitor of the tyrosine kinases associated with the KIT protein (stem cell factor receptor), ABL protein and platelet-derived growth factor receptors. "( Imatinib mesylate: in the treatment of gastrointestinal stromal tumours.
Croom, KF; Perry, CM, 2003)		3.2
"Imatinib mesylate (Glivec) is a selective inhibitor of bcr-abl tyrosine kinase, the product of the Philadelphia chromosome, which is the hallmark of chronic myeloid leukaemia (CML). "( Successful peripheral blood stem cell mobilisation with filgrastim in patients with chronic myeloid leukaemia achieving complete cytogenetic response with imatinib, without increasing disease burden as measured by quantitative real-time PCR.
Branford, S; Goh, KY; Grigg, A; Hoyt, R; Hughes, TP; Hui, CH; Kwan, YL; Ma, DD; Rudzki, B; Seymour, JF; To, LB; Trickett, A; Walsh, S; White, D, 2003)		1.76
"Imatinib mesylate is a selective tyrosine kinase inhibitor of c-abl, bcr/abl, c-kit, and platelet-derived growth factor-receptor (PDGF-R). "( Results of imatinib mesylate therapy in patients with refractory or recurrent acute myeloid leukemia, high-risk myelodysplastic syndrome, and myeloproliferative disorders.
Albitar, M; Cortes, J; Faderl, S; Garcia-Manero, G; Giles, F; Kantarjian, H; Letvak, L; O'Brien, S; Rios, MB; Salvado, A; Talpaz, M; Thomas, D, 2003)		2.15
"Imatinib mesylate is a tyrosine kinase inhibitor with high affinity for the BCR-ABL fusion protein expressed by the hematopoietic cells in chronic myelogenous leukemia (CML). "( The effect of dose increase of imatinib mesylate in patients with chronic or accelerated phase chronic myelogenous leukemia with inadequate hematologic or cytogenetic response to initial treatment.
Brandt, H; Mohamed, AN; Pemberton, P; Schiffer, CA; Zonder, JA, 2003)		2.05
"Imatinib mesylate (STI571) is a major therapeutic advance for the management of chronic myeloid leukaemia (CML), however, a proportion of patients are refractory to it, particularly those in more advanced phases of CML. "( ABL-kinase domain point mutation as a cause of imatinib (STI571) resistance in CML patient who progress to myeloid blast crisis.
Czekalska, S; Czopek, J; Hanfstein, B; Hochhaus, A; Jakóbczyk, M; Müller, MC; Rudzki, Z; Sacha, T; Salamanchuk, Z; Skotnicki, AB; Wolska-Smoleń, T, 2003)		1.76
"Imatinib mesylate is a 2-phenylaminopyrimidine tyrosine kinase inhibitor with specific activity for ABL, platelet-derived growth factor receptor, and c-kit receptor. "( [Molecular-target therapy of Ph-positive leukemia by imatinib (tyrosine kinase inhibitor)].
Ohyashiki, K; Tauchi, T, 2003)		1.76
"Imatinib mesylate is an inhibitor of Bcr/Abl tyrosine kinase, which essentially participates the pathogenesis of chronic myelogenous leukemia (CML). "( [Imatinib].
Urabe, A, 2003)		1.76
"Imatinib mesylate is a targeted agent for CML with efficacy to date, which is superior to all other nontransplant therapy and has limited toxicity."( Transplantation for chronic myelogenous leukemia: yes, no, maybe so. . . An Oregon perspective.
Mauro, MJ; Maziarz, RT, 2003)		1.04
"Imatinib mesylate is an inhibitor of a few tyrosine kinases including KIT, which is an important growth factor receptor of mast cells."( Treatment of rheumatoid arthritis with imatinib mesylate: clinical improvement in three refractory cases.
Eklund, KK; Joensuu, H, 2003)		2.03
"Imatinib mesylate is a specific inhibitor of the Bcr-Abl kinase and has shown promising results in clinical studies."( Phosphorylation of tyrosine 393 in the kinase domain of Bcr-Abl influences the sensitivity towards imatinib in vivo.
Bai, RY; Duyster, J; Grundler, R; Hoepfl, J; Miething, C; Mugler, C; Peschel, C, 2003)		1.04
"Imatinib mesylate (STI571) is a competitive Bcr-Abl tyrosine kinase inhibitor and has yielded encouraging results in treatment of chronic myelogenous leukemia (CML) and gastrointestinal stroma tumors (GISTs). "( Imatinib mesylate affects the development and function of dendritic cells generated from CD34+ peripheral blood progenitor cells.
Appel, S; Boehmler, AM; Brossart, P; Brümmendorf, TH; Grünebach, F; Hartmann, U; Kanz, L; Müller, MR; Reichardt, VL; Rupf, A; Weck, MM, 2004)		3.21
"Imatinib mesylate is a selective inhibitor of tyrosine kinase-mediated activity."( Surgical treatment of gastrointestinal stromal tumors in the imatinib (STI-571) era.
Hart, J; Langerman, A; Posner, MC; Ryan, CW; Swiger, S; Wu, PC, 2003)		1.04
"Imatinib mesylate (STI571) is a selective inhibitor of the bcr/abl tyrosine kinase with therapeutic potential in the blast crisis (BC) of chronic myelogenous leukemia (CML)."( Imatinib mesylate as treatment for blastic transformation of Philadelphia chromosome positive chronic myelogenous leukemia.
Carrasco, M; Conde, E; de Miguel, M; Díaz-Mediavilla, J; Martínez, JA; Sanz, MA; Sierra, J; Sureda, A, 2003)		3.2
"Imatinib mesylate is a tyrosine kinase inhibitor that targets the BCR-ABL protein in CML, c-kit (KIT) and platelet-derived growth factor receptors. "( Imatinib mesylate causes hypopigmentation in the skin.
Cortes, J; Kantarjian, H; O'Brien, S; Talpaz, M; Tsao, AS, 2003)		3.2
"Imatinib mesylate (STI571) is a very effective treatment option for Ph(+) chronic myeloid leukemia (CML) in chronic phase. "( CNS blast crisis of chronic myelogenous leukemia in a patient with a major cytogenetic response in bone marrow associated with low levels of imatinib mesylate and its N-desmethylated metabolite in cerebral spinal fluid.
Bornhauser, M; Ehninger, G; Freiberg-Richter, J; Jenke, A; Mohr, B; Radke, J; Schleyer, E; Schuler, US, 2004)		1.97
"Imatinib mesylate (Gleevec) is a specific inhibitor of KIT kinase activation, and in phase II clinical trials has proven to be remarkably efficacious in heavily pretreated GIST patients with advanced disease."( Imatinib mesylate: a molecularly targeted therapy for gastrointestinal stromal tumors.
Eisenberg, BL, 2003)		2.48
"Imatinib mesylate is a specific inhibitor of protein tyrosine kinase activity secondary to bcr-abl, mostly indicated for the treatment of patients with Philadelphia chromosome positive chronic myeloid leukaemia (CML). "( First case of immune-mediated haemolytic anaemia associated to imatinib mesylate.
Chamone, Dde A; Conchon, M; Dorlhiac-Llacer, PE; Fonseca, GH; Novaretti, MC, 2003)		2
"Imatinib mesylate is a potent, selective inhibitor of the tyrosine kinase activity of bcr-abl,which is now established as the state-of-the-art treatment for chronic, accelerated or even blastic phase of Philadelphia-positive [Ph(1)(+)] chronic myelogenous leukemia. "( Ida-FLAG plus imatinib mesylate-induced molecular remission in a patient with chemoresistant Ph1+ acute myeloid leukemia.
Giakoumi, X; Mantzouranis, M; Pangalis, GA; Vassilakopoulos, TP; Viniou, NA, 2004)		2.13
"Imatinib mesylate is an orally available tyrosine kinase inhibitor that specifically blocks Bcr-Abl function."( Innovations in the management of leukemia: role of biologic therapies.
Duffy, KM, 2003)		1.04
"Imatinib mesylate is a new drug that can inhibit the tyrosine kinase activity of Bcr-Abl, the receptors for platelet-derived growth factor receptor(PDGF) and stem cell factor, or c-kit. "( [Molecular targeted treatment--new treatment strategy for patients with chronic myeloid leukemia].
Usui, N, 2004)		1.77
"Imatinib mesylate is a drug with curative potential and can be used as a first line drug in the management of CML, however at present the cure rate is unknown."( Hematologic and cytogenetic findings in eleven chronic myelogenous leukemia patients treated with imatinib mesylate at a tertiary care hospital.
Adil, SN; Arain, S; Kakepoto, GN; Khurshid, M; Sajid, R; Usman, M, 2004)		1.98
"Imatinib mesylate is a selective inhibitor of a few tyrosine kinases including KIT, and it is the first effective treatment for gastrointestinal stromal tumors (GISTs). "( Serum KIT and KIT ligand levels in patients with gastrointestinal stromal tumors treated with imatinib.
Blanke, CD; Bono, P; Demetri, GD; Dimitrijevic, S; Heinrich, MC; Joensuu, H; Krause, A; von Mehren, M, 2004)		1.77
"Imatinib mesylate is a valuable therapy for patients with newly diagnosed Ph+ chronic-phase CML. "( Spotlight on imatinib mesylate in chronic myeloid leukemia.
Croom, KF; Curran, MP; Goa, KL, 2004)		2.14
"Imatinib mesylate is a small molecule drug that in vitro inhibits the Abelson (Abl), Arg (abl-related gene), stem cell factor receptor (Kit), and platelet-derived growth factor receptor A and B (PDGFRA and PDGFRB) tyrosine kinases. "( Imatinib targets other than bcr/abl and their clinical relevance in myeloid disorders.
Pardanani, A; Tefferi, A, 2004)		1.77
"Imatinib mesylate is a potent inhibitor of KIT tyrosine kinase, so we explored the possibility that ACC could be a potential target for this drug."( Imatinib mesylate as treatment for adenoid cystic carcinoma of the salivary glands: report of two successfully treated cases.
Alcedo, JC; Arosemena, JR; Fábrega, JM; Urrutia, A, 2004)		2.49
"Imatinib mesylate is a tyrosine kinase inhibitor targeting platelet-derived growth factor receptor-beta (PDGFRB), BCR-ABL, and KIT."( Imatinib mesylate in chordoma.
Bertieri, R; Bertulli, R; Casali, PG; Colecchia, M; Crippa, F; Fumagalli, E; Greco, A; Gronchi, A; Grosso, F; Messina, A; Olmi, P; Orlandi, R; Pierotti, MA; Pilotti, S; Ripamonti, C; Spreafico, C; Stacchiotti, S; Tamborini, E, 2004)		2.49
"Imatinib mesylate is a tyrosine kinase inhibitor that specifically targets c-Kit, Abl, and platelet-derived growth factor receptor (PDGFR). "( Expression of imatinib mesylate-targeted kinases in endometrial carcinoma.
Broaddus, RR; Burke, TW; Gershenson, DM; Lu, KH; Oh, JC; Ramondetta, LM; Schmandt, R; Slomovitz, BM; Wu, W, 2004)		2.13
"Imatinib mesylate is a relatively new drug that targets the BCR-ABL chimeric protein, the molecular basis of chronic myeloid leukemia (CML). "( Efficacy and safety of imatinib mesylate for patients in the first chronic phase of chronic myeloid leukemia: results of a Japanese phase II clinical study.
Bessho, M; Chiba, S; Emi, N; Fujimoto, M; Hirai, H; Hirano, M; Jinnai, I; Kawai, Y; Mizoguchi, H; Morishima, Y; Nakao, S; Nishimura, M; Ogura, M; Ohnishi, K; Ohno, R; Shimazaki, C; Taguchi, H; Takahashi, M; Tauchi, T; Urabe, A; Yazaki, F; Yokozawa, T, 2004)		2.08
"Imatinib mesylate is a selective tyrosine kinase inhibitor that is successfully used in the treatment of chronic myeloid leukaemias and gastrointestinal stromal tumours. "( Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.
Burger, H; Nooter, K, 2004)		2.05
"Imatinib mesylate is a targeted therapy for the treatment of chronic myeloid leukemia (CML)."( Cost-utility analysis of imatinib mesylate for the treatment of chronic myelogenous leukemia in the chronic phase.
Gordois, A; Scuffham, P; Ward, S; Warren, E, 2004)		2.07
"Imatinib mesylate is a molecular-targeted agent, shown to be effective in chronic myeloid leukemia and gastrointestinal stromal tumors (GIST). "( Some lessons learned from imatinib mesylate clinical development in gastrointestinal stromal tumors.
Bertulli, R; Casali, PG; Coco, P; Fumagalli, E; Grosso, F; Stacchiotti, S, 2004)		2.07
"Imatinib mesylate is a selective and potent small-molecule inhibitor of tyrosine kinases, including Kit, platelet-derived growth factor receptor, and the BCR-Abl fusion protein. "( Imatinib mesylate in the treatment of gastrointestinal stromal tumour.
McAuliffe, JC; Steinert, DM; Trent, JC, 2005)		3.21
"Imatinib mesylate is a small molecule inhibitor of the c-Abl, platelet-derived growth factor (PDGF) receptor and c-Kit tyrosine kinases that is approved for the treatment of Philadelphia chromosome-positive chronic myeloid leukemia (CML) and gastrointestinal stromal tumors. "( Imatinib mesylate radiosensitizes human glioblastoma cells through inhibition of platelet-derived growth factor receptor.
Appelt, C; Dörken, B; Hildebrandt, B; Holdhoff, M; Jordan, A; Kreuzer, KA; le Coutre, P; Na, IK; Riess, H; Schmidt, CA; Scholz, R; Van Etten, RA, )		3.02
"Imatinib mesylate is a potent and specific tyrosine kinase inhibitor against c-ABL, BCR-ABL, and c-KIT, and has been demonstrated to be highly active in chronic myeloid leukemia and gastrointestinal stromal tumors. "( Imatinib as a novel antifibrotic agent in bleomycin-induced pulmonary fibrosis in mice.
Aono, Y; Inayama, M; Izumi, K; Kishi, J; Nishioka, Y; Sone, S; Uehara, H; Ugai, M, 2005)		1.77
"Imatinib mesylate is a tyrosine kinase inhibitor initially developed against the bcr-abl fusion protein of CML, but also shows therapeutic inhibitory activity against c-Kit expressed in GISTs."( Expression of c-kit (CD117) in neuroendocrine tumours--a target for therapy?
Caplin, ME; Dhillon, AP; Hochhauser, D; Khan, K; Kostoula, V; Quaglia, A; Savage, K; Stubbs, M, 2005)		1.05
"Imatinib mesylate is a potent inhibitor of Abl, KIT, and PDGFR tyrosine kinases. "( A phase II trial of imatinib mesylate monotherapy in patients with metastatic breast cancer.
D'Andrea, G; Dickler, M; Hudis, CA; Menell, J; Moasser, M; Modi, S; Moynahan, ME; Norton, L; Panageas, KS; Seidman, AD; Tan, LK, 2005)		2.09
"Imatinib mesylate is a recently introduced KIT tyrosine kinase inhibitor with effect on metastatic GIST."( [Treatment of patients with gastrointestinal stromal tumour with imatinib mesylate].
Eide, J; Haugland, HK; Horn, A; Jebsen, NL; Jensen, DK; Lilleng, PK; Mannelqvist, M; Monge, OR; Skar, R; Øvrebø, K, 2005)		1.29
"Imatinib mesylate is a novel anti-tumor agent useful in the clinical management of chronic myelogenous leukemia and gastrointestinal stromal tumors with minimal toxicity relative to other forms of cancer therapy. "( Cyclooxygenase-2 induction and prostaglandin E2 accumulation in squamous cell carcinoma as a consequence of epidermal growth factor receptor activation by imatinib mesylate.
Donato, NJ; Johnson, FM; Newman, RA; Yang, P, 2004)		1.96
"Imatinib mesylate is a novel tyrosine kinase inhibitor used for the treatment of Philadelphia chromosome positive (Ph+) leukemia and other malignancies. "( Telomere length and telomerase activity in the BCR-ABL-transformed murine Pro-B cell line BaF3 is unaffected by treatment with imatinib.
Balabanov, S; Bokemeyer, C; Brümmendorf, TH; Duyster, J; Fellenberg, J; Hartmann, U; Kanz, L; Lipp, HP; van der Kuip, H; Ziegler, P, 2005)		1.77
"Imatinib mesylate is an oral drug designed to inhibit the kinase enzyme activity of KIT."( Nursing implications of imatinib as molecularly targeted therapy for gastrointestinal stromal tumors.
Amand, MS; Demetri, GD; Griffin, JM, 2005)		1.05
"Imatinib mesylate (IM) is a tyrosine kinase inhibitor, which inhibits phosphorylation of downstream proteins involved in BCR-ABL signal transduction. "( Imatinib mesylate (Gleevec) downregulates telomerase activity and inhibits proliferation in telomerase-expressing cell lines.
Bakhanashvili, M; Beery, E; Birenbaum, M; Fenig, E; Lahav, M; Luria, D; Nordenberg, J; Reshef, H; Sandbank, J; Uziel, O; Yerushalmi, R, 2005)		3.21
"Imatinib mesylate is a tyrosine kinase inhibitor of the ABL, platelet-derived growth factor receptor (PDGFR), and c-kit kinases. "( Induction of heparin-binding EGF-like growth factor and activation of EGF receptor in imatinib mesylate-treated squamous carcinoma cells.
Donato, NJ; Johnson, FM; Saigal, B, 2005)		1.99
"Imatinib mesylate is a selective tyrosine kinase inhibitor that is successfully used in the treatment of Philadelphia-positive chronic and acute leukaemia's, and gastrointestinal stromal tumors. "( Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.
Brok, M; Burger, H; de Boeck, G; de Bruijn, EA; Guetens, G; Nooter, K; Sparreboom, A; van Tol, H; Verweij, J; Wiemer, EA, 2005)		2.21
"Imatinib mesylate is a novel molecule, which inhibits the protein product of this fusion gene and hence has been used in the treatment of CML."( Imatinib mesylate in chronic myeloid leukemia: a prospective, single arm, non-randomized study.
Amare-Kadam, P; Baisane, C; Bakshi, A; Deshmukh, C; Parikh, P; Saikia, T, 2005)		2.49
"Imatinib mesylate (STI571) is an oral 2-phenylaminopyrimidine derivative that acts as a selective inhibitor against several receptor tyrosine kinases and has been viewed as one of the therapeutic success stories of the 21st century. "( Molecular research directions in the management of gastrointestinal stromal tumors.
Godwin, AK; Tarn, C, 2005)		1.77
"Imatinib mesylate is a selective Bcr/Abl kinase inhibitor and an effective anticancer agent for Bcr/Abl-positive chronic myelogenous leukemia. "( Detection of single nucleotide insertion of BCR/ABL region in imatinib-resistant human myelogenous leukemia SR-1 cells.
Han, HY; Han, JY; Jeong, JS; Kim, HJ; Kwak, JY; Kwon, HC; Park, JI; Park, TH; Seo, C, 2005)		1.77
"Imatinib mesylate is a protein tyrosine kinase inhibitor that inhibits the BCR-ABL tyrosine kinase, the receptor tyrosine kinases for platelet-derived growth factor, and stem cell factor c-kit. "( Acute renal failure secondary to imatinib mesylate treatment in prostate cancer.
Finkel, KW; Foringer, JR; Guntupalli, JS; Samuels, JA; Tjia, VM; Verani, RR, 2005)		2.05
"Imatinib mesylate is a specific inhibitor of BCR-ABL tyrosine kinase, which is now widely used for the treatment of chronic myeloid leukemia (CML) with a high efficacy. "( Severe hepatic injury caused by imatinib mesylate administered for the treatment of chronic myeloid leukemia and the efficacy of prednisolone for its management.
Ikuta, K; Inamura, J; Jimbo, J; Kohgo, Y; Miyokawa, N; Sato, K; Shindo, M; Tokusashi, Y; Torimoto, Y, 2005)		2.05
"Imatinib mesylate is a major advance in the therapy of patients with chronic myelogenous leukemia (CML). "( Targeting the kinase activity of the BCR-ABL fusion protein in patients with chronic myeloid leukemia.
Cortes, JE; Giles, FJ; Kantarjian, HM, 2005)		1.77
"Imatinib mesylate is a potent inhibitor of BCR-ABL, the constitutively active tyrosine kinase protein critical for the pathogenesis of chronic myeloid leukemia."( Comparison between patients with Philadelphia-positive chronic phase chronic myeloid leukemia who obtained a complete cytogenetic response within 1 year of imatinib therapy and those who achieved such a response after 12 months of treatment.
Abruzzese, E; Alimena, G; Amabile, M; Baccarani, M; Cilloni, D; Gobbi, M; Iacobucci, I; Iuliano, F; Martinelli, G; Martino, B; Montefusco, E; Ottaviani, E; Pane, F; Poerio, A; Rosti, G; Russo, D; Saglio, G; Soverini, S; Terragna, C; Testoni, N, 2006)		1.78
"Imatinib mesylate is a small molecule tyrosine kinase inhibitor that has significant efficacy in the treatment of chronic myelogenous leukaemia (CML). "( Multiple joint effusions associated with high-dose imatinib therapy in a patient with chronic myelogenous leukaemia.
Anavim, A; Dennehey, CF; Kong, KM; Moore, JC; Tiong Ong, S, 2006)		1.78
"Imatinib mesylate is an oral tyrosine kinase inhibitor that targets bcr-Abl, c-kit, platelet-derived growth factor receptor (PDGFR)-alpha, and PDGFR-beta, leading to remarkable clinical responses in several cancers."( Multicenter Phase II trial of high-dose imatinib mesylate in metastatic melanoma: significant toxicity with no clinical efficacy.
Atkins, MB; Byrnes, C; Eton, O; Hubbard, F; McDermott, DF; Prieto, V; Sanders, K; Sosman, JA; Wyman, K, 2006)		1.32
"Imatinib mesylate, STI571, is a novel anticancer drug used to treat Philadelphia chromosome positive (Ph+) chronic myeloid leukemia. "( An in vitro study of the cytogenetic and cytotoxic effects of imatinib mesylate, STI571 on murine erythroleukemia GM-86 cells.
Fotiadis, NA; Kirk, MJ; Majumdar, SK, 2006)		2.02
"Imatinib mesylate is a drug that has been recently approved for the treatment for chronic myeloid leukemia. "( Vitiligo-like lesions and diffuse lightening of the skin in a pediatric patient treated with imatinib mesylate: a noninvasive colorimetric assessment.
Barbagallo, T; Bellani, E; Borroni, G; Brazzelli, V; Locatelli, F; Prestinari, F; Rona, C; Roveda, E; Trevisan, V; Zecca, M, )		1.79
"Imatinib mesylate (Glivec) is a small molecule that binds to the ATP pocket of ABL and blocks downstream signalling events."( [Tyrosine kinase inhibitors for the treatment of CML].
Heim, D, 2006)		1.06
"Imatinib mesylate (Glivec) is an orally administered competitive inhibitor of tyrosine kinases associated with the KIT, ABL protein, licensed for the treatment of metastatic GIST since 2002 in Germany."( Treatment of gastrointestinal stromal tumor with imatinib mesylate: a retrospective single-center experience in Heidelberg.
Egerer, G; Geer, T; Herrmann, T; Ho, AD; Kallinowski, B; Kasper, B; Lehnert, T; Mechtersheimer, G, 2006)		1.31
"Imatinib mesylate is a very effective treatment in patients with Philadelphia (Ph)-positive chronic myeloid leukaemia (CML). "( Imatinib-associated neutropenia may not be overcome by filgrastim treatment in patients with blastic phase of chronic myeloid leukaemia.
Calbecka, M; Hellmann, A; Prejzner, W; Wyrowinska, E; Zaucha, JM, 2006)		1.78
"Imatinib Mesylate (Glivec) is a specific inhibitor of Bcr-Abl kinase."( [Chronic myeloid leukemia--resistance to imatinib mesylate (Glivec)--literature review and personal experience].
Divoký, V; Faber, E; Indrák, K; Jarosová, M; Nausová, J; Priwitzerová, M, 2006)		1.32
"Imatinib mesylate (IM), is a selective and competitive inhibitor of tyrosine kinases, including BCR-ABL, ABL, KIT, and the platelet-derived growth factor receptors (PDGF-R). "( Tyrosine kinase inhibitor imatinib mesylate as anticancer agent for advanced ocular melanoma expressing immunoistochemical C-KIT (CD 117): preliminary results of a compassionate use clinical trial.
Bernardeschi, P; Biancalani, M; De Giorgi, U; Dentico, P; Fiorentini, G; Lanzanova, G; Palomba, A; Rossi, S, 2003)		2.06
"Imatinib mesylate is a potent inhibitor of c-kit receptor tyrosine kinase activity."( Imatinib mesylate in the treatment of systemic mastocytosis: a phase II trial.
Droogendijk, HJ; Kluin-Nelemans, HJ; Oranje, AP; van Daele, PL; van de Loosdrecht, AA; van Doormaal, JJ, 2006)		2.5
"Imatinib mesylate is a selective tyrosine kinase inhibitor on ABL, c-Kit and PGDF-receptor, and functions through competitive inhibition at the ATP-binding site of the enzyme, which leads to growth arrest or apoptosis in cells that express BCR-ABL."( Treatment of chronic myeloid leukemia with imatinib mesylate.
Ohno, R, 2006)		1.32
"Imatinib mesylate (Gleevec) is a small-molecule inhibitor of the fusion protein Bcr-Abl, the causal agent in chronic myelogenous leukemia. "( Cardiotoxicity of the cancer therapeutic agent imatinib mesylate.
Alroy, J; Beahm, C; Clubb, FJ; Durand, JB; Force, T; Grazette, L; Iliescu, C; Kerkelä, R; Patten, R; Pesant, S; Rosenzweig, A; Salomon, RN; Shevtsov, S; Van Etten, RA; Walters, B; Yacobi, R, 2006)		2.03
"Imatinib mesylate (imatinib) is a potent inhibitor of defined tyrosine kinases (TKs) and is effective in the treatment of malignancies characterized by constitutive activation of these TKs such as chronic myeloid leukemia and gastrointestinal stromal tumors. "( Imatinib mesylate selectively impairs expansion of memory cytotoxic T cells without affecting the control of primary viral infections.
Matter, M; Mumprecht, S; Ochsenbein, AF; Pavelic, V, 2006)		3.22
"Imatinib mesylate is a novel therapeutic agent that targets the BCR-ABL tyrosine kinase, the molecular abnormality associated with Ph+ ALL."( Philadelphia chromosome-positive acute lymphoblastic leukemia: impact of imatinib treatment on remission induction and allogeneic stem cell transplantation.
Kovacsovics, T; Maziarz, RT, 2006)		1.06
"Imatinib mesylate (STI571) is a specific inhibitor of the BCR/ABL fusion tyrosine kinase that exhibits potent antileukemic effects in CML."( Comparative study of DNA damage, cell cycle and apoptosis in human K562 and CCRF-CEM leukemia cells: role of BCR/ABL in therapeutic resistance.
Majsterek, I; Pytel, D; Wysocki, T, 2006)		1.06
"Imatinib mesylate is a specific inhibitor of the Bcr-Abl protein tyrosine kinase that competes with ATP for its specific binding site in the kinase domain. "( The effect of imatinib mesylate (Glivec) on human tumor-derived cells.
Cree, IA; Di Nicolantonio, F; Glaysher, S; Hungerford, JL; Hurren, J; Knight, LA; Lamont, A; Mercer, SJ; Sharma, S; Whitehouse, PA, 2006)		2.14
"Imatinib mesylate is a tyrosine kinase inhibitor used for the treatment of chronic myeloid leukemia and hypereosinophilic syndrome. "( Desensitization to imatinib in patients with leukemia.
Cornetta, K; Cripe, LD; Fausel, C; Nelson, RP; Ramanuja, S; Ward, KE, 2006)		1.78
"Imatinib mesylate (imatinib) is a tyrosine kinase inhibitor developed to treat Bcr/Abl-expressing leukemias and subsequently found to treat c-Kit-expressing gastrointestinal stromal tumors."( Selective tyrosine kinase inhibition by imatinib mesylate for the treatment of autoimmune arthritis.
Chan, SM; Chang, A; Genovese, MC; Goodman, SB; Higgins, JP; Ho, PP; Lee, DM; Paniagua, RT; Robinson, WH; Sharpe, O; Song, JJ; Steinman, L; Thomas, FM; Tomooka, BH; Utz, PJ, 2006)		1.32
"Imatinib mesylate is a clinically well-tolerated small molecule inhibitor that exerts selective, dual inhibition of the transforming growth factor beta (TGFbeta) and platelet-derived growth factor (PDGF) pathways. "( Imatinib mesylate reduces production of extracellular matrix and prevents development of experimental dermal fibrosis.
Distler, JH; Distler, O; Gay, RE; Gay, S; Hauser, T; Huber, LC; Jüngel, A; Michel, BA; Schett, G; Schulze-Horsel, U; Zwerina, J, 2007)		3.23
"Imatinib mesylate is a selective protein kinase inhibitor, highly active in patients with chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GISTs). "( Severe skin reaction in a patient with gastrointestinal stromal tumor treated with imatinib mesylate.
Catricalà, C; Ciccarese, M; Cognetti, F; Ferraresi, V; Ferrari, A; Zeuli, M, )		1.8
"Imatinib mesylate is a selective inhibitor of the oncogenic tyrosine kinase, Bcr-Abl, and is widely used as a first-line treatment for chronic myeloid leukaemia (CML). "( Different target range and cytotoxic specificity of adaphostin and 17-allylamino-17-demethoxygeldanamycin in imatinib-resistant and sensitive cell lines.
Barnes, DJ; De, S; Melo, JV; Moravcsik, E; van Hensbergen, P, 2007)		1.78
"Imatinib mesylate is a small molecule inhibitor of certain tyrosine kinases, most notably the chimeric bcr-abl fusion protein found in CML. "( A phase II study of imatinib mesylate in children with refractory or relapsed solid tumors: a Children's Oncology Group study.
Adamson, PC; Bernstein, ML; Blaney, SM; Bond, M; Krailo, M; Pappo, A; Schultz, KR, 2008)		2.11
"Imatinib mesylate (Gleevec) is a well known drug for treating chronic myeloid leukemia and gastrointestinal stromal tumors. "( Synthesis and positron emission tomography studies of carbon-11-labeled imatinib (Gleevec).
Alexoff, D; Ding, YS; Fowler, JS; Kil, KE; Kim, SW; Lin, KS; Muench, L; Shea, C; Xu, Y, 2007)		1.78
"Imatinib mesylate is a selective inhibitor of tyrosine kinases such as bcr-abl, c-Kit, c-Fms and platelet derived growth factor receptor beta (PDGFRbeta)."( Preliminary data suggestive of a novel translational approach to mesothelioma treatment: imatinib mesylate with gemcitabine or pemetrexed.
Barbone, D; Bertino, P; Busacca, S; Favoni, R; Gaudino, G; Germano, S; Mutti, L; Pinato, S; Porta, C; Tassi, G, 2007)		1.28
"Imatinib mesylate is a potent and selective inhibitory of the BCR/ABL tyrosine kinase."( Central nervous system blastic crisis in chronic myeloid leukemia on imatinib mesylate therapy: a case report.
Altintas, A; Ayyildiz, O; Cil, T; Kaplan, MA; Kilinc, I, 2007)		1.3
"Imatinib mesylate is a potent inhibitor of ABL but also of PDGFR-alpha, and has been associated with durable hematologic responses in patients with HES."( The novel tyrosine kinase inhibitor EXEL-0862 induces apoptosis in human FIP1L1-PDGFR-alpha-expressing cells through caspase-3-mediated cleavage of Mcl-1.
Cortes, J; Giles, FJ; Kantarjian, H; Lamb, P; Manshouri, T; Pan, J; Quintás-Cardama, A; Tefferi, A; Verstovsek, S, 2007)		1.06
"Imatinib mesylate (imatinib) is an inhibitor that specifically targets a set of protein tyrosine kinase, such as abl, c-kit, and platelet-derived growth factor receptor (PDGFR) and it is widely used to treat chronic myeloid leukemia (CML)."( Imatinib mesylate both prevents and treats the arthritis induced by type II collagen antibody in mice.
Ando, T; Hamada, Y; Haro, H; Hatsushika, K; Kato, R; Koyama, K; Nakao, A; Ogawa, H; Sakuma, M; Sugiyama, H; Wako, M, 2007)		2.5
"Imatinib mesylate is a selective competitive inhibitor of the bcr-abl tyrosine kinase and c-KIT. "( Symptomatic hypoglycemia during imatinib mesylate in a non-diabetic female patient with gastrointestinal stromal tumor.
Gallwitz, B; Haap, M; Häring, HU; Hartmann, JT; Kanz, L; Müssig, K; Thamer, C, 2007)		2.07
"Imatinib Mesylate (STI-571) is a potent inhibitor of Kit Kinase activity and different reports demonstrated its efficacy in unresectable or metastatic Gists."( Gastric GISTs. Personal experience.
Artuso, S; La Donna, M; Linguerri, R; Mingolla, GP; Riccio, PA; Zannelli, M, )		0.85
"Imatinib mesylate is a selective inhibitor of the bcr/abl, c-kit and PDGF receptor tyrosine kinases. "( Ocular side effects in chronic myeloid leukemia patients treated with imatinib.
Alimena, G; Breccia, M; Cannella, L; Carmosino, I; Frustaci, A; Gentilini, F; Latagliata, R, 2008)		1.79
"Imatinib mesylate is a drug that has been approved for treatment of chronic myeloid leukemia (CML) in blast crisis, accelerated or chronic phase, and also for advanced gastrointestinal stromal tumors. "( Imatinib-induced fatal acute liver failure.
Cacchione, R; Gadano, AC; Mandó, OG; Marciano, S; Ridruejo, E; Villamil, AG, 2007)		1.78
"Imatinib mesylate (imatinib) is a new generation preparation that is now successfully used for treatment of cancer, particularly for chemotherapy of chronic myeloid leukemia (CML). "( Role of P-glycoprotein in evolution of populations of chronic myeloid leukemia cells treated with imatinib.
Kruglov, SS; Mechetner, EB; Rybalkina, EY; Stavrovskaya, AA; Stromskaya, TP; Turkina, AG; Zabotina, TN, 2008)		1.79
"Imatinib mesylate (Gleevec) is a small molecule tyrosine kinase inhibitor approved for use in the management of chronic myeloid leukemia in adults and children and in gastrointestinal stromal tumors in adults. "( Population pharmacokinetics of imatinib mesylate and its metabolite in children and young adults.
Barrett, JS; Bernstein, M; Blaney, SM; Bond, M; Champagne, M; Fossler, MJ; Jayaraman, B; Menon-Andersen, D; Mondick, JT; Thompson, PA, 2009)		2.08
"Imatinib mesylate is a BCR-ABL tyrosine kinase inhibitor used in the management of chronic myeloid leukemia. "( Imatinib-related bone marrow aplasia after complete cytogenetic response in chronic myeloid leukemia.
Junaid, A; Khan, KA; Mukhtar, K; Siddiqui, NS; Siddiqui, S, 2008)		1.79
"Imatinib mesylate is a selective inhibitor of several protein tyrosine kinases, including the receptor of platelet-derived growth factor, an important mediator of desmoplasia."( Imatinib mesylate inhibits proliferation and exerts an antifibrotic effect in human breast stroma fibroblasts.
Gioni, V; Karamanos, NK; Karampinas, T; Kletsas, D; Papadopoulos, S; Roussidis, AE; Voutsinas, G, 2008)		2.51
"Imatinib mesylate (STI571) is a promising new treatment for chronic myelogenous leukemia (CML). "( Imatinib mesylate (STI571) inhibits growth of primitive malignant progenitors in chronic myelogenous leukemia through reversal of abnormally increased proliferation.
Bhatia, R; Forman, SJ; Holtz, MS; Sawyers, CL; Slovak, ML; Zhang, F, 2002)		3.2
"Imatinib mesylate (STI571) is a specific inhibitor of BCR-ABL tyrosine kinase that can induce hematologic and cytogenetic remissions in patients with CML."( Imatinib mesylate (STI571) in the treatment of relapse of chronic myeloid leukemia after allogeneic stem cell transplantation.
Apperley, JF; Craddock, C; Dazzi, F; Goldman, JM; Marin, D; Marktel, S; Olavarria, E, 2002)		2.48

Effects

Imatinib mesylate has been shown to effectively block constitutively active KIT and delay tumor growth. It has considerable antineoplastic activity in patients with chronic myeloid leukaemia (CML) and some solid tumours.

ExcerptReferenceRelevance
"Imatinib mesylate has a substantial, but short term activity in the accelerated phase and blastic crisis of the Ph+ CML."( [Treatment of chronic myeloid leukemia with imatinib in the accelerated stage of the disease].
Boban, D; Bogdanić, V; Bulum, J; Kovacević, J; Krecak-Gverić, V; Labar, B; Mikulić, M; Mrsić-Davidović, S; Nemet, D; Sertić, D; Serventi-Seiwerth, R; Zadro, R, )		0.85
"Imatinib Mesylate (IMA) has been widely used to treat with chronic myeloid leukemia (CML). "( Role of ferroptosis in promoting cardiotoxicity induced by Imatinib Mesylate via down-regulating Nrf2 pathways in vitro and in vivo.
Li, D; Song, C; Zhang, J; Zhao, X, 2022)		2.41
"Imatinib mesylate (IM) has revolutionized the treatment of gastrointestinal stromal tumor (GIST). "( Targeting BCL6 in Gastrointestinal Stromal Tumor Promotes p53-Mediated Apoptosis to Enhance the Antitumor Activity of Imatinib.
Hao, Y; Jia, J; Jiang, Q; Li, C; Liu, W; Lou, Z; Ma, X; Tao, K; Wang, T; Zeng, X; Zhang, P; Zhang, R; Zhao, F, 2023)		2.35
"Imatinib mesylate has revolutionized the treatment of patients with chronic myeloid leukaemia (CML); however, some patients fail to respond and have a poor prognosis. "( Evaluation of Molecular Response to Imatinib Mesylate Treatment in Iranian Patients With Chronic Myeloid Leukemia.
Alimoghaddam, K; Babakhani, D; Chahardouli, B; Ghahremani, MH; Mohammadi, S; Nekoohesh, L; Nikbakht, M; Rostami, S, 2020)		2.28
"Imatinib mesylate (IM) therapy has been shown to induce lower T cell counts in chronic myelogenous leukemia (CML) patients and an interference of IM with T cell receptor (TCR) signaling has been invoked to explain this observation. "( Imatinib mesylate inhibits STAT5 phosphorylation in response to IL-7 and promotes T cell lymphopenia in chronic myelogenous leukemia patients.
Busque, L; Guimond, M; Laflamme, P; Leboeuf, DM; Moutuou, MM; Roy, J; Sidi Boumedine, R; Thiant, S, 2017)		3.34
"Imatinib mesylate has been associated with the changes in bone turnover. "( Soft tissue calcification secondary to imatinib mesylate in a patient with gastrointestinal stromal tumor.
Abushahin, F; Bossaer, JB; Enck, RE, 2014)		2.11
"Imatinib mesylate has been a breakthrough treatment for chronic myeloid leukemia. "( Quantification of imatinib in human serum: validation of a high-performance liquid chromatography-mass spectrometry method for therapeutic drug monitoring and pharmacokinetic assays.
Bendit, I; de Alencar Fisher Chamone, D; Novaes, MM; Rezende, VM; Rivellis, A, 2013)		1.83
"Imatinib mesylate (IM) has become a standard of care in chronic myeloid leukemia (CML) therapy. "( Reduced ABCG2 and increased SLC22A1 mRNA expression are associated with imatinib response in chronic myeloid leukemia.
Bueno, CT; Chiattone, CS; de Castro, FA; de Lima, LT; de Lourdes F Chauffaille, M; Guerra-Shinohara, EM; Hirata, MH; Hirata, RD; Hungria, VT; Luchessi, AD; Vivona, D; Zanichelli, MA, 2014)		1.85
"Imatinib mesylate has been the first of this novel family of drugs approved for the treatment of hematologic malignancies."( Tyrosine kinase inhibitors: muco-cutaneous side effects at the microscope.
Brazzelli, V; Croci, G; Grasso, V; Vassallo, C, 2014)		1.12
"Imatinib mesylate (IM) has so far been the standard of care for treating chronic myeloid leukemia (CML), but the initial striking efficacy of this drug has been overshadowed by the development of clinical resistance, which may in part be caused by pharmacogenetic variability. "( ABCB1 haplotypes but not individual SNPs predict for optimal response/failure in Egyptian patients with chronic-phase chronic myeloid leukemia receiving imatinib mesylate.
Ali, MA; Elsalakawy, WA, 2014)		2.04
"Imatinib mesylate (IM) has substantial efficacy in patients with metastatic gastrointestinal stromal tumors (GISTs), and pathological complete response (pCR) following IM treatment has been sporadically reported; however, its clinical significance for GIST needs to be clarified."( Clinical significance of pathological complete response in patients with metastatic gastrointestinal stromal tumors after imatinib mesylate treatment--lessons learned.
Chen, TC; Chen, TW; Chen, YY; Cheng, CT; Chiang, KC; Jung, SM; Tsai, CY; Tseng, JH; Wang, SY; Yeh, CN; Yeh, TS, 2014)		2.05
"Imatinib mesylate has been evaluated for possible potential in treatment of colon cancer in recent times. "( Hyaluronan coated liposomes as the intravenous platform for delivery of imatinib mesylate in MDR colon cancer.
Jaggi, M; Joshi, V; Negi, LM; Ronodip, K; Talegaonkar, S, 2015)		2.09
"Imatinib mesylate has dramatically improved the outcome of children with Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph* ALL) and is now included as first-line therapy. "( Imatinib-induced Severe Hepatitis in a 9-Year-old Girl With Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia.
Fukushima, H; Fukushima, T; Kobayashi, C; Nanmoku, T; Sakai, A; Satomi, K; Sumazaki, R; Suzuki, R; Tagawa, M, 2015)		1.86
"Imatinib mesylate has revolutionized the treatment of molecularly defined MN-eos, and novel agents have been successfully used to treat HES."( Eosinophilia in Hematologic Disorders.
Falchi, L; Verstovsek, S, 2015)		1.14
"Imatinib mesylate (IM) has effectively improved the prognosis of GIST patients and has been established as principle therapy in metastatic GIST."( [Lancet in the era of targeted drug therapy: the role of surgery in the management of advanced gastrointestinal stromal tumor].
Cao, H; Wang, M, 2016)		1.16
"Imatinib mesylate has activity against MCT in dogs, and response to treatment can be correlated to presence of mutation within exon 11 of c-kit."( Effect of tyrosine kinase inhibition by imatinib mesylate on mast cell tumors in dogs.
Bonkobara, M; Fujino, Y; Fujita, M; Ishida, N; Isotani, M; Kato, R; Kobayashi, T; Ochi, S; Ono, K; Setoguchi, A; Tamura, K; Tominaga, M; Washizu, T; Yagihara, H, )		1.84
"Imatinib mesylate has clinical activity against MCT in dogs. "( Effect of tyrosine kinase inhibition by imatinib mesylate on mast cell tumors in dogs.
Bonkobara, M; Fujino, Y; Fujita, M; Ishida, N; Isotani, M; Kato, R; Kobayashi, T; Ochi, S; Ono, K; Setoguchi, A; Tamura, K; Tominaga, M; Washizu, T; Yagihara, H, )		1.84
"Imatinib mesylate has shown promising results in chronic myeloid leukemia (CML) in all phases. "( Bone marrow morphological changes in patients of chronic myeloid leukemia treated with imatinib mesylate.
Amre, P; Deshmukh, C; Gujral, S; Joshi, S; Nair, CN; Sunita, P, )		1.8
"Imatinib mesylate (IM, Gleevec) has largely supplanted allogeneic hematopoietic cell transplantation (HCT) as first line therapy for chronic myeloid leukemia (CML). "( Impact of prior imatinib mesylate on the outcome of hematopoietic cell transplantation for chronic myeloid leukemia.
Abecasis, M; Antin, JH; Arora, M; Bolwell, BJ; Carabasi, MH; Cervantes, F; Champlin, RE; Copelan, E; Gale, RP; George, B; Giralt, SA; Gupta, V; Hale, GA; Halter, J; Horowitz, MM; Ilhan, O; Keating, A; Khoury, HJ; Kukreja, M; Lee, SJ; Liesveld, JL; Litzow, MR; Marks, DI; Maziarz, RT; McCarthy, PL; Olavarria, E; Rizzieri, DA; Schouten, HC; Stadtmauer, EA; Szer, J; Wang, T; Woolfrey, AE; Zander, AR, 2008)		2.13
"Imatinib mesylate has proven to be the most effective treatment in chronic myeloid leukemia. "( Specific assessment of BCR-ABL transcript overexpression and imatinib resistance in chronic myeloid leukemia patients.
Bengió, R; Bianchini, M; De Brasi, C; Gargallo, P; Gonzalez, M; Larripa, I, 2009)		1.8
"Imatinib mesylate has become the treatment of choice for chronic myeloid leukemia (CML): the standard dose for chronic- phase (CP) CML is 400 mg daily. "( Results of high-dose imatinib mesylate in intermediate Sokal risk chronic myeloid leukemia patients in early chronic phase: a phase 2 trial of the GIMEMA CML Working Party.
Alimena, G; Amabile, M; Baccarani, M; Breccia, M; Castagnetti, F; Galieni, P; Iacobucci, I; Iuliano, F; Luatti, S; Martinelli, G; Palandri, F; Pane, F; Rege Cambrin, G; Rosti, G; Saglio, G; Soverini, S; Specchia, G; Stagno, F; Testoni, N, 2009)		2.11
"Imatinib mesylate (imatinib) has been shown to be highly efficacious in the treatment of chronic myeloid leukemia (CML). "( Prevalence, determinants, and outcomes of nonadherence to imatinib therapy in patients with chronic myeloid leukemia: the ADAGIO study.
Abraham, I; Albrecht, T; Berneman, Z; De Bock, R; De Geest, S; MacDonald, K; Martiat, P; Mineur, P; Noens, L; Van Eygen, K; van Lierde, MA; Verhoef, G; Zachée, P, 2009)		1.8
"Imatinib mesylate has significantly improved the outcome of patients with CML. "( [Correlation of quantification of major bcr-abl mRNA between TMA (transcription mediated amplification) method and real-time quantitative PCR].
Abe, A; Bessyo, M; Ishikawa, M; Jinnai, I; Kato, C; Kyo, T; Miyamura, K; Niwa, T; Ogura, K; Sasaki, H; Yagasaki, F, 2009)		1.8
"Imatinib mesylate has significantly improved survival and quality of life of patients with gastrointestinal stromal tumors (GISTs). "( Insulin-like growth factor binding protein-3 has dual effects on gastrointestinal stromal tumor cell viability and sensitivity to the anti-tumor effects of imatinib mesylate in vitro.
Dupart, JJ; Godwin, AK; Hess, KR; Lee, HY; Taguchi, T; Trent, JC; Zhang, W, 2009)		1.99
"Imatinib mesylate has been demonstrated to allow the emergence of T cells directed against chronic myeloid leukemia cells. "( Emergence of BCR-ABL-specific cytotoxic T cells in the bone marrow of patients with Ph+ acute lymphoblastic leukemia during long-term imatinib mesylate treatment.
Barozzi, P; Basso, S; Comoli, P; D'Amico, R; Del Giovane, C; Forghieri, F; Locatelli, F; Luppi, M; Maccaferri, M; Morselli, M; Potenza, L; Quadrelli, C; Riva, G; Torelli, G; Vallerini, D; Volzone, F; Zanetti, E, 2010)		2.01
"Imatinib mesylate has proven to be an extremely effective and generally well tolerated drug, producing durable responses in most patients with chronic phase chronic myeloid leukaemia. "( Managing imatinib resistance in chronic myeloid leukaemia.
Hughes, T; Osborn, M, 2010)		1.8
"Imatinib mesylate has transformed the treatment for chronic myeloid leukemia (CML). "( Why doesn't imatinib cure chronic myeloid leukemia?
Redner, RL, 2010)		1.8
"Imatinib mesylate has been proved effective for advanced GIST."( A long-term follow-up of the imatinib mesylate treatment for the patients with recurrent gastrointestinal stromal tumor (GIST): the liver metastasis and the outcome.
Hou, M; Jiang, M; Yang, Y; Zhou, L; Zhu, J, 2010)		1.37
"Imatinib mesylate has been used for the treatment of unresectable or metastatic gastrointestinal stromal tumors (GIST). "( Imatinib induced severe skin reactions and neutropenia in a patient with gastrointestinal stromal tumor.
Bae, WK; Cho, SH; Chung, IJ; Hwang, JE; Shim, HJ; Yoon, JY, 2010)		1.8
"Imatinib mesylate has become a therapy of interest for the treatment of systemic sclerosis because of its ability to inhibit c-Abl and platelet-derived growth factor receptor, tyrosine kinases involved in profibrotic pathways. "( Imatinib and the treatment of fibrosis: recent trials and tribulations.
Gordon, J; Spiera, R, 2011)		1.81
"Imatinib mesylate has shown remarkable efficacy in the treatment of patients in the chronic phase of chronic myeloid leukemia. "( hTERT promotes imatinib resistance in chronic myeloid leukemia cells: therapeutic implications.
Deville, L; Hillion, J; Nguyen, E; Pendino, F; Samy, M; Ségal-Bendirdjian, E, 2011)		1.81
"Imatinib mesylate has shown significant safety and great effectiveness for patients with KIT-positive unresectable, advanced, or metastatic GIST."( [Evidence-based treatment of gastrointestinal stromal tumor (GIST) with tyrosine kinase inhibitors-imatinib and sunitinib].
Nishida, T; Omori, T; Ueshima, S, 2011)		1.09
"Imatinib mesylate has revolutionized the treatment of GIST. "( Advances in the surgical management of gastrointestinal stromal tumor.
Chaudhry, UI; DeMatteo, RP, 2011)		1.81
"Imatinib mesylate has become the treatment of choice for gastrointestinal stromal tumors (GISTs) and has made a revolutionary impact on survival rates. "( Bone marrow necrosis secondary to imatinib usage, mimicking spinal metastasis on magnetic resonance imaging and FDG-PET/CT.
Akcakaya, MO; Aras, Y; Bilgic, B; Unal, OF; Unal, SN, 2012)		1.82
"Imatinib mesylate has been commonly used in the treatment of patients with chronic myeloid leukemia (CML). "( [Molecular mechanism of imatinib-induced thrombocytopenia in treatment of patients with CML].
Jiang, QL; Meng, FY; Shu, LL; Yang, M, 2011)		1.81
"Imatinib mesylate has been the standard therapeutic treatment for chronic myeloid leukemia, advanced and metastatic gastrointestinal stromal tumor (GIST). "( Gynecomastia during imatinib mesylate treatment for gastrointestinal stromal tumor: a rare adverse event.
Liao, G; Liu, H; Yan, Z, 2011)		2.14
"Imatinib mesylate has revolutionized the treatment landscape for patients with newly diagnosed chronic myeloid leukemia. "( Chronic myeloid leukemia: mechanisms of resistance and treatment.
Cortes, J; Jabbour, E; Kantarjian, H; Parikh, SA, 2011)		1.81
"Imatinib mesylate has proven activity in treating locally advanced or metastatic gastrointestinal stromal tumors (GIST). "( Renal dysfunction in a renal transplant patient treated concurrently with cyclosporine and imatinib.
Egorin, MJ; Mulder, KE; Sawyer, MB, 2012)		1.82
"Imatinib mesylate has been efficacious in treating some of these MPDs."( Congenital and childhood myeloproliferative disorders with eosinophilia responsive to imatinib.
Abraham, S; Fluchel, M; Hancock, J; Jacobsen, J; Salama, M, 2012)		1.1
"Imatinib mesylate has been commonly used in the treatment of patients with chronic myeloid leukemia (CML). "( [Imatinib in treatment of thrombocythemia and other myeloproliferative diseases].
Shu, LL; Yang, M, 2012)		1.82
"Imatinib mesylate has been shown to be the first successful systemic therapy for patients with metastatic or unresectable disease and has revolutionized the treatment of this often rapidly progressive and fatal disease."( Management of gastrointestinal stromal tumors in the era of tyrosine kinase inhibitors.
Desai, J; George, S, 2002)		1.04
"Imatinib mesylate has been reported to have activity against desmoid tumor, most likely because of c-kit and PDGFR receptor tyrosine kinase activity inhibition, and warrants further study. "( Response of extraabdominal desmoid tumors to therapy with imatinib mesylate.
Baker, L; Hayes, C; Mace, J; McGinn, C; Sondak, V; Sybil Biermann, J; Thomas, D, 2002)		2
"Imatinib mesylate has recently been shown to be efficacious in MPDs with PDGFR activation."( Cloning of the t(1;5)(q23;q33) in a myeloproliferative disorder associated with eosinophilia: involvement of PDGFRB and response to imatinib.
Aguiar, RC; Aster, JC; Lee, C; Lopes, LF; Shipp, MA; Velloso, ER; Wilkinson, K, 2003)		1.04
"Imatinib mesylate has recently been shown to be highly effective in chronic-phase chronic myeloid leukemia (CML). "( Imatinib mesylate therapy of chronic phase chronic myeloid leukemia resistant or intolerant to interferon: results and prognostic factors for response and progression-free survival in 150 patients.
Alvarez-Larrán, A; Camós, M; Cervantes, F; Conde, E; García-Conde, J; Hernández-Boluda, JC; López-Jiménez, J; Odriozola, J; Osorio, S; Steegmann, JL; Villalón, L, 2003)		3.2
"Imatinib mesylate has promising single-agent antileukemic activity in patients with advanced Ph(+) acute leukemias."( Risk and prognosis of central nervous system leukemia in patients with Philadelphia chromosome-positive acute leukemias treated with imatinib mesylate.
Binckebanck, A; Brück, P; Gökbuget, N; Gschaidmeier, H; Hoelzer, D; Hofmann, WK; Komor, M; Leimer, L; Lübbert, M; Ottmann, OG; Pfeifer, H; Scheuring, U; Schleyer, E; Wassmann, B; Wolff, T, 2003)		1.24
"Imatinib mesylate has a substantial, but short term activity in the accelerated phase and blastic crisis of the Ph+ CML."( [Treatment of chronic myeloid leukemia with imatinib in the accelerated stage of the disease].
Boban, D; Bogdanić, V; Bulum, J; Kovacević, J; Krecak-Gverić, V; Labar, B; Mikulić, M; Mrsić-Davidović, S; Nemet, D; Sertić, D; Serventi-Seiwerth, R; Zadro, R, )		0.85
"Imatinib mesylate has become an effective agent for the treatment of chronic myeloid leukemia (CML). "( Imatinib mesylate effectively combines with chaperone-rich cell lysate-loaded dendritic cells to treat bcr-abl+ murine leukemia.
Feng, H; Graner, MW; Katsanis, E; Li, G; Zeng, Y, 2004)		3.21
"Imatinib mesylate has shown some promise in the treatment of HES. "( Imatinib mesylate treatment in two patients with idiopathic hypereosinophilic syndrome.
Kovacs, MJ; Payne, SM, )		3.02
"Imatinib mesylate has been found to have antitumor activity in patients with chordoma. "( Imatinib mesylate in chordoma.
Bertieri, R; Bertulli, R; Casali, PG; Colecchia, M; Crippa, F; Fumagalli, E; Greco, A; Gronchi, A; Grosso, F; Messina, A; Olmi, P; Orlandi, R; Pierotti, MA; Pilotti, S; Ripamonti, C; Spreafico, C; Stacchiotti, S; Tamborini, E, 2004)		3.21
"Imatinib mesylate has been reported to produce positive results in atypical chronic myeloproliferative disorders (CMD) with chromosomal translocations that disrupt the platelet-derived growth factor receptor beta gene (PDGFRB). "( Lack of response to imatinib mesylate in a patient with accelerated phase myeloproliferative disorder with rearrangement of the platelet-derived growth factor receptor beta-gene.
Bastie, JN; Castaigne, S; Cross, NC; Garcia, I; Mahon, FX; Terré, C, 2004)		2.09
"Imatinib mesylate has been useful in the treatment of Philadelphia chromosome-positive chronic myelogenous leukemia and B cell acute lymphoblastic leukemia through the inhibition of BCR-ABL tyrosine kinase activity."( Sole BCR-ABL inhibition is insufficient to eliminate all myeloproliferative disorder cell populations.
Cheng, D; McLaughlin, J; Shokat, KM; Witte, ON; Wong, S; Zhang, C, 2004)		1.04
"Imatinib mesylate (imatinib) has shown significant effects in patients with chronic myelogenous leukemia. "( [Imatinib mesylate plus G-CSF therapy for chronic myelogenous leukemia in the blastic crisis].
Asaka, M; Dazai, M; Hashino, S; Imamura, M; Izumiyama, K; Kobayashi, S; Kondo, T; Morita, R; Onozawa, M; Ota, S; Sogabe, S, 2004)		2.68
"Imatinib mesylate has become one of the main chemotherapeutic agents currently used to treat patients with chronic myeloid leukemia (CML). "( Imatinib-induced sweet syndrome in a patient with chronic myeloid leukemia.
Ayirookuzhi, SJ; Ma, L; Mills, G; Ramshesh, P, 2005)		1.77
"Imatinib mesylate has antitumor activity in vitro and in vivo against neuroblastoma cell lines and xenografts characterized by a different expression of receptor tyrosine kinases. "( Antitumor activity of imatinib mesylate in neuroblastoma xenografts.
Brueggen, J; Dominici, C; Gessi, M; Meco, D; Riccardi, A; Riccardi, R; Servidei, T, 2005)		2.09
"Imatinib mesylate has become the treatment of choice, especially for patients for whom allogenic stem cell transplantation is not an option."( Isolated central nervous system blast crisis in chronic myeloid leukemia.
Raghunadharao, D; Rajappa, S; Rao, IS; Surath, A; Uppin, SG, 2004)		1.04
"Imatinib mesylate has become the gold standard front-line treatment of chronic myelogenous leukemia through its ability to inhibit ABL tyrosine kinase. "( The role of the K247R substitution in the ABL tyrosine kinase domain in sensitivity to imatinib.
Cayuela, JM; Chabane, K; Hayette, S; Nicolini, FE; Rousselot, P; Thomas, X, 2006)		1.78
"Imatinib mesylate has considerable antineoplastic activity in patients with chronic myeloid leukaemia (CML) and some solid tumours. "( In vivo effects of imatinib mesylate on human haematopoietic progenitor cells.
Agis, H; Doninger, B; Drach, J; Jaeger, E; Marosi, C; Oehler, L; Schwarzinger, I; Sillaber, C; Valent, P, 2006)		2.1
"Imatinib mesylate has been shown to effectively block constitutively active KIT and delay tumor growth."( Flavopiridol targets c-KIT transcription and induces apoptosis in gastrointestinal stromal tumor cells.
Ambrosini, G; Chen, JH; Decarolis, P; Geha, RC; Kennealey, PT; Motwani, M; O'connor, R; Sambol, EB; Schwartz, GK; Singer, S; Wu, YV, 2006)		1.06
"Imatinib mesylate has been shown to induce hematologic and cytogenetic response in adults and children with CML."( Mobilization of Ph chromosome-negative peripheral blood stem cells in a child with chronic myeloid leukemia after imatinib-induced complete molecular remission.
Frangoul, H; Loken, MR; Manes, B; Vnencak-Jones, CL; Woods-Swafford, W, 2008)		1.07
"Imatinib mesylate has undoubted efficacy in the treatment of advanced gastrointestinal stromal tumors (GISTs), but complete responses have only been reported rarely."( Two cases of complete response after imatinib mesylate treatment of advanced GIST.
Economopoulos, T; Gaglia, A; Lianos, E; Nikolaou, M; Papaxoinis, G; Pectasides, D, )		1.85
"Imatinib mesylate (Gleevec) has dramatically changed the strategy of chronic myeloid leukemia (CML) therapy. "( [Innovation of clinical trials for anti-cancer drugs in Japan--proposals from academia with special reference to the development of novel Bcr-Abl/Lyn tyrosine kinase inhibitor INNO-406 (NS-187) for imatinib-resistant chronic myelogenous leukemia].
Maekawa, T, 2007)		1.78
"Imatinib mesylate has substantial activity in chronic phase of CML. "( Chronic phase chronic myeloid leukemia: response of imatinib mesylate and significance of Sokal score, age and disease duration in predicting the hematological and cytogenetic response.
Adil, SN; Kakepoto, GN; Khurshid, M; Syed, NN; Usman, M, 2007)		2.03
"Imatinib mesylate has revolutionised the treatment of GIST and offers good palliation and prolongation of overall survival."( Massive intraperitoneal stromal tumour: two-year follow-up.
Blasco, SB; Calvet, JD; Carbajo-Ferré, EM; Déjardin, Ddel C; González, MH; Lanao, MA; Lara, CD; Marín, AS; Moreno, VV; Pereferrer, FS; Pérez, JS, 2007)		1.78
"Imatinib mesylate has been well tolerable and widely used for chronic myeloid leukemia and gastrointestinal stromal tomor."( [Imatinib mesylate as a novel therapeutic drug for systemic rheumatic diseases].
Kameda, H, 2007)		1.97
"Imatinib mesylate (imatinib) has revolutionized clinical outcomes of patients with advanced gastrointestinal stromal tumor (GIST). "( Association of intratumoral vascular endothelial growth factor expression and clinical outcome for patients with gastrointestinal stromal tumors treated with imatinib mesylate.
Benjamin, RS; Lazar, AJ; McAuliffe, JC; Qiao, W; Raymond, AK; Steinert, DM; Thall, PF; Trent, JC; Yang, D, 2007)		1.98
"Imatinib mesylate (IM) has rapidly become the front-line treatment of Philadelphia-positive (Ph-pos) chronic myeloid leukemia, but the number of patients who were treated and are being treated with IM second-line is still substantial."( Long-term outcome of complete cytogenetic responders after imatinib 400 mg in late chronic phase, philadelphia-positive chronic myeloid leukemia: the GIMEMA Working Party on CML.
Abruzzese, E; Amabile, M; Baccarani, M; Breccia, M; Castagnetti, F; Cilloni, D; De Vivo, A; Iacobucci, I; Liberati, AM; Martinelli, G; Martino, B; Palandri, F; Pane, F; Poerio, A; Rosti, G; Saglio, G; Soverini, S; Specchia, G; Testoni, N, 2008)		1.79
"Imatinib mesylate has specific activity in inhibiting select tyrosine kinase receptors, including platelet-derived growth factor receptors (PDGFRs) and c-kit. "( Improving chemotherapeutic drug penetration in melanoma by imatinib mesylate.
Furuhashi, M; Kawamura, T; Ogawa, Y; Shimada, S; Tsukamoto, K, 2008)		2.03
"Imatinib mesylate has been proven to be effective in advanced GIST."( Imatinib mesylate treatment for advanced gastrointestinal stromal tumor: a pilot study focusing on patients experiencing sole liver metastasis after a prior radical resection.
Hou, M; Li, HY; Wang, Y; Zhang, J; Zhu, J, 2007)		2.5
"Imatinib mesylate also has activity as a single agent in CML blast crisis and in patients with Ph(+) acute lymphocytic leukemia (ALL)."( Signal transduction inhibition: results from phase I clinical trials in chronic myeloid leukemia.
Druker, B, 2001)		1.03

Actions

Imatinib mesylate plays a key role in the management of GISTs both as neoadjuvant therapy and in patients with recurrent and metastatic disease. Imatinib Mesylate (STI571) can inhibit c-kit tyrosine kinase activity.

ExcerptReferenceRelevance
"Imatinib mesylate plays a key role in the management of GISTs both as neoadjuvant therapy and in patients with recurrent and metastatic disease."( Duodenal gastrointestinal stromal tumor: From clinicopathological features to surgical outcomes.
Boccardi, V; Marano, L; Marrelli, D; Roviello, F, 2015)		1.14
"Imatinib mesylate and AMN107 inhibit orbital fibroblast proliferation and hyaluronan production induced by PDGF-BB; a factor highly expressed in orbital tissue from patients with GO. "( Imatinib mesylate and AMN107 inhibit PDGF-signaling in orbital fibroblasts: a potential treatment for Graves' ophthalmopathy.
Dik, WA; Dingjan, GM; Drexhage, HA; Hooijkaas, H; Paridaens, D; Schrijver, B; van Daele, PL; van den Bosch, WA; van Hagen, PM; van Steensel, L, 2009)		3.24
"Imatinib mesylate (STI571) can inhibit c-kit tyrosine kinase activity, but clinical trials have resulted in failure."( Imatinib mesylate (STI571) enhances amrubicin-induced cytotoxic activity through inhibition of the phosphatidylinositol 3-kinase/Akt pathway in small cell lung cancer cells.
Igishi, T; Kodani, M; Matsumoto, S; Matsunami, K; Morita, M; Nakazaki, H; Shigeoka, Y; Shimizu, E; Sumikawa, T; Suyama, H; Takeda, K; Ueda, Y, 2010)		2.52
"Imatinib mesylate may obviously inhibit the development of PF induced by bleomycin in mice."( [Effect of imatinib mesylate on bleomycin-induced pulmonary fibrosis in mice].
Li, L; Li, YQ, 2007)		2.17

Treatment

Imatinib mesylate treatment decreases fibrosis and results in the relatively rapid and steady improvement of skin changes and knee joint contractures in patients with stage 5 chronic kidney disease and NSF. Imatinib Mesylate is standard treatment for patients who have advanced gastrointestinal stromal tumor (GIST), but not all patients benefit equally.

ExcerptReferenceRelevance
"Imatinib mesylate (IM) treatment adherence is a challenge, especially in an economic-social population neglected from developing countries."( Pro-adherence complementary audiovisual educational intervention model for chronic myeloid leukemia patients treated with imatinib mesylate.
Barbosa, ADP; Carneiro, WJ; Cruz, AC; Cunha, LCD; Cunha, MMBD; Dewulf, NLS; Lemes, GA; Oliveira, FNM; Rodrigues Martins, M, 2023)		2.56
"Imatinib mesylate treatment was started postoperatively."( Prolapsed giant rectal gastrointestinal stromal tumor presented with incarceration A rare case of emergency rectal lesion.
Aydin, E; Erdogan, O; Rencuzogullari, A; Teke, Z, 2020)		1.28
"Imatinib mesylate treatment decreases fibrosis and results in the relatively rapid and steady improvement of skin changes and knee joint contractures in patients with stage 5 chronic kidney disease and NSF, despite the persistence of gadolinium in the tissues. "( Imatinib mesylate treatment of nephrogenic systemic fibrosis.
High, WA; Kay, J, 2008)		3.23
"Imatinib mesylate is standard treatment for patients who have advanced gastrointestinal stromal tumor (GIST), but not all patients benefit equally. "( Correlation of kinase genotype and clinical outcome in the North American Intergroup Phase III Trial of imatinib mesylate for treatment of advanced gastrointestinal stromal tumor: CALGB 150105 Study by Cancer and Leukemia Group B and Southwest Oncology Gr
Benjamin, RS; Bertagnolli, MM; Blanke, CD; Borden, EC; Bramwell, VH; Corless, CL; Demetri, GD; Fletcher, CD; Fletcher, JA; Heinrich, MC; Hollis, D; Owzar, K; Rankin, C; Ryan, CW; von Mehren, M, 2008)		2
"The imatinib mesylate treatment could prolong the survival of the patients who have recurrent GIST after the radical surgery in spite of an existence of the liver metastasis. "( A long-term follow-up of the imatinib mesylate treatment for the patients with recurrent gastrointestinal stromal tumor (GIST): the liver metastasis and the outcome.
Hou, M; Jiang, M; Yang, Y; Zhou, L; Zhu, J, 2010)		1.21
"Imatinib mesylate (IM) is the treatment of choice in patients with newly diagnosed chronic myeloid leukemia (CML), irrespectively of their age. "( Evaluation of tolerability and efficacy of imatinib mesylate in elderly patients with chronic phase CML: ELDERGLI study.
Avellaneda-Molina, C; Balanzat, J; Bargay, J; Boqué, C; del Cañizo, MC; Dios, A; Domingo, JM; Durán, S; Galende, J; García, I; Giraldo, P; Gracia, A; Hermosilla, M; López-Garrido, P; Luño-Fernandez, E; Moreno, MV; Nieto, JB; Salinas, R; Sánchez-Guijo, FM; Sanchez-Varela, JM; Soler, A, 2011)		2.07
"Imatinib mesylate treatment markedly reduces the burden of leukemia cells in chronic myelogenous leukemia (CML) patients. "( Persistence of leukemia stem cells in chronic myelogenous leukemia patients in prolonged remission with imatinib treatment.
Bhatia, R; Chakraborty, S; Chu, S; Huang, Q; Lin, A; McDonald, T; Snyder, DS, 2011)		1.81
"Imatinib mesylate treatment-induced activation of MAP kinases (including ERK1/2, p38, and JNK) and the phosphorylation of Akt and GSK-3beta."( BGP-15, a PARP-inhibitor, prevents imatinib-induced cardiotoxicity by activating Akt and suppressing JNK and p38 MAP kinases.
Berente, Z; Bognar, E; Gallyas, F; Gaszner, B; Kónyi, A; Sarszegi, Z; Sumegi, B, 2012)		1.1
"Imatinib mesylate treatment strongly suppressed STAT-5 tyrosine-phosphorylation in K562 and primary CML blasts."( In BCR-ABL-positive cells, STAT-5 tyrosine-phosphorylation integrates signals induced by imatinib mesylate and Ara-C.
Breitenbuecher, F; Carius, B; Fischer, T; Gschaidmeier, H; Huber, C; Kasper, S; Kindler, T; Stevens, T, 2003)		1.26
"Imatinib mesylate treatment is highly effective in chronic myeloid leukaemia and recent data have suggested that imatinib mesylate is also effective in the treatment of idiopathic hypereosinophilic syndrome (HES). "( Effective treatment of hypereosinophilic syndrome with imatinib mesylate.
Abboud, M; Bazarbachi, A; Bitar, N; Chami, B; Chehal, A; Kadri, A; Salem, Z; Zalloua, PA, 2003)		2.01
"Imatinib mesylate treatment causes remissions in a majority of patients with chronic myeloid leukemia (CML), but relapses are an increasing problem. "( Instability of BCR-ABL gene in primary and cultured chronic myeloid leukemia stem cells.
Eaves, A; Eaves, C; Jiang, X; Saw, KM, 2007)		1.78
"Imatinib mesylate treatment proved safe and effective for GIST patients who had liver metastasis alone. "( Imatinib mesylate treatment for advanced gastrointestinal stromal tumor: a pilot study focusing on patients experiencing sole liver metastasis after a prior radical resection.
Hou, M; Li, HY; Wang, Y; Zhang, J; Zhu, J, 2007)		3.23
"When treated with imatinib mesylate (STI571), a specific c-Abl family kinase inhibitor, the p38 expression was decreased and the loss of dopaminergic neurons was reduced."( c-Abl-p38
Fu, J; Mu, G; Ou, C; Qiu, L; Zhao, J, )		0.45
"Treatment with imatinib mesylate(imatinib) was initiated 13 days after surgery."( [A Case on the Long‒Term Effect of Imatinib on GIST of Unknown Primary Origin with Multiple Liver Metastases, Peritoneal Dissemination, and Bone Metastasis].
Ando, S; Fujiwara, Y; Kamei, R; Kitamura, Y; Matsui, H; Nagano, H; Sakamoto, K; Yamamoto, T; Yoshino, S, 2021)		0.96
"Treatment with imatinib mesylate suppressed cell proliferation, which was accompanied by apoptotic induction and cell cycle arrest in the investigated cell lines."( Antiproliferative effects of imatinib mesylate on ZR‑75‑1 and MDA‑MB‑231 cell lines via PDGFR‑β, PDGF‑BB, c‑Kit and SCF expression.
Aditya, A; Akbari Javar, H; Davoudi, ET; Ibrahim Noordin, M; Kadivar, A; Kamalidehghan, B; Sedghi, R, 2018)		1.11
"Treatment with imatinib mesylate, a tyrosine kinase inhibitor, results in rapid and complete resolution of hypereosinophilia and associated symptoms, except for those related to sub-endocardial fibrosis that may be irreversible."( Severe Prolonged Cough as Presenting Manifestation of FIP1L1-PDGFRA+ Chronic Eosinophilic Leukaemia: A Widely Ignored Association.
Bron, D; Cordier, JF; Cottin, V; Heimann, P; Lambert, F; Roufosse, F; Sidon, P, 2016)		0.77
"GIST treated with imatinib mesylate or second-line therapies that target mutant forms of these receptors generally escape disease control and progress over time."( Combination of Imatinib Mesylate and AKT Inhibitor Provides Synergistic Effects in Preclinical Study of Gastrointestinal Stromal Tumor.
Belinsky, MG; Devarajan, K; Gersz, L; Godwin, AK; Pathak, HB; Rink, L; von Mehren, M; Zhou, Y; Zook, P, 2017)		1.13
"Treatment with imatinib mesylate alone has been shown to have excellent long-term efficacy against myeloproliferative neoplasms; however, its long-term effects on ALL and AML have not been elucidated."( Marked response to imatinib mesylate in a patient with platelet-derived growth factor receptor beta-associated acute myeloid leukemia.
Ishikawa, T; Maruoka, H; Shimomura, Y, 2017)		1.12
"Treatment with imatinib mesylate (IM) results in an increased viable cell number of non-BCR-ABL-expressing cell lines by inhibiting spontaneous apoptosis. "( Cytoprotective effect of imatinib mesylate in non-BCR-ABL-expressing cells along with autophagosome formation.
Itoh, M; Kuroda, M; Miyazawa, K; Moriya, S; Naito, M; Ohtomo, T; Tomoda, A, 2010)		1.02
"Treatment with imatinib mesylate was started in an attempt to decrease the tumor load."( Disappearance of lentigines in a patient receiving imatinib treatment for familial gastrointestinal stromal tumor syndrome.
Campbell, T; Felsten, L; Moore, J, 2009)		0.69
"Treatment with imatinib mesylate at a daily dose of 75 mg/kg for 4 weeks reduced the graft size by an average of 80% (n = 8), significantly different from the original sizes within the group and from sizes of the grafts in 11 untreated mice in the control group (P < 0.001)."( Imatinib mesylate (Glivec) inhibits Schwann cell viability and reduces the size of human plexiform neurofibroma in a xenograft model.
Demestre, M; Friedrich, RE; Hagel, C; Herzberg, J; Holtkamp, N; Kluwe, L; Kurtz, A; Mautner, VF; Reuss, D; Von Deimling, A, 2010)		2.14
"Treatment by imatinib mesylate induced an haematological remission, the control of the infection and thoracotomy cicatrization."( [Clonal eosinophilia revealed by recurrent Staphylococcus aureus infection].
Dumon-Gubeno, MC; Figueredo, M; Medioni, LD; Mouroux, J; Naman, H; Nicolle, I; Tarhini, A; Vandenbos, F, 2011)		0.72
"Treatment with imatinib mesylate in previously treated chronic-phase chronic myeloid leukemia induced durable responses in a high proportion of patients and was related to satisfactory long-term and event-free survival."( Response to treatment with imatinib mesylate in previously treated chronic-phase chronic myeloid leukemia patients in a hospital in Brazil.
Daldegan, MB; Ferrari, I; Silveira, CA, 2011)		1.01
"Treatment with imatinib mesylate led to accumulation of the cells in G0/G1 phase of the cell cycle."( Imatinib mesylate inhibits T-cell proliferation in vitro and delayed-type hypersensitivity in vivo.
Bulur, PA; Dietz, AB; Knutson, GJ; Litzow, MR; Souan, L; Vuk-Pavlovic, S, 2004)		2.11
"Treatment with imatinib mesylate appears to reduce CML-associated bone marrow fibrosis in most patients who are treated during the chronic phase of disease. "( Imatinib mesylate therapy reduces bone marrow fibrosis in patients with chronic myelogenous leukemia.
Bueso-Ramos, CE; Cortes, J; Giles, F; Kantarjian, H; Medeiros, LJ; O'Brien, S; Rios, MB; Talpaz, M, 2004)		2.12
"Treatment with imatinib mesylate results in a high frequency of complete cytogenetic response, which can be further stratified using quantitative reverse-transcriptase polymerase chain reaction (qRT-PCR)."( Serial monitoring of BCR-ABL transcripts in chronic myelogenous leukemia (CML) treated with imatinib mesylate.
Ekeland-Sjöberg, K; Gustavsson, B; Hardling, M; Palmqvist, L; Ricksten, A; Stockelberg, D; Swolin, B; Wadenvik, H; Wei, Y, 2004)		0.88
"Treatment with imatinib mesylate and VK2 for 96 h resulted in suppression of cell growth in a dose-dependent manner in all cell lines tested."( Combination of vitamin K2 plus imatinib mesylate enhances induction of apoptosis in small cell lung cancer cell lines.
Miyazawa, K; Ohyashiki, K; Yokoyama, T; Yoshida, T, 2005)		0.95
"Treatment with Imatinib mesylate (Glivec), a recently discovered selective inhibitor of tyrosine kinases already used in chronic myeloid leukemia (in which an overexpression of tyrosine kinase is observed) was associated with tumor regression of more than 50% in the initial series of patients with GIST treated in 2001."( Treatment of gastrointestinal stromal tumors with imatinib mesylate: a major breakthrough in the understanding of tumor-specific molecular characteristics.
de Mestier, P; des Guetz, G, 2005)		0.92
"Treatment with imatinib mesylate (imatinib) alone rapidly normalized these parameters in parallel with a decrease in the number of blast cells."( Use of imatinib mesylate for favorable control of hypercalcemia mediated by parathyroid hormone-related protein in a patient with chronic myelogenous leukemia at blast phase.
Hyodo, H; Ito, T; Katayama, Y; Kimura, A; Miyoshi, N; Niimi, H; Tanaka, H, 2005)		1.12
"Treatment with imatinib mesylate (300 mg/day) promptly brought about complete remission."( Chronic eosinophilic leukemia with the FIP1L1-PDGFRalpha fusion gene in a patient with a history of combination chemotherapy.
Fujita, H; Kurata, M; Maeda, A; Matsui, T; Matsushita, A; Nagai, K; Sada, A; Takahashi, T; Tanaka, Y; Togami, K; Watanabe, N, 2006)		0.67
"Treatment with imatinib mesylate has been a well-accepted therapy for chronic myelogenous leukemia (CML) and gastrointestinal stromal tumors (GIST). "( Control of aggressive fibromatosis by treatment with imatinib mesylate. A case report and review of the literature.
Szarlej-Wcislo, K; Szczylik, C; Wcislo, G, 2007)		0.94
"Treatment with imatinib mesylate resulted within 6 months in a total disappearance of all chromosomal abnormalities with a complete cytogenetic and molecular response, which persists 3 years later."( Simultaneous regression of Philadelphia chromosome and multiple nonrecurrent clonal chromosomal abnormalities with imatinib mesylate in a patient autografted 22 years before for chronic myelogenous leukemia.
Barbu, V; Bories, D; Coppo, P; Gorin, NC; Portnoï, MF; Van Den Akker, J, 2007)		0.89

Toxicity

Imatinib mesylate is generally safe and has significant activity in the treatment of advanced GIST in Japanese patients. Despite its increasing use in the pediatric population, there are limited data regarding adverse event profiles. The patient was treated continuously with 400mg/day of imatinib Mesylate with no significant adverse events. The tumor gradually reduced in size.

ExcerptReferenceRelevance
" We did a phase I study to identify the dose-limiting toxic effects of imatinib in patients with advanced soft tissue sarcomas including GISTs."( Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a phase I study.
Dimitrijevic, S; Donato di Paola, E; Judson, I; Martens, M; Nielsen, OS; Sciot, R; Silberman, S; Stroobants, S; Van Glabbeke, M; van Oosterom, AT; Verweij, J; Webb, A, 2001)		0.31
" Toxic effects and haematological, biochemical, and radiological measurements were assessed during 8 weeks of follow-up."( Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a phase I study.
Dimitrijevic, S; Donato di Paola, E; Judson, I; Martens, M; Nielsen, OS; Sciot, R; Silberman, S; Stroobants, S; Van Glabbeke, M; van Oosterom, AT; Verweij, J; Webb, A, 2001)		0.31
"Five patients on 500 mg imatinib twice daily had dose-limiting toxic effects (severe nausea, vomiting, oedema, or rash)."( Safety and efficacy of imatinib (STI571) in metastatic gastrointestinal stromal tumours: a phase I study.
Dimitrijevic, S; Donato di Paola, E; Judson, I; Martens, M; Nielsen, OS; Sciot, R; Silberman, S; Stroobants, S; Van Glabbeke, M; van Oosterom, AT; Verweij, J; Webb, A, 2001)		0.31
" This report indicates that STI-571 is a safe and effective drug in heavily pretreated patients."( Safety and efficacy of STI-571 (imatinib mesylate) in patients with bcr/abl-positive chronic myelogenous leukemia (CML) after autologous peripheral blood stem cell transplantation (PBSCT).
Beck, J; Beltrami, G; Carella, A; Corsetti, MT; Fischer, T; Gschaidmeier, H; Hehlmann, R; Hess, GR; Hochhaus, A; Huber, C; Kreil, S; Meinhardt, P; Reifenrath, C; Schuch, B, 2002)		0.6
" There were no significant differences in toxic effects or response between the two doses."( Efficacy and safety of imatinib mesylate in advanced gastrointestinal stromal tumors.
Blanke, CD; Capdeville, R; Corless, C; Demetri, GD; Dimitrijevic, S; Druker, BJ; Eisenberg, B; Fletcher, CD; Fletcher, JA; Heinrich, MC; Janicek, M; Joensuu, H; Kiese, B; Peng, B; Roberts, PJ; Silberman, SL; Silverman, SG; Singer, S; Tuveson, DA; Van den Abbeele, AD; von Mehren, M, 2002)		0.63
" As a result of adverse effects, salvage therapy had to be discontinued or reduced in 14 patients (26%)."( Outcome and toxicity of salvage treatment on patients relapsing after autologous hematopoietic stem cell transplantation--experience from a single center.
Berlanga, J; Büchler, T; Encuentra, M; Ferra, C; Gallardo, D; Grañena, A; Hermosilla, M; Sarra, J, 2003)		0.32
" We conclude that filgrastim-induced CD34+ cell aphaeresis under simultaneous imatinib medication is safe and feasible in CML patients."( Filgrastim-induced stem cell mobilization in chronic myeloid leukaemia patients during imatinib therapy: safety, feasibility and evidence for an efficient in vivo purging.
Baskaynak, G; Dörken, B; Klühs, C; Kreuzer, KA; le Coutre, P; Movassaghi, K, 2004)		0.32
" In this article, we attempted to analyze the clinic efficacy and side effect of STI571 treatment on CML patients in different phase."( [Clinical efficacy and side effects of STI571 in treatment of patients with chronic myeloid leukemia].
Du, QF; Liu, QF; Liu, XL; Meng, FY; Song, LL; Xu, B; Zhang, S; Zheng, WY; Zhou, SY, 2004)		0.32
" At the same time, the side effects and adverse events of STI571 treatment were evaluated."( [Clinical efficacy and side effects of STI571 in treatment of patients with chronic myeloid leukemia].
Du, QF; Liu, QF; Liu, XL; Meng, FY; Song, LL; Xu, B; Zhang, S; Zheng, WY; Zhou, SY, 2004)		0.32
" To improve dosing flexibility, particularly with regard to the pediatric population and the management of adverse events, a scored 100-mg film-coated tablet has also been introduced."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
" After the third dosing, subjects were monitored to assess delayed drug-related adverse events."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
" Eight mild and one moderate adverse event considered to be drug related were reported."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
"Film-coated 100-mg (scored) and 400-mg tablet dose forms of imatinib are bioequivalent to the commercial 100-mg hard-gelatin capsule, and are as safe and well tolerated."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
" Mild non-hematologic adverse effects occurred in most of the patients, but were manageable and tolerable, or disappeared automatically."( [Efficacy and safety evaluation of imatinib in the treatment of patients with chronic granulocytic leukemia in accelerated phase].
Chen, SS; Jiang, B; Jiang, H; Jiang, Q; Lu, DP; Lu, Y, 2004)		0.32
" Although 29 of 39 patients required an adjustment of dosing because of grade 3 or 4 adverse events, most of the events were reversible, and 25 of the 29 patients were able to resume therapy."( Efficacy and safety of imatinib mesylate for patients in the first chronic phase of chronic myeloid leukemia: results of a Japanese phase II clinical study.
Bessho, M; Chiba, S; Emi, N; Fujimoto, M; Hirai, H; Hirano, M; Jinnai, I; Kawai, Y; Mizoguchi, H; Morishima, Y; Nakao, S; Nishimura, M; Ogura, M; Ohnishi, K; Ohno, R; Shimazaki, C; Taguchi, H; Takahashi, M; Tauchi, T; Urabe, A; Yazaki, F; Yokozawa, T, 2004)		0.63
" Severe adverse hematological effects of imatinib are extremely rare."( [Hematological side effects of tyrosine kinase inhibition using imatinib].
Hochhaus, A; Schmitt-Graeff, A, 2006)		0.33
" Maculopapular eruptions, erythematous eruptions, edema, and periorbital edema are the most common adverse events observed."( Imatinib mesylate and dermatology part 2: a review of the cutaneous side effects of imatinib mesylate.
Scheinfeld, N, 2006)		1.78
" iT with IM is a feasible and safe strategy for short-time 'bridging' management of patients with significant hematologic toxicity after standard daily dosing."( Intermittent dosage of imatinib mesylate in CML patients with a history of significant hematologic toxicity after standard dosing.
Divoký, V; Egorin, MJ; Faber, E; Holzerová, M; Indrák, K; Jarosová, M; Maresová, I; Nausová, J; Rozmanová, S, 2006)		0.64
" Transmission electron micrographs from humans and mice treated with imatinib show mitochondrial abnormalities and accumulation of membrane whorls in both vacuoles and the sarco- (endo-) plasmic reticulum, findings suggestive of a toxic myopathy."( Cardiotoxicity of the cancer therapeutic agent imatinib mesylate.
Alroy, J; Beahm, C; Clubb, FJ; Durand, JB; Force, T; Grazette, L; Iliescu, C; Kerkelä, R; Patten, R; Pesant, S; Rosenzweig, A; Salomon, RN; Shevtsov, S; Van Etten, RA; Walters, B; Yacobi, R, 2006)		0.59
" Adverse reactions (ARs) reported included: 33% (5) gastrointestinal events, 40% (6) dermatologic events and/or edema, 14% (2) blood toxicity, and 13% (2) asthenia."( [Effectiveness and safety of imatinib in seven gastrointestinal stromal tumor cases].
Gabella Bazarot, E; Giménez Castellanos, J; Grutzmancher Saiz, S; Marín Ariza, I; Reina Zoiló, JJ; Sánchez Gómez, E, )		0.13
" The incidence of adverse effect was 44."( [Efficacy and safety of adjuvant post-surgical therapy with imatinib in gastrointestinal stromal tumor patients with high risk of recurrence: interim analysis from a multicenter prospective clinical trial].
Bi, JW; Chen, DD; Ding, KF; Gu, J; Li, R; Lu, HS; Lu, YF; Shao, YF; Shi, YQ; Sun, YH; Wan, DS; Wang, PZ; Wu, XT; Yu, JR; Zhan, WH; Zhang, XH; Zou, XM, 2006)		0.33
"Imatinib is a promising postoperative adjuvant chemotherapy in GISTs patients with high risk of recurrence, and the adverse effects are receivable."( [Efficacy and safety of adjuvant post-surgical therapy with imatinib in gastrointestinal stromal tumor patients with high risk of recurrence: interim analysis from a multicenter prospective clinical trial].
Bi, JW; Chen, DD; Ding, KF; Gu, J; Li, R; Lu, HS; Lu, YF; Shao, YF; Shi, YQ; Sun, YH; Wan, DS; Wang, PZ; Wu, XT; Yu, JR; Zhan, WH; Zhang, XH; Zou, XM, 2006)		0.33
" Therapy was reasonably well tolerated; the most common treatment-related adverse events were fatigue, diarrhoea, skin discolouration, and nausea."( Efficacy and safety of sunitinib in patients with advanced gastrointestinal stromal tumour after failure of imatinib: a randomised controlled trial.
Baum, CM; Bello, CL; Blackstein, ME; Casali, PG; Demetri, GD; Desai, J; Fletcher, CD; Garrett, CR; George, S; Heinrich, MC; Huang, X; Judson, IR; McArthur, G; Morgan, JA; Shah, MH; van Oosterom, AT; Verweij, J, 2006)		0.33
" The monitoring of these toxic effects in clinical practice is impeded by a dearth of reliable laboratory methods."( Development and validation of a liquid chromatography method for the simultaneous determination of alpha-tocopherol, retinol and retinyl esters in human serum using a monolithic column for the monitoring of anticancer therapy side effects.
Krcmová, L; Melichar, B; Opletalová, V; Solich, P; Solichová, D; Urbánek, L, 2006)		0.33
" The most common adverse events reported included fluid retention, fatigue, diarrhea, and muscle cramps."( Emerging safety issues with imatinib and other Abl tyrosine kinase inhibitors.
Atallah, E; Cortes, J; Kantarjian, H, 2007)		0.34
" On the other hand, after 72 h pre-treatment, all concentrations of DHA tested (25, 50 and 100 microM) enhanced the toxic effect of imatinib."( Docosahexaenoic acid enhances the toxic effect of imatinib on Bcr-Abl expressing HL-60 cells.
Amarante-Mendes, GP; Curi, R; de Lima, TM, 2007)		0.34
" We here describe our experience on ocular complications in imatinib treated Ph+ CML patients, which consisted of a wide spectrum of adverse effects ranging from periobital oedema to serious adverse events such as glaucoma."( Ocular side effects in chronic myeloid leukemia patients treated with imatinib.
Alimena, G; Breccia, M; Cannella, L; Carmosino, I; Frustaci, A; Gentilini, F; Latagliata, R, 2008)		0.35
" We here describe the correlation of imatinib trough plasma concentrations (C(mins)) with clinical responses, event-free survival (EFS), and adverse events (AEs)."( Imatinib pharmacokinetics and its correlation with response and safety in chronic-phase chronic myeloid leukemia: a subanalysis of the IRIS study.
Druker, BJ; Gathmann, I; Guilhot, F; Krahnke, T; Larson, RA; O'Brien, SG; Riviere, GJ; Wang, Y, 2008)		0.35
" The overall and progression free survival, hematologic, cytogenetic and molecular response, and adverse events were evaluated."( [Efficacy and safety of imatinib in treatment of 151 chronic myeloid leukemia patients].
Li, JM; Shen, ZX; Wang, AH; Wang, L; You, JH; Zhou, L, 2008)		0.35
" (4) The adverse events of imatinib were moderate and tolerable."( [Efficacy and safety of imatinib in treatment of 151 chronic myeloid leukemia patients].
Li, JM; Shen, ZX; Wang, AH; Wang, L; You, JH; Zhou, L, 2008)		0.35
" The most frequent adverse effects related to the drug were nausea (78%), diarrhea (70%), dermatitis (62%), facial edema (61%), edema of the lower limbs (58%), vomiting (54%), and eyelid edema (51%)."( Efficacy and safety profile of imatinib mesylate (ST1571) in Japanese patients with advanced gastrointestinal stromal tumors: a phase II study (STI571B1202).
Hirota, S; Koseki, M; Miyakawa, K; Nishida, T; Ohtsu, A; Okamura, T; Sawaki, A; Shirao, K; Sugiyama, T, 2008)		0.63
"Imatinib mesylate is generally safe and has significant activity in the treatment of advanced GIST in Japanese patients."( Efficacy and safety profile of imatinib mesylate (ST1571) in Japanese patients with advanced gastrointestinal stromal tumors: a phase II study (STI571B1202).
Hirota, S; Koseki, M; Miyakawa, K; Nishida, T; Ohtsu, A; Okamura, T; Sawaki, A; Shirao, K; Sugiyama, T, 2008)		2.07
" Recently, dasatinib dose optimisation in chronic-phase has reduced the incidence of such adverse events without modification of the efficacy, however, their optimal overall management can efficiently reduce their severity and minimize their impact on disease response."( [Guidelines for the management of dasatinib (Sprycel)-induced side effects in chronic myelogenous leukemia and Philadelphia positive acute lymphoblastic leukemias].
Bergeron, A; Cony-Makhoul, P; Corm, S; Dubruille, V; Nicolini, FE; Rea, D; Rigal-Huguet, F, 2008)		0.35
" Cardiac toxicity is now recognized as a common adverse effect."( [Cardiac toxicity and edema].
Sakai, H; Takeuchi, S, 2008)		0.35
" The aim of our study was to analyse the frequency and type of hematological and non-hematological adverse events in our series of late and early chronic phase patients with CML treated with imatinib and correlate the grade of hematological toxicity with the response obtained."( Differences in hematological and non-hematological toxicity during treatment with imatinib in patients with early and late chronic phase chronic myeloid leukemia.
Alimena, G; Breccia, M; Cannella, L; Carmosino, I; Frustaci, AM; Latagliata, R; Santopietro, M; Stefanizzi, C, 2008)		0.35
" The most common ocular side effect associated with imatinib mesylate is periorbital edema."( Ocular side effects associated with imatinib mesylate and perifosine for gastrointestinal stromal tumor.
Dogan, SS; Esmaeli, B, 2009)		0.88
" We also review available data on the potential mechanisms by which these agents may cause adverse events (AEs) and we propose some general strategies to help clinicians to optimise treatment benefit with these agents."( Targeted therapies in the treatment of GIST: Adverse events and maximising the benefits of sunitinib through proactive therapy management.
Schöffski, P; Wolter, P, 2010)		0.36
" Adverse events included grade 4 hypocalcemia (n=1) and grade 3 fatigue, dehydration and anorexia, genitourinary/renal, lymphatic, metabolic, and ocular toxicity (n=1 each, 4%)."( Efficacy and safety of imatinib mesylate (Gleevec) and immunohistochemical expression of c-Kit and PDGFR-beta in a Gynecologic Oncology Group Phase Il Trial in women with recurrent or persistent carcinosarcomas of the uterus.
Alvarez, RD; Birrer, MJ; Boggess, JF; Darcy, KM; Elias, KM; Hoffman, JS; Huh, WK; Long, HJ; O'Malley, DM; Sill, MW, 2010)		0.67
"0 introduced the collection of attribution of adverse events (AEs) to study drug."( Evaluation of the value of attribution in the interpretation of adverse event data: a North Central Cancer Treatment Group and American College of Surgeons Oncology Group investigation.
Ballman, KV; Bot, B; Buckner, JC; DeMatteo, RP; Hillman, SL; Mandrekar, SJ; Nelson, H; Perez, EA; Sargent, DJ, 2010)		0.36
" This pilot study suggests that it is probably safe to perform cardiac monitoring on an annual basis."( The use of imatinib mesylate has no adverse effects on the heart function. Results of a pilot study in patients with chronic myeloid leukemia.
Barbosa, MM; Bittencourt, HN; Boersma, E; Clementino, NC; Geleijnse, ML; Marcolino, MS; Nunes, Mdo C; Ribeiro, AL; Silva, MH, 2011)		0.76
" Although these agents have largely revolutionized the treatment of the systemic autoimmune diseases, adverse reactions, which can be serious and life threatening, to the various immunosuppressive agents used in the treatment of CTD can occur."( Toxicity and monitoring of immunosuppressive therapy used in systemic autoimmune diseases.
Baughman, R; Decker, C; Meyer, KC, 2010)		0.36
" The most common motesanib treatment-related grade 3 adverse events included hypertension (23%), fatigue (9%), and diarrhea (5%)."( Efficacy and safety of motesanib, an oral inhibitor of VEGF, PDGF, and Kit receptors, in patients with imatinib-resistant gastrointestinal stromal tumors.
Baker, L; Benjamin, RS; Blay, JY; Bui, BN; Duyster, J; Hartmann, JT; McCoy, S; Reichardt, P; Rosen, LS; Schöffski, P; Schuetze, S; Skubitz, K; Stepan, DE; Sun, YN; Van Oosterom, A, 2011)		0.37
" The common adverse events were hand-foot syndrome, liver dysfunction, fatigue, anorexia and hypertension."( Clinical efficacy and safety of sunitinib after imatinib failure in Japanese patients with gastrointestinal stromal tumor.
Hara, K; Hijioka, S; Kawai, H; Kondo, S; Matsumoto, K; Mizuno, N; Niwa, Y; Sawaki, A; Tajika, M; Yamao, K, 2011)		0.37
" Although these agents are normally safe and effective, they can cause side effects that lead to intolerance and necessitate switching to an alternative treatment."( Management of adverse events associated with tyrosine kinase inhibitors in the treatment of chronic myeloid leukemia.
Deininger, M; Hochhaus, A; Jabbour, E, 2011)		0.37
" Many patients treated with imatinib experience adverse events (AEs) at some time during their treatment."( Uncommon or delayed adverse events associated with imatinib treatment for chronic myeloid leukemia.
Salie, R; Silver, RT, 2010)		0.36
" The foreseeable objective is to select personalized therapeutics, based on genetics characteristics that will result in more efficient and less toxic treatment."( How pharmacogenomics of biological response modifiers will influence clinical response and toxicity in dermatology.
Dalle, S; Shear, NH; Thomas, L, 2011)		0.37
" Treatment with imatinib is generally well tolerated, and the risk for severe adverse effects is low, generally occurring during the early phase of treatment and correlating with imatinib dose, phase of disease and patient's characteristics."( The safety profile of imatinib in CML and GIST: long-term considerations.
Judson, I; Thanopoulou, E, 2012)		0.38
"7%) experienced adverse events or severe adverse events with a suspected relationship to the study drug."( Activity and side effects of imatinib in patients with gastrointestinal stromal tumors: data from a German multicenter trial.
Bauer, S; Bokemeyer, C; Hartmann, JT; Hosius, C; Reichardt, P; Schlemmer, M; Schütte, R, 2011)		0.37
" Bosutinib exhibited an acceptable safety profile; the most common treatment-emergent adverse event was mild/moderate, typically self-limiting diarrhea."( Safety and efficacy of bosutinib (SKI-606) in chronic phase Philadelphia chromosome-positive chronic myeloid leukemia patients with resistance or intolerance to imatinib.
Abbas, R; Arkin, S; Besson, N; Brümmendorf, TH; Cortes, JE; Gambacorti-Passerini, C; Kantarjian, HM; Khoury, HJ; Kim, DW; Leip, E; Pasquini, R; Shen, ZX; Turkina, AG; Volkert, A; Wang, J, 2011)		0.37
"Cardiotoxicity was an unanticipated side effect elicited by the clinical use of imatinib (Imb)."( A multifaceted evaluation of imatinib-induced cardiotoxicity in the rat.
Agee, S; Estis, J; Hasinoff, B; Herman, EH; Knapton, A; Lipshultz, S; Lu, QA; Rosen, E; Rosenzweig, B; Thompson, K; Todd, JA; Zhang, J, 2011)		0.37
" It is well tolerated with mild adverse effects."( Gynecomastia during imatinib mesylate treatment for gastrointestinal stromal tumor: a rare adverse event.
Liao, G; Liu, H; Yan, Z, 2011)		0.69
"Long-term adverse effects of Imatinib in children with chronic myeloid leukemia (CML) are uncertain."( Imatinib has adverse effect on growth in children with chronic myeloid leukemia.
Bansal, D; Marwaha, RK; Shava, U; Trehan, A; Varma, N, 2012)		0.38
"Growth retardation is a significant adverse effect of imatinib in children with CML."( Imatinib has adverse effect on growth in children with chronic myeloid leukemia.
Bansal, D; Marwaha, RK; Shava, U; Trehan, A; Varma, N, 2012)		0.38
" Detailed information on the occurrence and management of defined cardiac adverse events was extracted."( Clinical cardiac safety profile of nilotinib.
Dörken, B; Fateh-Moghadam, S; Giles, FJ; Grille, P; Haverkamp, W; Kim, TD; Köhncke, C; le Coutre, P; Levitin, M; Schwarz, M, 2012)		0.38
" During a median follow-up of 44 months (range, 2-73), seven patients (9%), all of whom had received prior imatinib therapy, developed 11 clinical cardiac adverse events requiring treatment."( Clinical cardiac safety profile of nilotinib.
Dörken, B; Fateh-Moghadam, S; Giles, FJ; Grille, P; Haverkamp, W; Kim, TD; Köhncke, C; le Coutre, P; Levitin, M; Schwarz, M, 2012)		0.38
"Whereas new electrocardiographic abnormalities were recorded in 20% of all patients and some of them developed severe or even life-threatening coronary artery disease, QT prolongation, changes in left ventricular ejection fraction, and clinical cardiac adverse events were uncommon in patients treated with nilotinib."( Clinical cardiac safety profile of nilotinib.
Dörken, B; Fateh-Moghadam, S; Giles, FJ; Grille, P; Haverkamp, W; Kim, TD; Köhncke, C; le Coutre, P; Levitin, M; Schwarz, M, 2012)		0.38
" Sunitinib therapy was well tolerated, with most adverse events rated as grade 1 or 2 in severity."( Efficacy and safety of sunitinib in Chinese patients with imatinib-resistant or -intolerant gastrointestinal stromal tumors.
Gao, J; Hong, J; Li, J; Shen, L, 2012)		0.38
"5 mg/day continuous daily dose sunitinib dosing schedule appears to be the optimal choice for Chinese patients due to a decreased incidence of adverse events."( Efficacy and safety of sunitinib in Chinese patients with imatinib-resistant or -intolerant gastrointestinal stromal tumors.
Gao, J; Hong, J; Li, J; Shen, L, 2012)		0.38
" This rare but potentially fatal side effect has neither identified risk factors nor established treatment guideline."( Oxaliplatin-induced lung toxicity. Case report and review of the literature.
Abeni, C; Bertocchi, P; Prochilo, T; Zaniboni, A, 2012)		0.38
"This analysis confirms a slight 2-year PFS advantage of high-dose imatinib, but imatinib dose escalation could not lead to any other major clinical benefits, and brought more toxic effects for patients."( Efficacy and safety evaluation of two doses of imatinib for the treatment of advanced gastrointestinal stromal tumors (GISTs).
Chen, B; Wu, XT; Yang, P; Zhou, Y, 2012)		0.38
" Drug-related adverse events were reported in 130 (98%) patients assigned regorafenib and 45 (68%) patients assigned placebo."( Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumours after failure of imatinib and sunitinib (GRID): an international, multicentre, randomised, placebo-controlled, phase 3 trial.
Badalamenti, G; Bauer, S; Blackstein, M; Blay, JY; Casali, PG; Chung, J; Demetri, GD; Gelderblom, H; Hohenberger, P; Joensuu, H; Kang, YK; Kappeler, C; Kuss, I; Laurent, D; Le Cesne, A; Leahy, M; Maki, RG; Nguyen, BB; Nishida, T; Reichardt, P; Rutkowski, P; Schöffski, P; von Mehren, M; Xu, J, 2013)		0.39
" The hematologic/cytogenetic response, progression-free-survival (PFS), overall survival (OS) and adverse effects (AE) of the pts were assessed."( [Study on efficiency and safety of dasatinib in Chinese patients with chronic myelogenous leukemia who are resistant or intolerant to imatinib].
Hu, JD; Huang, XJ; Jin, J; Li, JY; Liu, T; Meng, FY; Shen, ZX; Wang, JM; Wang, JX; Wu, DP, 2012)		0.38
" Hand-foot syndrome was the most common adverse effect (25/48, 52."( [Efficacy and safety of sunitinib on patients with imatinib-resistant gastrointestinal stromal tumor].
Chen, ZF; Chi, P; Guan, GX; Jiang, WZ; Liu, X; Lu, HS, 2013)		0.39
" This review discusses the potential impact of treatment-, patient-, and disease-related characteristics on the emergence of adverse events during TKI therapy, with a focus on the underlying mechanisms believed to be responsible for a number of important adverse events associated with these agents and what implications they may have for treatment choice, particularly in the setting of first-line treatment."( Treatment-, patient-, and disease-related factors and the emergence of adverse events with tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia.
Irvine, E; Williams, C, 2013)		0.39
" Monitoring plasma levels of imatinib allowed us to judge if levels were toxic or not and to avoid discontinuation of imatinib in some cases."( [Imatinib plasma levels in the management of cutaneous side effects induced by imatinib (Glivec®): 2 case reports].
Daghfous, R; El Aïdli, S; Gaïes, E; Klouz, A; Lakhal, M; Sahnoun, R; Sraïri, S; Trabelsi, S, )		0.13
" (2) The drug-related adverse events were mostly grade 1/2 and were well-tolerated."( [Preliminary comparison of efficacy and safety of dasatinib and imatinib in newly diagnosed chronic myeloid leukemia].
Hu, JD; Huang, XJ; Shen, ZX; Wang, JX; Zhou, L, 2013)		0.39
"Dasatinib is an effective and safe therapy option and can be used as first-line therapy for newly diagnosed CML-CP patients."( [Preliminary comparison of efficacy and safety of dasatinib and imatinib in newly diagnosed chronic myeloid leukemia].
Hu, JD; Huang, XJ; Shen, ZX; Wang, JX; Zhou, L, 2013)		0.39
" Treatment-emergent adverse events (TEAEs) in each cohort were primarily gastrointestinal (diarrhea [86%/83%/74%], nausea [46%/48%/48%], and vomiting [37%/38%/43%])."( Bosutinib safety and management of toxicity in leukemia patients with resistance or intolerance to imatinib and other tyrosine kinase inhibitors.
Besson, N; Brümmendorf, TH; Cortes, JE; Durrant, S; Gambacorti-Passerini, C; Kantarjian, HM; Kelly, V; Khoury, HJ; Kim, DW; Leip, E; Martinelli, G; Porkka, K; Turnbull, K, 2014)		0.4
" The patient was treated continuously with 400mg/day of imatinib mesylate with no significant adverse events, and the tumor gradually reduced in size."( [A case of rectal gastrointestinal stromal tumor in an elderly patient who was successfully treated with imatinib mesylate with no significant adverse events].
Abe, M; Gomi, K; Ikeda, Y; Kajikawa, S; Maruyama, K; Mihara, M; Shimada, K; Shirota, H, 2014)		0.86
" After a 19-month median follow up, the safety profile of nilotinib 400 mg twice daily in patients switching from imatinib (n=35) was consistent with previous reports, and few new adverse events occurred in patients escalating from nilotinib 300 mg twice daily (n=19)."( Safety and efficacy of switching to nilotinib 400 mg twice daily for patients with chronic myeloid leukemia in chronic phase with suboptimal response or failure on front-line imatinib or nilotinib 300 mg twice daily.
Cervantes, F; Fan, X; Guilhot, F; Hochhaus, A; Hughes, TP; Kantarjian, HM; Kemp, C; Larson, RA; le Coutre, PD; Lobo, C; Menssen, HD; Niederwieser, D; Ossenkoppele, G; Rosti, G; Saglio, G; Shibayama, H, 2014)		0.4
" This article describes the results of the first investigation in which genotoxic and acute toxic properties of the drug were studied in higher plants."( Assessment of genotoxicity and acute toxic effect of the imatinib mesylate in plant bioassays.
Filipič, M; Knasmueller, S; Kundi, M; Mišík, M; Pichler, C; Rainer, B, 2014)		0.65
"2%); grade 3/4 drug-related non-hematologic adverse events included fatigue (3."( Efficacy and safety of radotinib in chronic phase chronic myeloid leukemia patients with resistance or intolerance to BCR-ABL1 tyrosine kinase inhibitors.
Cho, DJ; Choi, CW; Chung, JS; Do, YR; Jeong, SH; Jootar, S; Kim, DW; Kim, DY; Kim, H; Kim, HJ; Kim, JA; Kim, SH; Kim, YK; Kwak, JY; Lee, GY; Menon, H; Oh, SJ; Park, HL; Park, JS; Park, S; Saikia, T; Shin, HJ; Shin, JS; Sohn, SK; Zang, DY, 2014)		0.4
" The most common toxicities were primarily gastrointestinal adverse events (diarrhea [84%], nausea [45%], vomiting [37%]), which were primarily mild to moderate, typically transient, and first occurred early during treatment."( Bosutinib efficacy and safety in chronic phase chronic myeloid leukemia after imatinib resistance or intolerance: Minimum 24-month follow-up.
Assouline, S; Besson, N; Brümmendorf, TH; Cervantes, F; Cortes, JE; Durrant, S; Gambacorti-Passerini, C; Jin, J; Kantarjian, HM; Kelly, V; Khoury, HJ; Kim, DW; Leip, E; Masszi, T; Mathews, V; Pasquini, R; Shen, ZX; Turkina, AG; Turnbull, K; Vellenga, E; Zaritskey, A, 2014)		0.4
" Following the switch from branded imatinib to non-branded imatinib, 5/8 patients (63%) experienced treatment failure and 6/8 (75%) experienced severe and recurrent adverse events."( Deleterious effects of non-branded versions of imatinib used for the treatment of patients with chronic myeloid leukemia in chronic phase: a case series on an escalating issue impacting patient safety.
Saavedra, D; Vizcarra, F, 2014)		0.4
" The major adverse effects of combination therapy were rash, asthenia, edema and musculoskeletal events, and combination therapy was more prone to inducing neutropenia, thrombocytopenia and mild anemia."( [Efficacy and safety analysis of interferon combined with imatinib in treating chronic myeloid leukemia].
Bao, EN; Liu, Y; Lu, XC; Zhong, WW; Zhu, HL, 2014)		0.4
" In particular, muco-cutaneous side effects represent the most frequent non-hematological adverse events."( Tyrosine kinase inhibitors: muco-cutaneous side effects at the microscope.
Brazzelli, V; Croci, G; Grasso, V; Vassallo, C, 2014)		0.4
" Adverse events (AEs; any grade) with bosutinib versus imatinib were significantly more common for certain gastrointestinal events (diarrhea, 70% vs."( Safety of bosutinib versus imatinib in the phase 3 BELA trial in newly diagnosed chronic phase chronic myeloid leukemia.
Brümmendorf, TH; Cortes, JE; Dmoszynska, A; Duvillié, L; Gambacorti-Passerini, C; Gogat Marchant, K; Kantarjian, HM; Khattry, N; Lipton, JH; Pavlov, D; Rossiev, V; Wong, RS, 2014)		0.4
"Chronic myeloid leukemia (CML) treatment relies on tyrosine kinase inhibitors (TKIs), but their use can be associated with low-grade adverse events (AEs)."( Impact of low-grade adverse events on health-related quality of life in adult patients receiving imatinib or nilotinib for newly diagnosed Philadelphia chromosome positive chronic myelogenous leukemia in chronic phase.
Chen, L; Guérin, A; Hiscock, R; Ionescu-Ittu, R; Keir, C; Marynchenko, M; Nitulescu, R; Wu, EQ, 2014)		0.4
" Despite its increasing use in the pediatric population, there are limited data regarding adverse event profiles of imatinib mesylate in children, and few reports exist in the literature focusing on nonhematologic toxicity in this population."( Nonhematologic toxicity of imatinib mesylate in pediatric patients with chronic myelogenous leukemia: a predominance of musculoskeletal pain.
Gressett Ussery, SM; Heym, KM; Philpot, LM; Trinkman, H, 2015)		0.92
"Rare but serious cardiovascular and pulmonary adverse events (AEs) have been reported in patients with chronic myeloid leukemia treated with BCR-ABL inhibitors."( Cardiovascular and pulmonary adverse events in patients treated with BCR-ABL inhibitors: Data from the FDA Adverse Event Reporting System.
Cortes, J; Malhotra, R; Mauro, M; Saglio, G; Steegmann, JL; Ukropec, JA; Wallis, NT, 2015)		0.42
" Eight-year probabilities of adverse drug reactions (ADR) were 76%, of grades 3-4 22%, of non-hematologic 73%, and of hematologic 28%."( Safety and efficacy of imatinib in CML over a period of 10 years: data from the randomized CML-study IV.
Burchert, A; Dengler, J; Dietz, CT; Fabarius, A; Falge, C; Hanfstein, B; Hasford, J; Hehlmann, R; Heinrich, L; Hochhaus, A; Kalmanti, L; Kanz, L; Krause, SW; Lauseker, M; Müller, MC; Neubauer, A; Oppliger-Leibundgut, E; Pfirrmann, M; Pfreundschuh, M; Proetel, U; Rinaldetti, S; Saussele, S; Scheid, C; Spiekermann, K; Stegelmann, F, 2015)		0.42
" With regard to safety issues, grade 3/4 non-hematologic adverse events (AEs) were infrequent."( A prospective analysis of clinical efficacy and safety in chronic myeloid leukemia-chronic phase patients with imatinib resistance or intolerance as evaluated using European LeukemiaNet 2013 criteria.
Akagi, T; Chou, T; Harigae, H; Ishida, Y; Ishizawa, K; Ito, S; Kimura, J; Kubo, K; Motegi, M; Murai, K; Noji, H; Oba, K; Ogawa, K; Sakamoto, J; Shimosegawa, K; Sugawara, T; Tajima, K; Yokoyama, H, 2015)		0.42
"Patients with non-optimal responses (who meet ELN 2013 warning and failure criteria) to imatinib should be switched quickly to dasatinib, which is less toxic in CML-CP patients, to improve their prognoses."( A prospective analysis of clinical efficacy and safety in chronic myeloid leukemia-chronic phase patients with imatinib resistance or intolerance as evaluated using European LeukemiaNet 2013 criteria.
Akagi, T; Chou, T; Harigae, H; Ishida, Y; Ishizawa, K; Ito, S; Kimura, J; Kubo, K; Motegi, M; Murai, K; Noji, H; Oba, K; Ogawa, K; Sakamoto, J; Shimosegawa, K; Sugawara, T; Tajima, K; Yokoyama, H, 2015)		0.42
"6%) and adverse events (31."( Long-term safety and efficacy of imatinib in pulmonary arterial hypertension.
Barst, RJ; Chang, HJ; Dario Vizza, C; Felser, JM; Frantz, RP; Frost, AE; Fukumoto, Y; Galié, N; Ghofrani, HA; Hassoun, PM; Hoeper, MM; Klose, H; Lawrence, D; Matsubara, H; Morrell, NW; Peacock, AJ; Pfeifer, M; Quinn, DA; Simonneau, G; Tapson, VF; Torres, F; Yang, W, 2015)		0.42
"Severe adverse events, significant side effects, and a high discontinuation rate limit the utility of imatinib in the treatment of PAH."( Long-term safety and efficacy of imatinib in pulmonary arterial hypertension.
Barst, RJ; Chang, HJ; Dario Vizza, C; Felser, JM; Frantz, RP; Frost, AE; Fukumoto, Y; Galié, N; Ghofrani, HA; Hassoun, PM; Hoeper, MM; Klose, H; Lawrence, D; Matsubara, H; Morrell, NW; Peacock, AJ; Pfeifer, M; Quinn, DA; Simonneau, G; Tapson, VF; Torres, F; Yang, W, 2015)		0.42
" Compared with the HR group, the TKI+HR group had no increase in the toxic responses to chemotherapy and had a decrease in the infection rate during the induction period."( [Efficacy and safety of imatinib for the treatment of Philadelphia chromosome-positive acute lymphoblastic leukemia in children].
Chen, XJ; Guo, Y; Liu, F; Liu, TF; Liu, XM; Qi, BQ; Ruan, M; Wang, SC; Yang, WY; Zhang, JY; Zhang, L; Zhu, XF; Zou, Y, 2015)		0.42
" Adverse cutaneous reactions induced by imatinib are frequent, generally moderate, and dose-dependent."( Possible Role of Interleukin-31/33 Axis in Imatinib Mesylate-Associated Skin Toxicity.
Allegra, A; Alonci, A; Calapai, G; Gangemi, S; Maisano, V; Mannucci, C; Musolino, C; Russo, S, 2015)		0.68
" Although all TKIs are associated with nonhematologic adverse events (AEs), experience with imatinib suggested that toxicities are typically manageable and apparent early during drug development."( Tyrosine Kinase Inhibitor-Associated Cardiovascular Toxicity in Chronic Myeloid Leukemia.
Deininger, M; Moslehi, JJ, 2015)		0.42
"The purpose of this study was to determine the frequency of major cytogenetic response (MCyR) and adverse events with nilotinib in adults with imatinib-resistant Philadelphia chromosome-positive chronic myeloid leukemia (CML)."( Response and Adverse Effects of Nilotinib in Imatinib-resistant Chronic Myeloid Leukemia Patients: Data From a Developing Country.
Hussain, S; Usman Shaikh, M, 2015)		0.42
" The frequency of adverse effects was assessed at 6 months, and the patient overall survival was calculated after 3 years."( Response and Adverse Effects of Nilotinib in Imatinib-resistant Chronic Myeloid Leukemia Patients: Data From a Developing Country.
Hussain, S; Usman Shaikh, M, 2015)		0.42
" The most frequent nonhematologic adverse events were myalgia and headache."( Response and Adverse Effects of Nilotinib in Imatinib-resistant Chronic Myeloid Leukemia Patients: Data From a Developing Country.
Hussain, S; Usman Shaikh, M, 2015)		0.42
"The nilotinib response rates were higher in chronic phase patients, and the most common adverse events were thrombocytopenia, myalgia, and headache."( Response and Adverse Effects of Nilotinib in Imatinib-resistant Chronic Myeloid Leukemia Patients: Data From a Developing Country.
Hussain, S; Usman Shaikh, M, 2015)		0.42
" The hematologic, cytogenetic and molecular responses were assessed at 3- and 6-month, and adverse effects were evaluated throughout the study."( [A prospective, multi-centre clinical trial to evaluate the early clinical efficacy and safety of a generic imatinib in treating patients with chronic phase of chronic myelogenous leukemia].
DU, X; Han, X; Hou, M; Hu, J; Jiang, Q; Jin, J; Li, Y; Liu, B; Liu, T; Ma, J; Meng, F; Shen, Z; Wu, D; Zhao, D, 2015)		0.42
" No adverse effects related death occurred."( [A prospective, multi-centre clinical trial to evaluate the early clinical efficacy and safety of a generic imatinib in treating patients with chronic phase of chronic myelogenous leukemia].
DU, X; Han, X; Hou, M; Hu, J; Jiang, Q; Jin, J; Li, Y; Liu, B; Liu, T; Ma, J; Meng, F; Shen, Z; Wu, D; Zhao, D, 2015)		0.42
" In this study, we investigated the toxic potential of the mixture of 5-FU + IM + ET against green alga Pseudokirchneriella subcapitata and cyanobacterium Synechococcus leopoliensis, and the stability and sorption of these drugs to algal cells."( Toxicity of the mixture of selected antineoplastic drugs against aquatic primary producers.
Barceló, D; Brezovsek, P; de Alda, ML; Elersek, T; Filipič, M; Heath, E; Korošec, M; Milavec, S; Negreira, N; Ščančar, J; Zonja, B, 2016)		0.43
"This review describes key efficacy data on imatinib for the treatment of GIST, and focuses on safety and tolerability of imatinib, with emphasis on common adverse events management and long term toxicity profile."( A safety evaluation of imatinib mesylate in the treatment of gastrointestinal stromal tumor.
Ben Ami, E; Demetri, GD, 2016)		0.74
" The toxicity profile of imatinib has been well characterized, and although the majority of patients experience an adverse event during treatment with imatinib, these side effects are usually mild and manageable, with the majority of patients continuing treatment uninterruptedly."( A safety evaluation of imatinib mesylate in the treatment of gastrointestinal stromal tumor.
Ben Ami, E; Demetri, GD, 2016)		0.74
" We evaluated vascular/cardiac toxicities associated with long-term bosutinib treatment for Philadelphia chromosome-positive (Ph+) leukemia based on treatment-emergent adverse events (TEAEs) and changes in QTc intervals and ejection fraction in two studies: a phase 1/2 study of second-/third-/fourth-line bosutinib for Ph+ leukemia resistant/intolerant to prior TKIs (N = 570) and a phase 3 study of first-line bosutinib (n = 248) versus imatinib (n = 251) in chronic phase chronic myeloid leukemia."( Long-term evaluation of cardiac and vascular toxicity in patients with Philadelphia chromosome-positive leukemias treated with bosutinib.
Aguiar, JM; Brümmendorf, TH; Cortes, JE; Dimitrov, S; Durand, JB; Fly, KD; Gambacorti-Passerini, C; Jean Khoury, H; Kantarjian, H; Leip, E; Lipton, JH; Matczak, E; Mauro, MJ; Pavlov, D; Shapiro, M, 2016)		0.43
"Many patients with chronic myeloid leukemia in chronic phase experience chronic treatment-related adverse events (AEs) during imatinib therapy."( Evaluating the Impact of a Switch to Nilotinib on Imatinib-Related Chronic Low-Grade Adverse Events in Patients With CML-CP: The ENRICH Study.
Akard, LP; Busque, L; Cortes, JE; Keir, C; Lin, FP; Lipton, JH; Mauro, MJ; Miller, CB; Pinilla-Ibarz, J; Warsi, G, 2016)		0.43
"In the phase II ENRICH (Exploring Nilotinib to Reduce Imatinib Related Chronic Adverse Events) study (N = 52), the effect of switching patients with imatinib-related chronic low-grade nonhematologic AEs from imatinib to nilotinib was evaluated."( Evaluating the Impact of a Switch to Nilotinib on Imatinib-Related Chronic Low-Grade Adverse Events in Patients With CML-CP: The ENRICH Study.
Akard, LP; Busque, L; Cortes, JE; Keir, C; Lin, FP; Lipton, JH; Mauro, MJ; Miller, CB; Pinilla-Ibarz, J; Warsi, G, 2016)		0.43
" The most common grade 3 or 4 adverse event was a hand-foot skin reaction (25%)."( Efficacy and Safety of Regorafenib in Korean Patients with Advanced Gastrointestinal Stromal Tumor after Failure of Imatinib and Sunitinib: A Multicenter Study Based on the Management Access Program.
Im, SA; Kang, YK; Kim, TY; Lee, SJ; Park, JO; Park, SR; Ryoo, BY; Ryu, MH; Son, MK, 2017)		0.46
" The most common Glivec related adverse effects were edema (n=278, 51% ), fatigue (n=218, 40% ), gastrointestinal disorders (n=190, 35%), muscle cramps (n=118, 22%), skin color changes (n=118, 22%), weight gain (n=71, 13%), rash (n=60, 11%), hepatic function abnormality (n=55, 10%), and cytopenia (n=38, 7%)."( [The impact of Glivec related side effects on daily life in Chinese patients with chronic myeloid leukemia in the chronic phase].
Huang, XJ; Jiang, Q; Wang, HB; Yu, L, 2016)		0.43
" The most frequently reported adverse reactions (>30%) include edema, nausea, vomiting, muscle cramps, musculoskeletal pain, diarrhea, rash, fatigue and abdominal pain."( New Drug and Possible New Toxicity - Squamous Cell Carcinoma Following Imatinib in Patients with Gastrointestinal Stromal Tumors.
Inayat, F; Saif, MW, 2016)		0.43
"0ng/L, which are several orders of magnitude lower from those that caused adverse effects in fish and human derived cells."( Assessment of the genotoxicity of the tyrosine kinase inhibitor imatinib mesylate in cultured fish and human cells.
Filipič, M; Gajski, G; Garaj-Vrhovac, V; Gerić, M; Novak, M; Nunić, J; Žegura, B, 2017)		0.69
"BCR-ABL1 tyrosine kinase inhibitors (TKIs) are established treatments for chronic myelogenous leukemia (CML); however, they are associated with infrequent, but clinically serious adverse events (AEs)."( Healthcare and economic burden of adverse events among patients with chronic myelogenous leukemia treated with BCR-ABL1 tyrosine kinase inhibitors.
Bilmes, R; Lin, J; Lingohr-Smith, M; Makenbaeva, D, 2017)		0.46
" Most (85%; n = 144) adverse events were mild."( Generic Imatinib Therapy Among Jordanians: An Observational Assessment of Efficacy and Safety in Routine Clinical Practice.
Abbasi, S; Alrabi, K; Awidi, A; Kheirallah, KA, 2017)		0.46
"Short-term mucocutaneous adverse effects are well documented with imatinib."( Long-term mucocutaneous adverse effects of imatinib in Indian chronic myeloid leukemia patients.
Dogra, S; Handa, S; Khadwal, A; Kumari, S; Lad, D; Malhotra, P; Prakash, G; Suri, V; Varma, S; Vinay, K; Yanamandra, U, 2018)		0.48
"To study the long-term mucocutaneous adverse effects of imatinib and factors predicting these adverse effects."( Long-term mucocutaneous adverse effects of imatinib in Indian chronic myeloid leukemia patients.
Dogra, S; Handa, S; Khadwal, A; Kumari, S; Lad, D; Malhotra, P; Prakash, G; Suri, V; Varma, S; Vinay, K; Yanamandra, U, 2018)		0.48
"98 cutaneous adverse effects were seen per patient."( Long-term mucocutaneous adverse effects of imatinib in Indian chronic myeloid leukemia patients.
Dogra, S; Handa, S; Khadwal, A; Kumari, S; Lad, D; Malhotra, P; Prakash, G; Suri, V; Varma, S; Vinay, K; Yanamandra, U, 2018)		0.48
"Cutaneous hyperpigmentation and periorbital edema are common long-term adverse effects of imatinib in Indian patients."( Long-term mucocutaneous adverse effects of imatinib in Indian chronic myeloid leukemia patients.
Dogra, S; Handa, S; Khadwal, A; Kumari, S; Lad, D; Malhotra, P; Prakash, G; Suri, V; Varma, S; Vinay, K; Yanamandra, U, 2018)		0.48
" Hypertension (20%; 95% CI 7-33), hand-foot skin reaction (22%; 95% CI 17-27), and hypophosphatemia (18%; 95% CI 5-41) were common grade ≥3 regorafenib-related adverse events in patients treated with regorafenib after failure with imatinib and sunitinib treatments."( Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumor after failure with imatinib and sunitinib treatment: A meta-analysis.
Jiang, T; Piao, D; Wang, W; Zhang, Z, 2017)		0.46
" Close monitoring and appropriate management of grade ≥3 regorafenib-related adverse events should be considered during treatment."( Efficacy and safety of regorafenib for advanced gastrointestinal stromal tumor after failure with imatinib and sunitinib treatment: A meta-analysis.
Jiang, T; Piao, D; Wang, W; Zhang, Z, 2017)		0.46
" Adverse events were consistent with those reported in other nilotinib studies."( Efficacy and safety of switching to nilotinib in patients with CML-CP in major molecular response to imatinib: results of a multicenter phase II trial (NILSw trial).
Akashi, K; Hino, M; Hirase, C; Ishikawa, J; Kamimura, T; Kanakura, Y; Kawaguchi, T; Kuroda, J; Matsumura, I; Matsuoka, KI; Miyamoto, T; Nakamae, H; Shibayama, H; Shimose, T, 2018)		0.48
"Some patients receiving a tyrosine kinase inhibitor (TKI) for the first-line treatment of chronic phase chronic myeloid leukemia (CML-CP) experience intolerable adverse events."( Efficacy and safety of nilotinib 300 mg twice daily in patients with chronic myeloid leukemia in chronic phase who are intolerant to prior tyrosine kinase inhibitors: Results from the Phase IIIb ENESTswift study.
Anderson, L; Branford, S; D'Rozario, J; Gervasio, O; Hiwase, D; Hughes, T; Irving, I; Levetan, C; Powell, A; Roberts, W; Solterbeck, A; Tan, P; Taper, J; Traficante, R; Wright, M; Yeung, DT, 2018)		0.48
" Of the non-hematological adverse events associated with intolerance to prior imatinib or dasatinib, 74% resolved within 12 weeks of switching to nilotinib 300 mg bid."( Efficacy and safety of nilotinib 300 mg twice daily in patients with chronic myeloid leukemia in chronic phase who are intolerant to prior tyrosine kinase inhibitors: Results from the Phase IIIb ENESTswift study.
Anderson, L; Branford, S; D'Rozario, J; Gervasio, O; Hiwase, D; Hughes, T; Irving, I; Levetan, C; Powell, A; Roberts, W; Solterbeck, A; Tan, P; Taper, J; Traficante, R; Wright, M; Yeung, DT, 2018)		0.48
"Chronic, low-grade adverse events are common in patients with chronic myeloid leukemia who are treated with imatinib."( Outcomes of switching to dasatinib after imatinib-related low-grade adverse events in patients with chronic myeloid leukemia in chronic phase: the DASPERSE study.
Abruzzese, E; Kim, DW; Mohamed, H; Pinilla-Ibarz, J; Rong, Y; Saussele, S; Williams, LA; Zyczynski, T, 2018)		0.48
" To prevent adverse side effects of drugs, it is important to investigate potential toxicity in vitro."( ATP-based cell viability assay is superior to trypan blue exclusion and XTT assay in measuring cytotoxicity of anticancer drugs Taxol and Imatinib, and proteasome inhibitor MG-132 on human hepatoma cell line HepG2.
Kammerer, S; Küpper, JH; Nowak, E, 2018)		0.48
"This multicenter cooperative study aimed to analyze the adverse events (AEs) associated with tyrosine kinase inhibitors (TKIs) used as initial treatment for chronic-phase chronic myeloid leukemia (CML-CP) and their impact on outcome."( Severe adverse events by tyrosine kinase inhibitors decrease survival rates in patients with newly diagnosed chronic-phase chronic myeloid leukemia.
Fukuhara, T; Haseyama, Y; Hirayama, Y; Ikeda, H; Imamura, M; Ishihara, T; Ito, S; Kakinoki, Y; Kobayashi, H; Kobayashi, R; Kohda, K; Kondo, T; Kuroda, H; Kurosawa, M; Matsukawa, T; Mori, A; Nishio, M; Ota, S; Sakai, H; Sarashina, T; Sato, K; Shindo, M; Takahashi, T; Yamamoto, M; Yamamoto, S; Yoshida, M, 2018)		0.48
" Most adverse events initially occurred within two years."( Safety and efficacy of second-line bosutinib for chronic phase chronic myeloid leukemia over a five-year period: final results of a phase I/II study.
Bardy-Bouxin, N; Brümmendorf, TH; Cortes, JE; Crescenzo, R; DeAnnuntis, L; Gambacorti-Passerini, C; Kantarjian, HM; Khoury, HJ; Kim, DW; Leip, E; Lipton, JH; Noonan, K; Schafhausen, P; Shapiro, M, 2018)		0.48
" On the brink of commercialization of generic imatinib, this study aims to evaluate the therapeutic pattern of CP-CML and the occurrence of adverse events (AEs) over a decade of local real clinical practice."( Pattern of Use and Long-Term Safety of Tyrosine Kinase Inhibitors: A Decade of Real-World Management of Chronic Myeloid Leukemia.
Bettiol, A; Chinellato, A; Crescioli, G; Gherlinzoni, F; Giusti, P; Lombardi, N; Marconi, E; Vannacci, A; Walley, T, 2018)		0.48
" The adverse event (AE) profile of dasatinib at 4 years was similar to that at 6 and 18 months."( Four-year follow-up of patients with imatinib-resistant or intolerant chronic myeloid leukemia receiving dasatinib: efficacy and safety.
Hu, J; Huang, X; Jiang, Q; Jin, J; Li, J; Liu, T; Meng, F; Shen, Z; Wang, J; Wu, D, 2019)		0.51
" The NMAs were built for six outcomes at 12 months: complete cytogenetic response (CCyR), major cytogenetic response (MCyR), deep molecular response, major molecular response (MMR), complete haematologic response and incidence of serious adverse events."( Comparative efficacy and safety of tyrosine kinase inhibitors for chronic myeloid leukaemia: A systematic review and network meta-analysis.
Aguiar, KS; Fachi, MM; Fernandez-Llimos, F; Figueiredo, BC; Lenzi, L; Leonart, LP; Pontarolo, R; Tonin, FS, 2018)		0.48
"5 months after switch to generic imatinib, 17% of patients reported new or worsening side effects, but grade 3-4 non-hematological adverse events were rare."( Safety and efficacy of switching from branded to generic imatinib in chronic phase chronic myeloid leukemia patients treated in Italy.
Basso, M; Bertoldero, G; Binotto, G; Bonalumi, A; Bonifacio, M; D'Amore, F; Danini, M; De Biasi, E; Fanin, R; Fortuna, S; Frison, L; Griguolo, D; Krampera, M; Marin, L; Miggiano, MC; Minotto, C; Pizzolo, G; Ruggeri, M; Sartori, R; Scaffidi, L; Semenzato, G; Stulle, M; Tinelli, M; Tiribelli, M, 2018)		0.48
" Although 12 patients experienced vascular adverse events, no new safety issues were observed in patients with adverse events."( Efficacy and safety of tyrosine kinase inhibitors for newly diagnosed chronic-phase chronic myeloid leukemia over a 5-year period: results from the Japanese registry obtained by the New TARGET system.
Inokuchi, K; Iriyama, N; Kawaguchi, T; Kizaki, M; Kurokawa, M; Matsumura, I; Nakamura, F; Nakaseko, C; Naoe, T; Ohnishi, K; Okamoto, S; Ono, T; Sumi, M; Suzuki, R; Takahashi, N; Usui, N; Yamamoto, K, 2019)		0.51
"Cardiovascular or arteriothrombotic adverse events (CV- or AT-AEs) are reported in chronic myeloid leukemia (CML) patients treated with tyrosine kinase inhibitors (TKIs)."( Analysis of cardiovascular and arteriothrombotic adverse events in chronic-phase CML patients after frontline TKIs.
Ahaneku, H; Boddu, PC; Borthakur, G; Cortes, JE; Estrov, Z; Garcia-Manero, G; Jabbour, E; Jain, P; Kadia, TM; Kantarjian, H; Nogueras-González, GM; O'Brien, S; Ravandi, F; Sam, P; Sasaki, K; Verstovsek, S, 2019)		0.51
"2%) had grade 1-2 adverse events (AEs) and 12 patients (41."( Activity and Safety of Palbociclib in Patients with Advanced Gastrointestinal Stromal Tumors Refractory to Imatinib and Sunitinib: A Biomarker-driven Phase II Study.
Bellera, CA; Blay, JY; Boidot, R; Bompas, E; Bouche, O; Duffaud, F; Esnaud, T; Geneste, D; Ghiringhelli, F; Isambert, N; Italiano, A; Le Loarer, F; Lucchesi, C; Mir, O; Penel, N; Toulmonde, M, 2019)		0.51
" The dire clinical course of paediatric CML is further exacerbated by the adverse effects of long-term imatinib therapy."( Efficacy and Safety of Imatinib in Paediatric CML - A Single Centre Study.
Grzeszkiewicz, K; Pawelec, K; Pieluszczak, K; Smeding, C; Szydło, A, )		0.13
"There is little information about cardiovascular adverse event (CV-AE) incidence in chronic myeloid leukemia (CML) patients treated with bosutinib in the real-life practice."( Incidence and evaluation of predisposition to cardiovascular toxicity in chronic myeloid leukemia patients treated with bosutinib in the real-life practice.
Abruzzese, E; Annunziata, M; Baratè, C; Binotto, G; Bonifacio, M; Breccia, M; Caocci, G; Cattaneo, D; De Gregorio, F; Elena, C; Foà, R; Fozza, C; Galimberti, S; Iurlo, A; La Nasa, G; Luciano, L; Martino, B; Molica, M; Mulas, O; Orlandi, EM; Russo Rossi, A; Sgherza, N; Trawinska, MM, 2019)		0.51
" Pleural effusion is a frequent side effect in patients during dasatinib treatment."( Lupus-like symptoms with anti-RNP/Sm and anti-nuclear antibodies positivity: An extremely rare adverse event of dasatinib.
Bakanay, SM; Dilek, I; Kucuksahin, O; Maral, S, 2020)		0.56
" After switching, 15 (39%) patients reported new or worsening adverse events, including 5 (13%) patients with edema, 8 (21%) muscle cramps, 7 (18%) nausea, 6 (16%) diarrhea, and 5 (13%) fatigue."( Efficacy and safety of generic imatinib after switching from original imatinib in patients treated for chronic myeloid leukemia in the United States.
Abou Dalle, I; Borthakur, G; Burger, J; Cortes, J; Estrov, Z; Garcia-Manero, G; Jabbour, E; Kantarjian, H; Ohanian, M; Ravandi, F; Verstovsek, S, 2019)		0.51
" Adverse events noted were mild and well tolerated."( Efficacy and safety of generic imatinib after switching from original imatinib in patients treated for chronic myeloid leukemia in the United States.
Abou Dalle, I; Borthakur, G; Burger, J; Cortes, J; Estrov, Z; Garcia-Manero, G; Jabbour, E; Kantarjian, H; Ohanian, M; Ravandi, F; Verstovsek, S, 2019)		0.51
" All patients experienced at least one treatment-related adverse event (AE), including diarrhoea (80."( Efficacy and safety of TAS-116, an oral inhibitor of heat shock protein 90, in patients with metastatic or unresectable gastrointestinal stromal tumour refractory to imatinib, sunitinib and regorafenib: a phase II, single-arm trial.
Doi, T; Komatsu, Y; Kurokawa, Y; Naito, Y; Nishida, T; Ohkubo, S; Ozaka, M; Sawaki, A; Takahashi, T, 2019)		0.51
"In this multicenter, open-label, single-arm trial, safety was assessed based on the frequency of adverse events (AEs)."( Safety of Imatinib Mesylate in a Multicenter Expanded Access Program in Adult Patients with Gastrointestinal Stromal Tumors in the Adjuvant Setting.
Barone, C; Bauer, S; Castellana, R; Crippa, S; Delgado Perez, JR; Fumagalli, E; Le Cesne, A; Melichar, B; Papai, Z; Prausova, J; Pustowka, A; Quiering, C; Reichardt, P; Schlemmer, M, 2019)		0.92
"Hematological toxicity is a common adverse effect of tyrosine kinase inhibitors (TKIs) for the treatment of chronic myeloid leukemia (CML)."( Marrow fibrosis is an independent predictor of hematological toxicity of tyrosine kinase inhibitors for the treatment of chronic myeloid leukemia.
Hong, J; Li, Q; Ni, J; Sun, G; Xia, R; Zeng, Q; Zhang, Z, 2020)		0.56
" None of the patients in this group had treatment-related deaths or IM discontinuation due to drug toxicities, and only 1 patient had a grade III-IV nonhematologic adverse event."( Clinical efficacy and safety of imatinib treatment in children and adolescents with chronic myeloid leukemia: A single-center experience in China.
An, X; Deng, M; Guan, X; Wen, X; Xiao, J; Yu, J, 2020)		0.56
" However, the novel strategy is required to reduce life-threatening adverse effects of PNT including ischemic cardiovascular disease."( Involvement of MCL1, c-myc, and cyclin D2 protein degradation in ponatinib-induced cytotoxicity against T315I(+) Ph+leukemia cells.
Abe, A; Hayakawa, F; Ichihara, M; Inoue, C; Kawamoto, Y; Murate, T; Nishizawa, Y; Nozawa, Y; Sobue, S; Suzuki, M, 2020)		0.56
" Adverse cardiovascular events were recorded in both groups."( Cardiovascular Toxicity in Cancer Patients Treated with Tyrosine Kinase Inhibitors: A Real-World Single-Center Experience.
Accurso, V; Badalamenti, G; Bronte, E; Di Lisi, D; Macaione, F; Novo, G; Novo, S; Rinaldi, G; Russo, A; Siragusa, S, 2020)		0.56
"Our study confirms that imatinib is a relatively safe drug, while it reveals that the latest-generation TKIs may cause a burden of cardiovascular complications."( Cardiovascular Toxicity in Cancer Patients Treated with Tyrosine Kinase Inhibitors: A Real-World Single-Center Experience.
Accurso, V; Badalamenti, G; Bronte, E; Di Lisi, D; Macaione, F; Novo, G; Novo, S; Rinaldi, G; Russo, A; Siragusa, S, 2020)		0.56
" The most common adverse events were diarrhoea (76%), palmar-plantar erythrodysesthesia syndrome (60%), fatigue (50%), hypertension (42%), weight loss (40%) and oral mucositis (30%), with 32 (64%) patients requiring dose reductions, 27 (54%) having treatment interruptions and no cabozantinib-related deaths observed."( Activity and safety of the multi-target tyrosine kinase inhibitor cabozantinib in patients with metastatic gastrointestinal stromal tumour after treatment with imatinib and sunitinib: European Organisation for Research and Treatment of Cancer phase II tri
Ali, N; Benson, C; Blay, JY; Cousin, S; Dileo, P; Gelderblom, H; Italiano, A; Kasper, B; Kopeckova, K; LeCesne, A; Litiere, S; Marreaud, S; Menge, F; Mir, O; Nzokirantevye, A; Papai, Z; Schöffski, P; Vanden Bempt, I; Wardelmann, E; Wozniak, A; Zaffaroni, F, 2020)		0.56
" The objective of this study is to develop a target-oriented drug carrier to minimize these adverse effects by the controlled release of the drug."( Encapsulation of Imatinib in Targeted KIT-5 Nanoparticles for Reducing its Cardiotoxicity and Hepatotoxicity.
Fardshouraki, S; Jandaghian, S; Mirian, M; Safaeian, L; Taymouri, S; Varshosaz, J, 2020)		0.56
" The most common adverse events were anemia, proteinuria, fatigue, neutropenia, and diarrhea."( A prospective multicenter phase II study on the efficacy and safety of dasatinib in the treatment of metastatic gastrointestinal stromal tumors failed by imatinib and sunitinib and analysis of NGS in peripheral blood.
Li, J; Li, Y; Liu, X; Shen, L; Wu, X; Zhang, B; Zhang, X; Zhou, Y, 2020)		0.56
" All results suggest that the ultra-long circulating pro-drug NP may provide an effective and safe therapeutic strategy for BCR-ABL-positive CML."( An ultra-long circulating nanoparticle for reviving a highly selective BCR-ABL inhibitor in long-term effective and safe treatment of chronic myeloid leukemia.
Fu, L; Liang, H; Liang, X; Liu, J; Liu, Q; Shi, J; Wang, B; Wang, J; Zou, F, 2020)		0.56
" Safety was assessed according to the occurrence of adverse events."( Evaluation of the use, effectiveness and safety of tyrosine kinase inhibitors in chronic myelogenous leukaemia in a general university hospital.
Escudero-Vilaplana, V; González-Haba, E; Marquinez-Alonso, I; Osorio, S; Rodriguez-Gonzalez, CG; Sanjurjo-Sáez, M, 2020)		0.56
" Finally, regarding safety, the authors found a pooled dropout rate due to all adverse events of 22% and a rate of serious adverse events of 17%."( Efficacy and safety of imatinib mesylate in systemic sclerosis. A systematic review and meta-analysis.
Ciaffi, J; Ciccia, F; Cipriani, P; Giacomelli, R; Liakouli, V; Meliconi, R; Ruscitti, P; Ursini, F, 2020)		0.87
" Adverse effects, if any, were documented as per the NCI-CTCAE criteria v4."( Efficacy and safety profile of generic imatinib in patients with newly diagnosed chronic myeloid leukemia-chronic phase: sharing experience of a hemato-oncology center from eastern India.
Dolai, TK; Mandal, PK; Phukan, A, 2021)		0.62
"Cutaneous adverse effects (AE) related to tyrosine-kinase inhibitor (TKI) drugs have been mainly described as case reports."( Cutaneous side effects in a cohort of patients with chronic myeloid leukemia treated with tyrosine kinase inhibitors: General description and further characterization, correlation with photoexposition and study of hypopigmentation as treatment's prognosti
Daudén, E; García-Diez, A; Llamas-Velasco, M; Ovejero-Merino, E; Requena, L; Steegmann, JL, 2020)		0.56
" Moreover, prolonged treatment produces various adverse effects, such as serious vascular adverse events including stroke, myocardial infarction, and peripheral arterial occlusive disease."( [Management of vascular adverse events during tyrosine kinase inhibitors in patients with chronic myeloid leukemia].
Takaku, T, 2020)		0.56
" However, it can cause some serious adverse effects."( Sigmoid Sinus Thrombosis Followed by Splenic Infarction Due to Imatinib Therapy in a Patient with Gastrointestinal Stromal Tumor; Hematological Side Effects of Imatinib.
Demirağ, G; Yılmaz, A; Yilmaz, H, 2021)		0.62
" Treatment-emergent adverse events in both subpopulations were consistent with the primary BFORE results."( Efficacy and safety of bosutinib versus imatinib for newly diagnosed chronic myeloid leukemia in the Asian subpopulation of the phase 3 BFORE trial.
Brümmendorf, TH; Chuah, C; Cortes, JE; Do, YR; Koh, LP; Numbenjapon, T; Ohkura, M; Ong, KH; Ono, C; Viqueira, A; Zang, DY, 2021)		0.62
" There were significantly more hematologic adverse events (AEs) in elderly patients (P = ."( Efficacy and Safety of Imatinib Treatment in Elderly Patients With Chronic Myeloid Leukemia: Real-Life Data and a Single-Center Experience.
Ar, MC; Aydın, Y; Başlar, Z; Bayraktar, EA; Bektaş, F; Elverdi, T; Eşkazan, AE; Keskin, D; Öngören, Ş; Özgür Yurttaş, N; Özmen, D; Öztaş, M; Sadri, S; Salihoğlu, A; Soysal, T, 2021)		0.62
" The most common all-cause adverse events were increased blood bilirubin (53."( A phase 2 study of nilotinib in pediatric patients with CML: long-term update on growth retardation and safety.
Aimone, P; Allepuz, A; Bautista, F; Ducassou, S; Dufour, C; Goto, H; Guinipero, T; Hijiya, N; Kang, HJ; Karakas, Z; Maschan, A; Millot, F; Patterson, B; Rizzari, C; Samis, J; Shimada, H; Sosothikul, D; Titorenko, K; Yoo, KH; Zwaan, CM, 2021)		0.62
" Imatinib + SOC-treated participants exhibited no increase in number or severity of adverse events, a significantly accelerated decline in parasite density and pyrexia, and no DPC."( Imatinib augments standard malaria combination therapy without added toxicity.
Chien, HD; Kesely, KR; Low, PS; Noomuna, P; Pantaleo, A; Putt, KS; Tuan, TA; Turrini, FM, 2021)		0.62
" We extracted data on the trial and patient characteristics, and the following primary outcomes: all-cause mortality, the ratios of virological cure, and treatment-emergent adverse events."( Efficacy and safety of current medications for treating severe and non-severe COVID-19 patients: an updated network meta-analysis of randomized placebo-controlled trials.
Chen, J; Cheng, Q; Fang, Z; Jia, Q; Zhao, G, 2021)		0.62
" However, some patients may require dose reductions to manage the occurrences of adverse events (AEs)."( Efficacy and safety following bosutinib dose reduction in patients with Philadelphia chromosome‒positive leukemias.
An, F; Brümmendorf, TH; Cortes, JE; Crescenzo, RJ; Ferdinand, R; Gambacorti-Passerini, C; Kim, DW; Kota, V; Leip, E; Lipton, JH, 2021)		0.62
" Measurements included medications, follow-ups, adverse events, allogeneic stem cell transplantation and quality-adjusted life years (QALYs)."( Safety and cost-effectiveness of ponatinib versus other tyrosine kinase inhibitors as second-line therapy in patients with chronic myeloid leukemia in the United States.
Guo, JJ; Hincapie, AL; Li, Y; Yue, X, 2022)		0.72
" Within this context, we present a case of a 25-year-old woman diagnosed with Ph+ ALL during the third trimester and the safe and effective use of imatinib as treatment after failure of conventional chemotherapy."( Safe and Effective Use of Imatinib to Treat Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia During Pregnancy.
Ashraf, S; Bachiashvili, K; Bhatia, R; Jamy, O; Rangaraju, S; Vachhani, P; Wolfson, J, 2022)		0.72
" A total of four treatment-emergent adverse events (TEAEs) occurred during the study."( Safety, tolerability, and pharmacokinetics of single and multiple topical ophthalmic administration of imatinib mesylate in healthy subjects.
Chung, JY; Huh, KY; Hyon, JY; Koo, HC; Lee, JH; Na, JY; You, JC; Yu, KS, 2022)		0.94
" Ponatinib, a third generation TKI, has shown a relatively high incidence of serious adverse effects including thrombotic vascular occlusion and heart failure, particularly in patients with a prior history of cardiovascular impairment."( Cardiovascular Toxicity Associated With Tyrosine Kinase Inhibitor Therapy In Chronic Myeloid Leukemia.
Al Nahedh, M; Aljurf, M; Baqal, OJ; Binzaid, AA; Samarkandi, HH; Soheib, M, 2021)		0.62
" We evaluated patients' treatments with or without AC, completion rates, adverse events (AEs), recurrence-free survival (RFS), and overall survival (OS)."( Real-world data on the efficacy and safety of adjuvant chemotherapy in Japanese patients with a high-risk of gastrointestinal stromal tumor recurrence.
Doki, Y; Eguchi, H; Hirota, S; Kawabata, R; Kurokawa, Y; Makino, T; Motoori, M; Nakajima, K; Nishida, T; Nishikawa, K; Omori, T; Saito, T; Takahashi, T; Tanaka, K; Teranishi, R; Ushimaru, Y; Yamamoto, K; Yamashita, K, 2022)		0.72
"8%) patients experienced Common Terminology Criteria for Adverse Events Grade 2 or higher AEs."( Real-world data on the efficacy and safety of adjuvant chemotherapy in Japanese patients with a high-risk of gastrointestinal stromal tumor recurrence.
Doki, Y; Eguchi, H; Hirota, S; Kawabata, R; Kurokawa, Y; Makino, T; Motoori, M; Nakajima, K; Nishida, T; Nishikawa, K; Omori, T; Saito, T; Takahashi, T; Tanaka, K; Teranishi, R; Ushimaru, Y; Yamamoto, K; Yamashita, K, 2022)		0.72
" This study aimed to evaluate the response and the adverse events of treatment with imatinib mesylate (IM) compared to conventional therapy using vinblastine and prednisolone (VP) in canine cutaneous MCTs."( Imatinib Mesylate for the Treatment of Canine Mast Cell Tumors: Assessment of the Response and Adverse Events in Comparison with the Conventional Therapy with Vinblastine and Prednisone.
Alexandre, PA; Brandão, PE; Casagrande, TAC; Dagli, MLZ; de Queiroz, GF; Fukumasu, H; Macedo, TR; Matera, JM; Melo, SR; Pinto, ACBCF, 2022)		2.39
"Imatinib (IM), a milestone drug used in the field of molecular targeted therapy, has been reported to cause serious adverse liver effects, including liver failure and even death."( Imatinib-induced hepatotoxicity via oxidative stress and activation of NLRP3 inflammasome: an in vitro and in vivo study.
Cheng, ZP; Fang, WT; Huang, FR; Shen, Y; Sun, LN; Wang, DJ; Wang, YQ, 2022)		0.72
" However, other proteins are also inhibited, so they can cause a wide range of adverse effects (AEs)."( [Prevalence of Adverse Effects of Tyrosine Kinase Inhibitors Used in Management of Chronic Myeloid Leukemia at Sidi Bel-Abbès University Hospital Center].
Belfrak, F; Beloufa, S; Benlazar, M; Benmehimda, NC; Mahi, E; Matmour, D; Merad, Y; Si-Ali, N; Toumi, H, 2022)		0.72
" Safety endpoints included the incidence and severity of adverse events (AE)."( Efficacy and Safety of Ripretinib in Chinese Patients with Advanced Gastrointestinal Stromal Tumors as a Fourth- or Later-Line Therapy: A Multicenter, Single-Arm, Open-Label Phase II Study.
Cai, S; Cao, H; Deng, Y; Dong, J; Huang, Z; Li, J; Shen, L; Wu, X; Zhang, J; Zhou, Y, 2022)		0.72
" No grade 4 adverse events were observed."( Efficacy and Safety of Generic Dasatinib in Patients With Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase: A Multicenter Prospective Study in China.
Du, X; Jin, J; Liu, P; Lou, J; Meng, L; Wang, W; Yu, W, 2022)		0.72
" Severe cardiac adverse events were monitored for 28 days or until death occurred."( Cardiac Safety of Imatinib for the Treatment of COVID-19: A Secondary Analysis of a Randomized, Double-Blind, Placebo-Controlled Trial.
Aman, J; Bogaard, HJ; de Man, FS; Duijvelaar, E; Pinto, Y; Schippers, JR; Smeele, PJ; Vanhove, A, 2022)		0.72
"Endoscopic resection for intermediate-risk gastric GIST is a feasible and safe method, and there is no significant benefit for patients with intermediate-risk gastric GIST to accept imatinib adjuvant treatment after ER."( Comparison of Safety and Outcomes between Endoscopic and Surgical Resections of Intermediate-Risk Primary Gastric Gastrointestinal Stromal Tumors.
Hassan, S; Liu, J; Ni, M; Ren, X; Wang, L; Xu, G; Yang, J; Zhu, T; Zou, X, 2023)		0.91
" We extracted data on trials and patient characteristics, and the following primary outcomes: all-cause mortality (ACM), and treatment-emergent adverse events (TEAEs)."( Comparative efficacy and safety of pharmacological interventions for severe COVID-19 patients: An updated network meta-analysis of 48 randomized controlled trials.
Chen, J; Cheng, Q; Fang, Z; Jia, Q; Zhao, G, 2022)		0.72
" We found that most medications were safe in treating severe COVID-19."( Comparative efficacy and safety of pharmacological interventions for severe COVID-19 patients: An updated network meta-analysis of 48 randomized controlled trials.
Chen, J; Cheng, Q; Fang, Z; Jia, Q; Zhao, G, 2022)		0.72
"Sunitinib therapy for patients with imatinib-resistant and/or intolerant gastrointestinal stromal tumors (GISTs) often causes severe adverse events (AEs) that lead to treatment discontinuation."( Sunitinib therapy for imatinib-resistant and/or intolerant gastrointestinal stromal tumors: comparison of safety and efficacy between standard and reduced dosage regimens.
Hirota, S; Ishikawa, T; Kanda, T; Matsumoto, Y; Saijo, Y; Sasaki, K, 2023)		0.91
"003] in randomized controlled trials, but adverse events (AEs) were higher than those in the control group (P < 0."( A meta-analysis of the efficacy and toxicity of tyrosine kinase inhibitors in treating patients with different types of thyroid cancer: how to choose drugs appropriately?
Lin, S; Lu, J; Su, J; Wang, M; Yan, J; Zhang, J, 2023)		0.91
" Despite some reports from overseas, the relationship between Cmin, adverse events (AEs), and treatment efficacy in Japanese patients with GIST has still been lacking."( Plasma trough concentration of imatinib and its effect on therapeutic efficacy and adverse events in Japanese patients with GIST.
Doki, Y; Eguchi, H; Hayashi, Y; Hirota, S; Koh, M; Kurokawa, Y; Makino, T; Motoori, M; Nakajima, K; Nishida, T; Nishigaki, T; Omori, T; Saito, T; Takahashi, T; Takehara, T; Tanaka, K; Teranishi, R; Yamamoto, K; Yamashita, K, 2023)		0.91
" Our data showed that nilotinib could be, as first-line treatment, effective and relatively safe even in elderly CML patients."( Efficacy and safety of nilotinib as frontline treatment in elderly (> 65 years) chronic myeloid leukemia patients outside clinical trials.
Albano, F; Annunziata, M; Bocchia, M; Breccia, M; Castagnetti, F; Dragani, M; Esposito, MR; Galimberti, S; Gugliotta, G; Iovine, M; Iurlo, A; Latagliata, R; Luciano, L; Martino, B; Palmieri, R; Pregno, P; Rosti, G; Sica, A; Sica, S; Sorà, F; Tiribelli, M, 2023)		0.91
"We report a 51-year-old man, suffering from acute toxic hepatitis after 5 months of imatinib treatment for chronic myeloid leukemia."( Imatinib mesylate-induced acute hepatotoxicity.
Chtourou, L; Elloumi, M; Fakhfakh, Y; Frikha, I; Medhaffar, M; Sahnoun, R, 2023)		2.35
"This study aimed to conduct a thorough analysis of fluid retention-associated adverse events (AEs) associated with BCR::ABL inhibitors."( Fluid retention-associated adverse events in patients treated with BCR::ABL1 inhibitors based on FDA Adverse Event Reporting System (FAERS): a retrospective pharmacovigilance study.
Cai, J; Huang, J; Jiang, Q; Lin, H; Wu, L; Ye, Q, 2023)		0.91
"Food and Drug Administration Adverse Event Reporting System (FAERS) database for BCR::ABL inhibitors was searched from 1 January 2004 to 30 September 2021."( Fluid retention-associated adverse events in patients treated with BCR::ABL1 inhibitors based on FDA Adverse Event Reporting System (FAERS): a retrospective pharmacovigilance study.
Cai, J; Huang, J; Jiang, Q; Lin, H; Wu, L; Ye, Q, 2023)		0.91
"Patients with chronic myeloid leukemia (CML) treated with tyrosine kinase inhibitors (TKIs) often experience cutaneous adverse events, such as rashes and pruritus."( Comparison of cutaneous adverse events between second-generation tyrosine kinase inhibitors and imatinib for chronic myeloid leukemia: a systematic review and meta-analysis.
Cha, SH; Kim, K; Song, YK, 2023)		0.91
" Two independent reviewers screened the results and selected articles on cutaneous adverse events."( Comparison of cutaneous adverse events between second-generation tyrosine kinase inhibitors and imatinib for chronic myeloid leukemia: a systematic review and meta-analysis.
Cha, SH; Kim, K; Song, YK, 2023)		0.91
"This study shows that neoadjuvant imatinib is effective and safe for patients with large or locally advanced GIST."( Neoadjuvant Imatinib in Locally Advanced Gastrointestinal Stromal Tumors (GISTs) is Effective and Safe: Results from a Prospective Single-Center Study with 108 Patients.
Hartemink, KJ; Ijzerman, N; Kerst, M; Koenen, AM; Roets, E; Schrage, YM; Steeghs, N; van Coevorden, F; van de Wal, D; van der Burg, SJC; van der Graaf, WTA; van Houdt, WJ; van Sandick, JW; Veenhof, XAAFA, 2023)		0.91

Pharmacokinetics

ExcerptReferenceRelevance
"1 h); half-life (11."( [Efficacy and pharmacokinetics of imatinib mesylate in a child with chronic myeloid leukemia].
Chida, S; Endo, M; Hosokawa, T; Nakatuji, Y; Sugawara, W, 2003)		0.6
" Two additional blood samples were taken for imatinib pharmacokinetic (PK) assessment on day 8 before, and 24 h after, imatinib administration."( Effects of imatinib mesylate (STI571, Glivec) on the pharmacokinetics of simvastatin, a cytochrome p450 3A4 substrate, in patients with chronic myeloid leukaemia.
Beck, J; Bond, E; Capdeville, R; Dutreix, C; Fischer, T; Huber, C; Mehring, G; Meinhardt, P; Milosavljev, S; O'Brien, SG; Peng, B, 2003)		0.71
"Despite the remarkable clinical response rates to imatinib in the treatment of bcr-abl leukemic patients, pharmacokinetic data on this relatively novel substance are needed to improve our understanding of the emergence of resistance, the interindividual variations of clinical response and the clinical and biologic relevance of its main metabolite N-desmethyl-imatinib."( Pharmacokinetics and cellular uptake of imatinib and its main metabolite CGP74588.
Baskaynak, G; Bonin, Mv; Bornhäuser, M; Dörken, B; Ehninger, G; Jenke, A; Kreuzer, KA; le Coutre, P; Leopold, T; Ottmann, O; Pursche, S; Schleyer, E, 2004)		0.32
"To evaluate the basic pharmacokinetic (PK) characteristics of imatinib mesylate and assess the relationship between the PK and pharmacodynamic (PD) properties of the drug."( Pharmacokinetics and pharmacodynamics of imatinib in a phase I trial with chronic myeloid leukemia patients.
Capdeville, R; Druker, BJ; Ford, J; Hayes, M; Lloyd, P; Peng, B; Racine-Poon, A; Resta, D; Rosamilia, M; Sawyers, CL; Talpaz, M, 2004)		0.56
" Pharmacokinetic parameters were estimated using model-independent methods."( Plasma and cerebrospinal fluid pharmacokinetics of imatinib after administration to nonhuman primates.
Aleksic, A; Balis, FM; Berg, SL; Blaney, SM; Egorin, MJ; McCully, C; McGuffey, L; Neville, K; Parise, RA; Thompson, P, 2004)		0.32
" Imatinib and CGP74588 (main metabolite of imatinib) concentrations were measured using LC/MS/MS method and pharmacokinetic parameters were estimated by a non-compartmental analysis."( Pharmacokinetic interaction between ketoconazole and imatinib mesylate (Glivec) in healthy subjects.
Capdeville, R; Dutreix, C; Hayes, M; Mehring, G; Peng, B; Pokorny, R; Seiberling, M, 2004)		0.57
" Imatinib half-life (12."( Effect of St John's wort on imatinib mesylate pharmacokinetics.
Egorin, MJ; Fitzgerald, SM; Frye, RF; Hruska, MW; Lagattuta, TF, 2004)		0.62
"Open-label, complete crossover, fixed-sequence, pharmacokinetic study."( The influence of St. John's wort on the pharmacokinetics and protein binding of imatinib mesylate.
Berenson, CS; Booker, BM; Bullock, JM; Haas, CE; Jusko, WJ; Smith, P, 2004)		0.55
"005), and 21% in half-life (p=0."( The influence of St. John's wort on the pharmacokinetics and protein binding of imatinib mesylate.
Berenson, CS; Booker, BM; Bullock, JM; Haas, CE; Jusko, WJ; Smith, P, 2004)		0.55
" However, we have now evidence, based on several in vitro and in vivo observations suggesting that pharmacokinetic resistance may also play a definitive role in the ultimate resistance of patients on chronic imatinib."( Pharmacokinetic resistance to imatinib mesylate: role of the ABC drug pumps ABCG2 (BCRP) and ABCB1 (MDR1) in the oral bioavailability of imatinib.
Burger, H; Nooter, K, 2004)		0.61
"The pharmacokinetic values for imatinib and CGP74588, respectively, were: maximum concentration (3,340 and 781 ng/ml), time to maximum concentration (2 h), half-life (18."( Pharmacokinetics of imatinib mesylate in end stage renal disease. A case study.
Briasoulis, E; Karavasilis, V; Marselos, M; Pappas, P; Pavlidis, N, 2005)		0.65
" Nonlinear mixed effects modelling was used for the population pharmacokinetic analysis."( Population pharmacokinetics of imatinib mesylate in patients with chronic-phase chronic myeloid leukaemia: results of a phase III study.
Bolton, AE; Capdeville, R; Gathmann, I; Hensley, M; Peng, B; Racine-Poon, A; Riviere, GJ; Schmidli, H, 2005)		0.61
" Pharmacokinetic studies of imatinib in healthy volunteers and patients with CML, GIST and other cancers show that orally administered imatinib is well absorbed, and has an absolute bioavailability of 98% irrespective of oral dosage form (solution, capsule, tablet) or dosage strength (100 mg, 400 mg)."( Clinical pharmacokinetics of imatinib.
Lloyd, P; Peng, B; Schran, H, 2005)		0.33
"A population pharmacokinetic analysis was performed using NONMEM based on 321 plasma samples from 59 patients with either chronic myeloid leukaemia or gastrointestinal stromal tumours."( Population pharmacokinetics of imatinib and the role of alpha-acid glycoprotein.
Biollaz, J; Buclin, T; Csajka, C; Decosterd, LA; Duchosal, MA; Eap, CB; Henry, H; Leyvraz, S; Rochat, B; Rosselet, A; Widmer, N, 2006)		0.33
"Because of the high pharmacokinetic variability of imatinib and the reported relationships between its plasma concentration and efficacy and toxicity, the usefulness of therapeutic drug monitoring as an aid to optimizing therapy should be further investigated."( Population pharmacokinetics of imatinib and the role of alpha-acid glycoprotein.
Biollaz, J; Buclin, T; Csajka, C; Decosterd, LA; Duchosal, MA; Eap, CB; Henry, H; Leyvraz, S; Rochat, B; Rosselet, A; Widmer, N, 2006)		0.33
" However, pharmacokinetic parameters of imatinib in vivo were not statistically significantly different in 16 patients who were heterozygous for ABCG2 421C>A compared with 66 patients carrying the wild-type sequence (P = ."( Association of enzyme and transporter genotypes with the pharmacokinetics of imatinib.
Baker, SD; Bates, SE; Burger, H; de Bruijn, EA; de Jong, FA; Figg, WD; Gardner, ER; Guetens, G; Nooter, K; Prenen, H; Sparreboom, A; van Oosterom, AT; van Schaik, RH; Verweij, J, 2006)		0.33
"This study explored factors affecting the pharmacokinetic variability of imatinib and CGP 74588, and the pharmacokinetic-pharmacodynamic correlations in patients with advanced gastrointestinal stromal tumors."( Pharmacokinetic-pharmacodynamic relationships of imatinib and its main metabolite in patients with advanced gastrointestinal stromal tumors.
Berthaud, P; Blay, JY; Chatelut, E; Delbaldo, C; Deroussent, A; Jambu, A; Le Cesne, A; Ré, M; Séronie-Vivien, S; Vassal, G, 2006)		0.33
" Plasma imatinib and CGP 74588 concentrations were quantified by reverse-phase high-performance liquid chromatography coupled with tandem mass spectrometry, and analyzed by the population pharmacokinetic method (NONMEM program)."( Pharmacokinetic-pharmacodynamic relationships of imatinib and its main metabolite in patients with advanced gastrointestinal stromal tumors.
Berthaud, P; Blay, JY; Chatelut, E; Delbaldo, C; Deroussent, A; Jambu, A; Le Cesne, A; Ré, M; Séronie-Vivien, S; Vassal, G, 2006)		0.33
" Pharmacokinetic (PK) analysis showed that imatinib displayed linear PK in patients with advanced GIST."( [Pharmacokinetic-pharmacodynamics relationships of imatinib (Glivec)].
Delbaldo, C, )		0.13
" In this phase-I/II trial pharmacokinetic parameters of imatinib given for hepatocellular cancer were similar to those previously derived from CML patients."( Imatinib for hepatocellular cancer--focus on pharmacokinetic/pharmacodynamic modelling and liver function.
Hosius, C; Malfertheiner, P; Schleyer, E; Treiber, G; Troeger, U; Wex, T, 2008)		0.35
" Pharmacokinetic analyses revealed lowered exposures and enhanced clearance among patients on EIAEDs."( Safety and pharmacokinetics of dose-intensive imatinib mesylate plus temozolomide: phase 1 trial in adults with malignant glioma.
Desjardins, A; Egorin, MJ; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Lagattuta, TF; McLendon, R; Quinn, JA; Reardon, DA; Rich, JN; Salvado, AJ; Sathornsumetee, S; Vredenburgh, JJ, 2008)		0.6
" Population pharmacokinetic (PPK) studies evaluating the effect of population covariates on the pharmacokinetics of imatinib and its active metabolite have been developed in adults with chronic myeloid leukemia (CML) and gastrointestinal stromal tumor (GIST)."( Population pharmacokinetics of imatinib mesylate and its metabolite in children and young adults.
Barrett, JS; Bernstein, M; Blaney, SM; Bond, M; Champagne, M; Fossler, MJ; Jayaraman, B; Menon-Andersen, D; Mondick, JT; Thompson, PA, 2009)		0.64
" Of the over 325 members of the solute carrier superfamily, this review focuses on the molecular features, expressional regulation, and genetic polymorphisms of the organic cation transporter (OCT) family, and the pharmacokinetic or pharmacodynamic consequences for organic cationic drugs."( Organic cation transporters and their pharmacokinetic and pharmacodynamic consequences.
Choi, MK; Song, IS, 2008)		0.35
" Plasma imatinib and CGP74588 concentrations observed on day 1 and at steady-state were analyzed by a population pharmacokinetic method (NONMEM) to evaluate the effect of age, body weight, age, sex, albuminemia, plasma alpha1-acid glycoprotein (AGP), and eight polymorphisms corresponding to ABCB1, ABCG2, CYP3A4, CYP3A5, and AGP (pharmacogenetic data available for 46 of 67 patients)."( Population pharmacokinetics and pharmacogenetics of imatinib in children and adults.
Azard, J; Barrois, M; Chatelut, E; Delbaldo, C; Geoerger, B; Kattygnarath, D; LeCesne, A; Petain, A; Séronie-Vivien, S; Vassal, G, 2008)		0.35
"This study assessed the pharmacokinet-ics of single and multiple oral doses of nilotinib in Chinese patients with CML and compared the pharmacokinetic profiles of nilotinib between the Chinese patients and a subgroup of white patients with CML."( Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Hu, P; Meng, F; Shen, Z; Wang, J; Wang, Y; Wei, Y; Yin, O; Zhou, L, 2009)		0.35
" Serum nilotinib concentrations were determined using a validated liquid chromatography-tandem mass spectrometry assay, and pharmacokinetic parameters of nilotinib were calculated using a noncompartmental method."( Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Hu, P; Meng, F; Shen, Z; Wang, J; Wang, Y; Wei, Y; Yin, O; Zhou, L, 2009)		0.35
" Two patients withdrew consent and discontinued after administration of the first dose; thus, 21 patients were included in the pharmacokinetic analysis."( Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Hu, P; Meng, F; Shen, Z; Wang, J; Wang, Y; Wei, Y; Yin, O; Zhou, L, 2009)		0.35
"In this pharmacokinetic study in Chinese patients with CML resistant to or intolerant of imatinib, nilotinib 400 mg BID was rapidly absorbed after a single dose and multiple doses."( Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Hu, P; Meng, F; Shen, Z; Wang, J; Wang, Y; Wei, Y; Yin, O; Zhou, L, 2009)		0.35
" The agent, administered orally, has approximately 98% oral bioavailability, achieves maximum plasma concentration approximately 2-4 hours after ingestion, and has a plasma half-life of approximately 18 hours."( Imatinib mesylate pharmacokinetics before and after sleeve gastrectomy in a morbidly obese patient with chronic myeloid leukemia.
Beumer, JH; Egorin, MJ; Pavlovsky, C; Pavlovsky, S; Rogel, S; Shah, DD, 2009)		1.8
" Post marketing study commitments have been made upon (accelerated) approval such as additional pharmacokinetic studies in patients with renal- or hepatic impairment, in children, additional interactions studies and studies on the relative or absolute bioavailability."( Clinical pharmacokinetics of tyrosine kinase inhibitors.
Gelderblom, H; Guchelaar, HJ; van Erp, NP, 2009)		0.35
"97), or half-life (13."( Effect of a proton pump inhibitor on the pharmacokinetics of imatinib.
Appleman, LR; Beumer, JH; Christner, SM; Egorin, MJ; Komazec, KA; Miller, BM; Redner, RL; Shah, DD; Yerk, MA, 2009)		0.35
" Pharmacokinetic parameters were determined using WinNonLin software."( Interleukin-2 treatment effect on imatinib pharmacokinetic, P-gp and BCRP expression in mice.
Abbara, C; Bonhomme-Faivre, L; Cibert, M; Farinotti, R; Gonin, P; Hosten, B; Petit, B, 2010)		0.36
" The method is found to be rapid, reliable, and suitable for in vivo pharmacokinetic study."( Validation of an HPLC method for determination of imatinib mesylate in rat serum and its application in a pharmacokinetic study.
Bende, G; Kollipara, S; Moorthy, G; Movva, S; Saha, R, )		0.38
" Noncompartmental pharmacokinetic parameters were estimated."( Differential effects of ketoconazole and primaquine on the pharmacokinetics and tissue distribution of imatinib in mice.
Bukhari, NI; Chay, G; Kan, E; Law, JH; Lim, WY; Segarra, I; Soo, GW; Tan, SY, 2010)		0.36
" Pharmacokinetic (PK) and pharmacodynamic factors, adherence, and drug-drug interactions can affect exposure to imatinib and impact clinical outcomes."( Correlations between imatinib pharmacokinetics, pharmacodynamics, adherence, and clinical response in advanced metastatic gastrointestinal stromal tumor (GIST): an emerging role for drug blood level testing?
von Mehren, M; Widmer, N, 2011)		0.37
" The pharmacokinetics of paracetamol and imatinib in Korean patients with CML were similar to previous pharmacokinetic results in white patients with CML."( Effects of imatinib mesylate on the pharmacokinetics of paracetamol (acetaminophen) in Korean patients with chronic myelogenous leukaemia.
Demirhan, E; Hayes, M; Jin, Y; Kim, DW; Park, S; Schran, H; Tan, EY; Wang, Y, 2011)		0.76
" Pharmacokinetic parameters were estimated by a population pharmacokinetic analysis based on 622 plasma samples from 34 patients at steady state."( Association of genetic polymorphisms in the influx transporter SLCO1B3 and the efflux transporter ABCB1 with imatinib pharmacokinetics in patients with chronic myeloid leukemia.
Hamada, A; Hirayama, C; Kawaguchi, T; Nakashima, R; Saito, H; Yamakawa, Y; Yuki, M, 2011)		0.37
"The pharmacokinetic interaction between metronidazole, an antibiotic-antiparasitic drug used to treat anaerobic bacterial and protozoal infections, and imatinib, a CYP3A4, P-glycoprotein substrate kinase inhibitor anticancer drug, was evaluated."( Metronidazole leads to enhanced uptake of imatinib in brain, liver and kidney without affecting its plasma pharmacokinetics in mice.
Bukhari, NI; Chay, G; Kan, E; Law, JH; Lim, WY; Segarra, I; Soo, GW; Tan, SY, 2011)		0.37
" Imatinib plasma, brain, kidney and liver concentrations were measured by HPLC and non-compartmental pharmacokinetic parameters estimated."( Metronidazole leads to enhanced uptake of imatinib in brain, liver and kidney without affecting its plasma pharmacokinetics in mice.
Bukhari, NI; Chay, G; Kan, E; Law, JH; Lim, WY; Segarra, I; Soo, GW; Tan, SY, 2011)		0.37
" Considering that a retrospective pharmacokinetic analysis has also suggested that imatinib clearance increases over time in patients with soft tissue sarcoma and GIST, the primary aim of this study was to assess systemic exposure to imatinib at multiple time points in a long-term prospective population pharmacokinetic study."( A long-term prospective population pharmacokinetic study on imatinib plasma concentrations in GIST patients.
De Giorgi, U; de Jong, FA; Eechoute, K; Fransson, MN; Friberg, LE; Loos, WJ; Mathijssen, RH; Reyners, AK; Schiavon, G; Sparreboom, A; van der Graaf, WT; Verweij, J; Wiemer, EA, 2012)		0.38
"Full pharmacokinetic blood sampling was conducted in 50 patients with GIST on the first day of imatinib treatment, and after one, six, and 12 months."( A long-term prospective population pharmacokinetic study on imatinib plasma concentrations in GIST patients.
De Giorgi, U; de Jong, FA; Eechoute, K; Fransson, MN; Friberg, LE; Loos, WJ; Mathijssen, RH; Reyners, AK; Schiavon, G; Sparreboom, A; van der Graaf, WT; Verweij, J; Wiemer, EA, 2012)		0.38
"This is the first prospective pharmacokinetic study in patients with GIST, showing a significant decrease of approximately 30% in imatinib exposure after long-term treatment."( A long-term prospective population pharmacokinetic study on imatinib plasma concentrations in GIST patients.
De Giorgi, U; de Jong, FA; Eechoute, K; Fransson, MN; Friberg, LE; Loos, WJ; Mathijssen, RH; Reyners, AK; Schiavon, G; Sparreboom, A; van der Graaf, WT; Verweij, J; Wiemer, EA, 2012)		0.38
"Concentration data from 493 patients with CML in chronic phase (CML-CP), accelerated phase, or blast crisis were used to perform a population pharmacokinetic analysis using nonlinear mixed-effect modeling."( Nilotinib population pharmacokinetics and exposure-response analysis in patients with imatinib-resistant or -intolerant chronic myeloid leukemia.
Baccarani, M; Giles, FJ; Kantarjian, HM; le Coutre, PD; Ottmann, OG; Sallas, WM; Woodman, RC; Yin, OQ, 2013)		0.39
" Patients with a lower Cmin had significantly longer time to complete cytogenetic response (P = 0."( Nilotinib population pharmacokinetics and exposure-response analysis in patients with imatinib-resistant or -intolerant chronic myeloid leukemia.
Baccarani, M; Giles, FJ; Kantarjian, HM; le Coutre, PD; Ottmann, OG; Sallas, WM; Woodman, RC; Yin, OQ, 2013)		0.39
"When tolerability allows, adherence to the nilotinib dose (400 mg twice daily) in order to maintain sufficient Cmin is important in maximizing the efficacy of nilotinib in patients with imatinib-resistant or -intolerant CML."( Nilotinib population pharmacokinetics and exposure-response analysis in patients with imatinib-resistant or -intolerant chronic myeloid leukemia.
Baccarani, M; Giles, FJ; Kantarjian, HM; le Coutre, PD; Ottmann, OG; Sallas, WM; Woodman, RC; Yin, OQ, 2013)		0.39
"Several population pharmacokinetic (PPK) analyses of the anticancer drug imatinib have been performed to investigate different patient populations and covariate effects."( Systematic review of population pharmacokinetic analyses of imatinib and relationships with treatment outcomes.
Buclin, T; Csajka, C; Gotta, V; Widmer, N, 2013)		0.39
" The relationships between imatinib exposure and therapeutic efficacy or toxicity were examined by grouping patients into quartiles according to Cmin and its percent change after dose escalation."( Efficacy, safety, and pharmacokinetics of imatinib dose escalation to 800 mg/day in patients with advanced gastrointestinal stromal tumors.
Beck, MY; Kang, YK; Ryoo, BY; Ryu, MH; Yoo, C, 2013)		0.39
"Given that the validated method has proved to be linear, accurate, precise, and robust, it is suitable for pharmacokinetic assays, such as bioavailability and bioequivalence, and is being successfully applied in routine therapeutic drug monitoring in the hospital service."( Quantification of imatinib in human serum: validation of a high-performance liquid chromatography-mass spectrometry method for therapeutic drug monitoring and pharmacokinetic assays.
Bendit, I; de Alencar Fisher Chamone, D; Novaes, MM; Rezende, VM; Rivellis, A, 2013)		0.39
" When co-administered with voriconazole, pharmacokinetic parameters of imatinib were not significantly altered except for a 36."( Differential effects of ketoconazole, itraconazole and voriconazole on the pharmacokinetics of imatinib and its main metabolite GCP74588 in rat.
Han, A; Hu, G; Kan, X; Lin, G; Qiu, X; Wang, C; Wang, Z; Xu, T, 2014)		0.4
" In this paper, the pharmacokinetic characteristics (absorption, distribution, metabolism and excretion) and drug-drug interactions of the approved TKIs are reviewed."( [Clinical pharmacokinetics of small molecule tyrosine kinase inhibitors].
Ding, JF; Zhong, DF, 2013)		0.39
" A population pharmacokinetic analysis was performed to investigate imatinib disposition in every patient and the role of transporter polymorphisms."( The c.480C>G polymorphism of hOCT1 influences imatinib clearance in patients affected by chronic myeloid leukemia.
Angelini, S; Arici, R; Baratè, C; Bocci, G; Capecchi, M; Cervetti, G; Ciabatti, E; Danesi, R; Di Paolo, A; Fontanelli, G; Galimberti, S; Grassi, S; Guerrini, F; Hrelia, P; Petrini, M; Polillo, M, 2014)		0.4
" We describe a kinetic and pharmacodynamic (PD) model of Bcr-Abl signalling in myeloid cells that is used to simulate effects of four classes of drugs: Bcr-Abl signalling inhibitors, such as imatinib, cyclin-dependent kinase inhibitors, and pro- and anti-oxidants."( A pharmacodynamic model of Bcr-Abl signalling in chronic myeloid leukaemia.
Jackson, RC; Radivoyevitch, T, 2014)		0.4
"This study examined whether oral administration of dasatinib to the rats with imatinib led to any pharmacokinetic interactions."( Pharmacokinetic interaction study of combining imatinib with dasatinib in rats by UPLC-MS/MS.
Ding, T; Geng, P; Ma, J; Wang, S; Wu, M; Zhang, Q; Zhou, Y, 2015)		0.42
"To prepare, optimize and characterize imatinib-loaded nanostructured lipid carriers (IMT-NLC), and evaluate their pharmacokinetic and cytotoxicity characteristics."( Modulation of Pharmacokinetic and Cytotoxicity Profile of Imatinib Base by Employing Optimized Nanostructured Lipid Carriers.
Cho, HJ; Choi, HG; Gupta, B; Jeong, JH; Kim, JO; Poudel, BK; Pradhan, R; Shin, BS; Tran, TH; Yong, CS, 2015)		0.42
" An in vivo pharmacokinetic study was conducted in rats after both oral and intravenous administration."( Modulation of Pharmacokinetic and Cytotoxicity Profile of Imatinib Base by Employing Optimized Nanostructured Lipid Carriers.
Cho, HJ; Choi, HG; Gupta, B; Jeong, JH; Kim, JO; Poudel, BK; Pradhan, R; Shin, BS; Tran, TH; Yong, CS, 2015)		0.42
"A combined DoE approach enabled accurate optimization and successful preparation of IMT-NLC with enhanced in vivo pharmacokinetic and in vitro cytotoxicity characteristics."( Modulation of Pharmacokinetic and Cytotoxicity Profile of Imatinib Base by Employing Optimized Nanostructured Lipid Carriers.
Cho, HJ; Choi, HG; Gupta, B; Jeong, JH; Kim, JO; Poudel, BK; Pradhan, R; Shin, BS; Tran, TH; Yong, CS, 2015)		0.42
" The aim of this study was to investigate the absorption and distribution kinetics of imatinib in healthy Iranian volunteers using nonlinear mixed effects modeling (NLMEM) to assess the overall, intra- and inter-subject variabilities in pharmacokinetic parameters after oral administration."( Population Pharmacokinetic Analysis of the Oral Absorption Process and Explaining Intra-Subject Variability in Plasma Exposures of Imatinib in Healthy Volunteers.
Dinan, NM; Golabchifar, AA; Kebriaeezadeh, A; Rezaee, S; Rouini, MR, 2016)		0.43
" To simultaneously describe the imatinib pharmacokinetic profiles obtained with both formulations, a population pharmacokinetic model was applied to data using SAEM algorithm implemented in MONOLIX, whilst simulations were used by numerical solving of ordinary differential equations to calculate secondary parameters in individuals for bioequivalence studies."( Population Pharmacokinetic Analysis of the Oral Absorption Process and Explaining Intra-Subject Variability in Plasma Exposures of Imatinib in Healthy Volunteers.
Dinan, NM; Golabchifar, AA; Kebriaeezadeh, A; Rezaee, S; Rouini, MR, 2016)		0.43
"According to goodness-of-fit criteria, a two-compartment open model with sequential zero- then first-order absorption and first-order elimination was used as the structural pharmacokinetic model."( Population Pharmacokinetic Analysis of the Oral Absorption Process and Explaining Intra-Subject Variability in Plasma Exposures of Imatinib in Healthy Volunteers.
Dinan, NM; Golabchifar, AA; Kebriaeezadeh, A; Rezaee, S; Rouini, MR, 2016)		0.43
" Future studies should focus on other pharmacokinetic processes so as to identify the major contributor to patient variability in imatinib plasma concentrations."( In Vivo Cytochrome P450 3A Isoenzyme Activity and Pharmacokinetics of Imatinib in Relation to Therapeutic Outcome in Patients With Chronic Myeloid Leukemia.
Aagesen, J; Alsenhed, J; Aluthgedara, W; Bergquist, J; Gréen, H; Hägg, S; Johnsson, A; Lotfi, K; Olsson-Strömberg, U; Peterson, C; Richter, J; Sandstedt, A; Skoglund, K; Söderlund, S; Svedberg, A; Ubhayasekera, SJ; Vikingsson, S, 2016)		0.43
" Concomitant use after hematopoietic stem cell transplantation (HSCT) for chronic myeloid leukemia (CML) or Philadelphia chromosome-positive (Ph+) acute lymphatic leukemia (ALL) may therefore result in a pharmacokinetic interaction."( A clinically relevant pharmacokinetic interaction between cyclosporine and imatinib.
Andrews, LM; Atiq, F; Broers, AE; Doorduijn, JK; Koch, BC; Van Gelder, T; Versmissen, J, 2016)		0.43
" We also describe key success factors that are useful for judging the quality of clinical pharmacodynamic studies, including biopsy quality and suitability, specimen handling, assay fitness-for-purpose, and reagent quality control."( Theory and practice of clinical pharmacodynamics in oncology drug development.
Doroshow, JH; Parchment, RE, 2016)		0.43
"A population pharmacokinetic analysis was performed on 170 plasma samples from 74 adult Iranian chronic myeloid leukemia patients."( Population Pharmacokinetics of Imatinib and its application to the therapeutic drug monitoring: Middle East CML population.
Ansari, M; Kalantary-Khandani, B; Mohajeri, E; Mosavi, N; Pardakhty, A; Safavi, M, 2016)		0.43
"By considering morphological and biological covariates, a unique covariate model could be used to accurately describe Imatinib pharmacokinetics in our population and because of the pharmacokinetic variability of Imatinib and the reported relationships between its plasma concentration and efficacy and toxicity, the usefulness of therapeutic drug monitoring as an aid to optimizing therapy should be further investigated."( Population Pharmacokinetics of Imatinib and its application to the therapeutic drug monitoring: Middle East CML population.
Ansari, M; Kalantary-Khandani, B; Mohajeri, E; Mosavi, N; Pardakhty, A; Safavi, M, 2016)		0.43
" Several studies have established interindividual and interpopulation variations in imatinib disposition although no pharmacokinetic study have been conducted in an African population since the introduction of the drug."( Population Pharmacokinetics of Imatinib in Nigerians With Chronic Myeloid Leukemia: Clinical Implications for Dosing and Resistance.
Adeagbo, BA; Bolaji, OO; Bolarinwa, RA; Durosinmi, MA; Ogungbenro, K; Olugbade, TA, 2017)		0.46
" In the same way, suboptimal adherence may also bias the results of pharmacokinetic modeling studies, which will affect in turn Bayesian TDM interpretation that relies on such population models."( Effect of Adherence on Pharmacokinetic/Pharmacodynamic Relationships of Oral Targeted Anticancer Drugs.
Cardoso, E; Csajka, C; Schneider, MP; Widmer, N, 2018)		0.48
" Pharmacokinetic variables (e."( Pharmacology and pharmacokinetics of imatinib in pediatric patients.
Bornhäuser, M; Metzler, M; Millot, F; Schleyer, E; Suttorp, M, 2018)		0.48
"Preclinical pharmacokinetic studies are an essential part of modern drug development."( Using miniature MS system with automatic blood sampler for preclinical pharmacokinetics study.
Bateman, KP; Helmy, R; Liu, Y; Ouyang, Z; Pu, F; Zhang, W, 2017)		0.46
" The miniature MS system was used to obtain drug concentrations, which were subsequently used to calculate the pharmacokinetic parameters."( Using miniature MS system with automatic blood sampler for preclinical pharmacokinetics study.
Bateman, KP; Helmy, R; Liu, Y; Ouyang, Z; Pu, F; Zhang, W, 2017)		0.46
"The growing interest of cancerous patients in using vitamins, while on imatinib (IMA) therapy, increased the risk of their pharmacokinetic interactions."( Ultra-performance LC-MS/MS study of the pharmacokinetic interaction of imatinib with selected vitamin preparations in rats.
Alzoman, NZ; Maher, HM; Shehata, SM, 2018)		0.48
" Co-administered vitamin preparations could affect IMA pharmacokinetic profiling through either an increase (vitamin A and E) or a decrease (vitamin C) in IMA bioavailability."( Ultra-performance LC-MS/MS study of the pharmacokinetic interaction of imatinib with selected vitamin preparations in rats.
Alzoman, NZ; Maher, HM; Shehata, SM, 2018)		0.48
"To enable such efficacy studies of two clinically approved TKIs, nilotinib, and imatinib, we first conducted comprehensive pharmacokinetic (PK) studies in relevant rodent and non-rodent animal models."( Preclinical pharmacokinetic evaluation to facilitate repurposing of tyrosine kinase inhibitors nilotinib and imatinib as antiviral agents.
Ananthula, HK; Buller, RM; Damon, IK; Desai, PB; Gallardo-Romero, N; Kalman, D; Moir-Savitz, T; Olson, V; Parker, S; Patel, G; Sallans, L; Salzer, JS; Sherwin, CM; Touchette, E; Werner, MH, 2018)		0.48
" The longer nilotinib elimination half-life in prairie dogs (i."( Preclinical pharmacokinetic evaluation to facilitate repurposing of tyrosine kinase inhibitors nilotinib and imatinib as antiviral agents.
Ananthula, HK; Buller, RM; Damon, IK; Desai, PB; Gallardo-Romero, N; Kalman, D; Moir-Savitz, T; Olson, V; Parker, S; Patel, G; Sallans, L; Salzer, JS; Sherwin, CM; Touchette, E; Werner, MH, 2018)		0.48
" The objective of this study was to develop and evaluate a physiologically based pharmacokinetic (PBPK) model for hyperforin (the constituent of SJW responsible for interactions), which has the potential to provide unique insights into SJW interactions and allow prediction of the likely extent of interactions with SJW compared to published interaction reports."( Physiologically Based Pharmacokinetic Modelling of Hyperforin to Predict Drug Interactions with St John's Wort.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2019)		0.51
" Currently, multiple oral TKIs have been introduced in the treatment of solid tumours, all administered in a fixed dose, although large interpatient pharmacokinetic (PK) variability is described."( Imatinib, sunitinib and pazopanib: From flat-fixed dosing towards a pharmacokinetically guided personalized dose.
Desar, IME; Steeghs, N; van der Graaf, WTA; van Erp, NP; Westerdijk, K, 2020)		0.56
" Physiologically-based pharmacokinetic (PBPK) models for the lignans accounting for reversible and mechanism-based inhibitions and induction of CYP3A enzymes were built in the Simcyp Simulator (version 17) and evaluated for their capability to predict interactions with midazolam and tacrolimus."( Potential for pharmacokinetic interactions between Schisandra sphenanthera and bosutinib, but not imatinib: in vitro metabolism study combined with a physiologically-based pharmacokinetic modelling approach.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2020)		0.56
"This study aimed to investigate the potential pharmacokinetic interactions between curcumin, imatinib and bosutinib, combining In Vitro and in silico methods."( Physiologically-Based Pharmacokinetic Predictions of the Effect of Curcumin on Metabolism of Imatinib and Bosutinib: In Vitro and In Vivo Disconnect.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2020)		0.56
" A physiologically-based pharmacokinetic (PBPK) model for curcumin formulated as solid lipid nanoparticles (SLN) was constructed using In Vitro glucuronidation kinetics and published clinical pharmacokinetic data."( Physiologically-Based Pharmacokinetic Predictions of the Effect of Curcumin on Metabolism of Imatinib and Bosutinib: In Vitro and In Vivo Disconnect.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2020)		0.56
" Being a CYP3A4 substrate, imatinib co-administration with CYP3A4 modulators would change its pharmacokinetic profile."( The effect of grape seed and green tea extracts on the pharmacokinetics of imatinib and its main metabolite, N-desmethyl imatinib, in rats.
Al Sharie, AH; Arafat, T; Babaresh, WM; Darweesh, RS; El-Elimat, T; Khamis, TN; Zayed, A, 2020)		0.56
" Plasma samples were collected and analyzed for imatinib and N-desmethyl imatinib concentrations using LC-MS/MS method, then their non-compartmental pharmacokinetic parameters were determined."( The effect of grape seed and green tea extracts on the pharmacokinetics of imatinib and its main metabolite, N-desmethyl imatinib, in rats.
Al Sharie, AH; Arafat, T; Babaresh, WM; Darweesh, RS; El-Elimat, T; Khamis, TN; Zayed, A, 2020)		0.56
" Pharmacokinetic studies were performed in male SD rats."( In vivo Pharmacokinetics and in vitro Release of Imatinib Mesylate-Loaded Liposomes for Pulmonary Delivery.
Ji, H; Li, Z; Qiao, W; Tang, J; Wang, C; Xu, H, 2021)		0.88
" Following intratracheal administration to rats, IM-LPs not only extended the half-life of IM, but also prolonged retention of IM compared with plain IM solution after intratracheal and intravenous administration."( In vivo Pharmacokinetics and in vitro Release of Imatinib Mesylate-Loaded Liposomes for Pulmonary Delivery.
Ji, H; Li, Z; Qiao, W; Tang, J; Wang, C; Xu, H, 2021)		0.88
" Several imatinib population pharmacokinetic (popPK) models have been developed."( External evaluation of population pharmacokinetic models of imatinib in adults diagnosed with chronic myeloid leukaemia.
Corral Alaejos, Á; Jiménez Cabrera, S; Otero, MJ; Pérez-Blanco, JS; Sánchez-Guijo, F; Zarzuelo Castañeda, A, 2022)		0.72
"This study implements a physiologically based pharmacokinetic (PBPK) modelling approach to predict the effect of hydrastine and berberine, two major alkaloids present in goldenseal extract, on pharmacokinetics of imatinib and bosutinib."( Physiologically based pharmacokinetic model predictions of natural product-drug interactions between goldenseal, berberine, imatinib and bosutinib.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2022)		0.72
"PBPK models of hydrastine and berberine were developed in the Simcyp Simulator (version 17), integrating prior in vitro knowledge and published clinical pharmacokinetic data."( Physiologically based pharmacokinetic model predictions of natural product-drug interactions between goldenseal, berberine, imatinib and bosutinib.
Adiwidjaja, J; Boddy, AV; McLachlan, AJ, 2022)		0.72
" Steady-state pharmacokinetic sampling was performed either in a sparse (4 samples each, n = 44) or intensive manner (9 samples each, n = 5)."( Role of ADME gene polymorphisms on imatinib disposition: results from a population pharmacokinetic study in chronic myeloid leukaemia.
Gokarn, A; Gota, V; Govalkar, R; Jadhav, S; Khattry, N; Krishnamurthy, MN; Kumar, S; Mehta, P; Patil, A; Punatar, S; Puri, AS; Shriyan, B, 2022)		0.72
" Pharmacokinetic parameters were calculated with WinNonlin software."( Pharmacokinetics, Bioequivalence, and Safety Studies of a Generic Selective Tyrosine Kinase Inhibitor Nilotinib Capsule Versus a Branded Product in Healthy Chinese Volunteers.
Huang, M; Lu, D; Wang, H; Wang, M; Zhang, Q; Zhou, W; Zhu, Y, 2022)		0.72
"Virtual TDM highlights the benefit of pharmacokinetic modelling to optimising treatments in challenging oncology population groups."( The Application of Virtual Therapeutic Drug Monitoring to Assess the Pharmacokinetics of Imatinib in a Chinese Cancer Population Group.
Badhan, RKS; Yu, H, 2023)		0.91
"We aimed to use physiologically based pharmacokinetic (PBPK) modeling and simulation to predict imatinib steady-state plasma exposure in patients with chronic myeloid leukemia (CML) to investigate variability in outcomes."( Application of physiologically based pharmacokinetic modeling to understand real-world outcomes in patients receiving imatinib for chronic myeloid leukemia.
Adattini, JA; Adiwidjaja, J; Gross, AS; McLachlan, AJ, 2023)		0.91
"In hepatic dysfunction, renal pharmacokinetic adaptation can be observed, although information on the changes in drug exposure and the interorgan regulation of membrane transporters in kidney in liver diseases is limited."( Renal Pharmacokinetic Adaptation to Cholestasis Causes Increased Nephrotoxic Drug Accumulation by Mrp6 Downregulation in Mice.
Arakawa, H; Horike, SI; Kato, Y; Kawanishi, T; Meguro-Horike, M; Nishiuchi, T; Shengyu, D; Sugimoto, M, 2023)		0.91

Compound-Compound Interactions

Imatinib mesylate, a recently introduced specific tyrosine kinase inhibitor of BCR-ABL, in combination with chemotherapy, resulted in more than 90% hematologic CR in adult Ph-positive ALL.

ExcerptReferenceRelevance
" The cytotoxic effects of STI571 were studied in combination with antileukemic agents against Ph(+) leukemia cell lines, KU812, K-562, TCC-S, and TCC-Y."( In vitro cytotoxic effects of a tyrosine kinase inhibitor STI571 in combination with commonly used antileukemic agents.
Akutsu, M; Furukawa, Y; Honma, Y; Kano, Y; Mano, H; Sato, Y; Tsunoda, S, 2001)		0.31
" These represent regimens where imatinib is combined with conventional chemotherapeutic drugs or with inhibitors of other key signal transduction molecules that may be preferentially activated in CML cells."( Imatinib mesylate in combination with other chemotherapeutic drugs: in vitro studies.
Melo, JV; Tipping, AJ, 2003)		1.76
" Thus several groups decided to investigate this new combination with the hypothesis that cell resistance would be less frequent."( Imatinib in combination with cytarabine for the treatment of Philadelphia-positive chronic myelogenous leukemia chronic-phase patients: rationale and design of phase I/II trials.
Berthaud, P; Berthou, C; Buzyn, A; Facon, T; Gardembas, M; Guilhot, F; Guilhot, J; Legros, L; Mahon, FX; Maloisel, F; Michallet, M; Najman, A; Rigal-Huguet, F; Rousselot, P; Tulliez, M; Vigier, M, 2003)		0.32
" In this paper, we analyzed effectiveness of Glivec in combination with homoharringtonine (HHT) and cytarabine (Ara-C) for patients with Ph chromosome positive acute leukemia (Ph(+)-AL), and investigated patients' tolerance to side effects of this trial."( [Glivec in combination with HA regimen for treatment of 20 patients with Ph chromosome positive acute leukemia].
Huang, F; Liu, XL; Meng, FY; Song, LL; Xu, B; Zhang, Y; Zheng, WY, 2003)		0.32
"Regimen of Glivec in combination with HA could increase chemotherapy effect for the patients with Ph(+)-AL, prolong their life time and the side-effects were tolerable."( [Glivec in combination with HA regimen for treatment of 20 patients with Ph chromosome positive acute leukemia].
Huang, F; Liu, XL; Meng, FY; Song, LL; Xu, B; Zhang, Y; Zheng, WY, 2003)		0.32
" Imatinib combined with low-dose IFN-alpha may achieve prolonged hematologic and molecular remissions in a subset of patients with advanced Ph+ALL, who are not candidates for allogeneic SCT."( Efficacy and safety of imatinib mesylate (Glivec) in combination with interferon-alpha (IFN-alpha) in Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph+ALL).
Binckebanck, A; Gschaidmeier, H; Hoelzer, D; Käbisch, A; Leimer, L; Lübbert, M; Ottmann, OG; Pfeifer, H; Scheuring, U; Wassmann, B, 2003)		0.63
" Thus, the efficacy of other antileukemic agents combined with ZOL should be evaluated experimentally."( Antiproliferative efficacy of the third-generation bisphosphonate, zoledronic acid, combined with other anticancer drugs in leukemic cell lines.
Kimura, S; Kuroda, J; Maekawa, T; Nogawa, M; Ottmann, OG; Sato, K; Segawa, H; Yuasa, T, 2004)		0.32
"The effects of monoterpene perilly alcohol (POH) alone or in combination with STI571 on the proliferation and apoptosis of the cell line K562 positive for Bcr/Abl were investigated."( Effects of POH in combination with STI571 on the proliferation and apoptosis of K562 cells.
Chen, Y; Hu, D, 2004)		0.32
" We therefore investigated the therapeutic efficacy of STI571, alone or combined with chemotherapy, in human SCLC cells or tumors xenografted into nude mice."( In vivo efficacy of STI571 in xenografted human small cell lung cancer alone or combined with chemotherapy.
de Cremoux, P; Decaudin, D; Fréneaux, P; Judde, JG; Livartowski, A; Nemati, F; Pouillart, P; Poupon, MF; Sastre, X; Tran-Perennou, C, 2005)		0.33
"To study the synergistic effect of STI571, an inhibitor of tyrosine kinase in combination with arsenic trioxide (As(2)O(3)) on a multidrug-resistant leukemia cell line expressing bcr-abl."( [Synergistic inhibitory effect of STI571 in combination with arsenic trioxide on a multidrug-resistant leukemia cell line expressing bcr-abl].
Chen, L; Fei, XH; Gao, L; Huang, ZX; Lou, JW; Wang, JM; Xu, XP, 2004)		0.32
"The cytotoxic effect of STI571 alone or in combination with different concentrations of As(2)O(3) on both bcr-abl and mdr1 positive leukemia cell line K562-n/VCR was detected by MTT method."( [Synergistic inhibitory effect of STI571 in combination with arsenic trioxide on a multidrug-resistant leukemia cell line expressing bcr-abl].
Chen, L; Fei, XH; Gao, L; Huang, ZX; Lou, JW; Wang, JM; Xu, XP, 2004)		0.32
" We examined the cytotoxic effects of imatinib in combination with other anticancer agents in the human prostate cancer cell lines LNCaP, PC-3, and DU 145."( In vitro cytotoxic effects of imatinib in combination with anticancer drugs in human prostate cancer cell lines.
Battistel, C; Hartung, R; Kübler, HR; Lehmer, A; Paul, R; Treiber, U; van Randenborgh, H; Wagenpfeil, S; Wutzler, S, 2005)		0.33
" In combination with etoposide imatinib produced additive effects in two of three cell lines."( In vitro cytotoxic effects of imatinib in combination with anticancer drugs in human prostate cancer cell lines.
Battistel, C; Hartung, R; Kübler, HR; Lehmer, A; Paul, R; Treiber, U; van Randenborgh, H; Wagenpfeil, S; Wutzler, S, 2005)		0.33
" Imatinib was evaluated both alone and in combination with established chemotherapeutic agents in adenoid cystic carcinoma (ACC) primary cultures and established cell lines representing squamous cell carcinoma of the head and neck (HNSCC)."( Synergistic effects of imatinib (STI 571) in combination with chemotherapeutic drugs in head and neck cancer.
Bruce, IA; Homer, JJ; McGown, AT; Slevin, NJ; Ward, TH, 2005)		0.33
"To study the effect of nonmyeloablative allogeneic peripheral blood stem cell (NST) transplantation combined with imatinib in the treatment of chronic myeloid leukemia (CML)."( [Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].
Chen, RA; Hao, MW; He, H; Jiang, SS; Liang, YM; Liu, L; Liu, Q; Wang, LH; Zhang, JL, 2005)		0.33
" The preparative regimen included cytoxin (CTX), Ara-C, and fludarabine combined with antithymocyte globulin (ATG) or anti-CD3 monoclonal antibody."( [Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].
Chen, RA; Hao, MW; He, H; Jiang, SS; Liang, YM; Liu, L; Liu, Q; Wang, LH; Zhang, JL, 2005)		0.33
"An effective and safer method for CML, especially advanced CML treatment of NST transplantation combined with imatinib before and after transplantation reduces the leukemic cell load before transplantation, inhibits the proliferation of residual leukemic cells, promotes full chimerism change and enhanced the effect of graft versus leukemia."( [Nonmyleoablative allogeneic stem cell transplantation combined with imatinib in treatment of chronic myeloid leukemia: a clinical study].
Chen, RA; Hao, MW; He, H; Jiang, SS; Liang, YM; Liu, L; Liu, Q; Wang, LH; Zhang, JL, 2005)		0.33
" injection of gemcitabine did not inhibit tumor growth, its combination with AEE788 and STI571 produced >80% inhibition of tumor growth and prolonged survival in parallel with increases in number of tumor cells and tumor-associated endothelial cell apoptosis, decreased microvascular density, decreased proliferation rate, and prolonged survival."( Simultaneous inhibition of EGFR, VEGFR, and platelet-derived growth factor receptor signaling combined with gemcitabine produces therapy of human pancreatic carcinoma and prolongs survival in an orthotopic nude mouse model.
Abbruzzese, JL; Baker, CH; Bucana, CD; Fan, D; Fidler, IJ; Kitadai, Y; Kuwai, T; Sasaki, T; Yokoi, K, 2005)		0.33
"The maximum tolerated dose for this combination with granulocyte-colony-stimulating factor support was identified as imatinib at a dose of 300 mg/day with irinotecan (at a dose of 65 mg/m(2)) and cisplatin (at a dose of 30 mg/m(2)) given on Days 1 and 8, every 21 days."( Phase I studies of imatinib mesylate combined with cisplatin and irinotecan in patients with small cell lung carcinoma.
Glisson, BS; Johnson, FM; Krug, LM; Patel, J; Peeples, B; Prieto, VG; Shoaf, S; Tamboli, P; Tran, HT, 2006)		0.66
"Imatinib combined with high-dose chemotherapy is now becoming the gold standard for treatment of Philadelphia chromosome-positive acute leukemias."( High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia.
Choufi, B; Dombret, H; Dupriez, B; Huguet, F; Legros, L; Maury, S; Ojeda-Uribe, M; Pigneux, A; Raffoux, E; Rea, D; Recher, C; Reman, O; Rousselot, P; Royer, B; Stéphane, D; Thomas, X; Turlure, P; Vigier, M, 2006)		0.74
" Treatment of NB with STI-571 in combination with 9-cis RA might be a therapeutic strategy for patients in consolidation therapy who have completed gamma-irradiation therapy."( Effect of STI-571 (imatinib mesylate) in combination with retinoic acid and gamma-irradiation on viability of neuroblastoma cells.
Kontny, U; Lagodny, J; Niemeyer, CM; Rössler, J; Zambrzycka, I, 2006)		0.66
" Our goals were to deliver small interfering RNA (siRNA) using a liposome-based method, and to show Bcr-Abl siRNA specificity against K-562 cells, alone or in combination with Gleevec."( Effects of siRNAs in combination with Gleevec on K-562 cell proliferation and Bcr-Abl expression.
Baker, BE; Ichiki, AT; Kestler, DP, 2006)		0.33
"We analyzed IGF1R blockade by ADW742, a small molecule specific for this receptor, alone and in combination with imatinib, vincristine, and doxorubicin on Ewing tumor cell lines."( Insulin-like growth factor I receptor pathway inhibition by ADW742, alone or in combination with imatinib, doxorubicin, or vincristine, is a novel therapeutic approach in Ewing tumor.
Campos, M; de Alava, E; Hernández, T; Mackintosh, C; Martín, DH; Martins, AS; Ordóñez, JL, 2006)		0.33
" Combination with usual chemotherapeutic agents vincristine and doxorubicin showed synergistic interactions."( Insulin-like growth factor I receptor pathway inhibition by ADW742, alone or in combination with imatinib, doxorubicin, or vincristine, is a novel therapeutic approach in Ewing tumor.
Campos, M; de Alava, E; Hernández, T; Mackintosh, C; Martín, DH; Martins, AS; Ordóñez, JL, 2006)		0.33
" STI571 combined with VCR significantly suppressed the proliferation of K562-n/VCR cells."( STI571 combined with vincristine greatly suppressed the tumor formation of multidrug-resistant K562 cells in a human-nude mice xenograft model.
Chen, L; Fei, XH; Gao, L; Qiu, HY; Wang, JM; Zhou, H, 2006)		0.33
" VCR combined with STI571 had an excellent tumor-suppressing effect on both K562-n/VCR and K562-n in the human-nude mice xenograft model."( STI571 combined with vincristine greatly suppressed the tumor formation of multidrug-resistant K562 cells in a human-nude mice xenograft model.
Chen, L; Fei, XH; Gao, L; Qiu, HY; Wang, JM; Zhou, H, 2006)		0.33
"This study was aimed to investigate the clinical features and therapy of Ph(+) acute lymphoblastic leukemia (Ph(+)ALL) combined with invasive aspergillosis."( [Ph+ acute lymphoblastic leukemia combined with lung and brain invasive aspergillosis].
Huang, M; Liu, WL; Ran, D; Sun, HY; Zhang, YC; Zhou, JF, 2006)		0.33
" These in vitro studies appear to provide data for the decision of G-CSF administration in combination with imatinib in the treatment of neutropenic patients with advanced-stage CML."( Effect of imatinib mesylate combined with granulocyte colony-stimulating factor on leukaemic blast cells derived from advanced-stage chronic myelogenous leukaemia patients.
Asaka, M; Hashino, S; Imamura, M; Kondo, K; Matsuno, K; Mori, A; Musashi, M; Onozawa, M; Ota, S; Tanaka, J; Toubai, T; Toyoshima, N, 2006)		0.74
" Because of its wide spectrum of actions, it is reasonable to consider the combination with other anticancer drugs in clinical application."( Cytotoxic effects of histone deacetylase inhibitor FK228 (depsipeptide, formally named FR901228) in combination with conventional anti-leukemia/lymphoma agents against human leukemia/lymphoma cell lines.
Akutsu, M; Furukawa, Y; Izumi, T; Kano, Y; Kobayashi, H; Mano, H; Tsunoda, S, 2007)		0.34
" During 2004 and 2005, 45 patients with newly diagnosed Ph+ ALL were treated in the Group for Research on Adult Acute Lymphoblastic Leukemia (GRAAPH) 2003 study, in which imatinib was started with HAM (mitoxantrone with intermediate-dose cytarabine) consolidation in good early responders (corticosensitive and chemosensitive ALL) or earlier during the induction course in combination with dexamethasone and vincristine in poor early responders (corticoresistant and/or chemoresistant ALL)."( Imatinib combined with induction or consolidation chemotherapy in patients with de novo Philadelphia chromosome-positive acute lymphoblastic leukemia: results of the GRAAPH-2003 study.
Buzyn, A; Cayuela, JM; Chalandon, Y; de Labarthe, A; Delabesse, E; Dombret, H; Escoffre, M; Huguet-Rigal, F; Ifrah, N; Lhéritier, V; MacIntyre, E; Maury, S; Pigneux, A; Réa, D; Reman, O; Rousselot, P; Thomas, X; Vekemans, MC; Vernant, JP; Witz, F, 2007)		0.34
" Overall, our findings strongly suggest that either TZD18, either alone or in combination with imatinib may be beneficial for the treatment of CML in myeloid blast crisis."( Dual PPARalpha/gamma ligand TZD18 either alone or in combination with imatinib inhibits proliferation and induces apoptosis of human CML cell lines.
Bertz, J; Elstner, E; Eucker, J; Koeffler, HP; Liu, H; Possinger, K; Waechter, M; Zang, C, 2006)		0.33
" A Phase II study was performed on low-dose decitabine, a DNA methyltransferase inhibitor, in combination with imatinib in patients with CML in accelerated phase (AP) and myeloid blastic phase (BP)."( Phase II study of low-dose decitabine in combination with imatinib mesylate in patients with accelerated or myeloid blastic phase of chronic myelogenous leukemia.
Cortes, J; Garcia-Manero, G; Gharibyan, V; Issa, JP; Jones, D; Kantarjian, HM; Morris, GM; O'brien, S; Oki, Y; Verstovsek, S, 2007)		0.58
" The objective of this Phase I study was to define the dose-limiting toxicity (DLT) and maximum tolerated dose (MTD) of imatinib in combination with fluorouracil and leucovorin in patients with chemotherapy-refractory gastrointestinal cancer."( Imatinib mesylate for targeting the platelet-derived growth factor beta receptor in combination with fluorouracil and leucovorin in patients with refractory pancreatic, bile duct, colorectal, or gastric cancer--a dose-escalation Phase I trial.
Al-Batran, SE; Atmaca, A; Ehninger, G; Hosius, C; Jäger, E; Pauligk, C; Schleyer, E, 2007)		1.78
"To observe the efficacy of Gleevec combined with myeloablative allogeneic stem cells transplantation(Allo-SCT) for the treatment of chronic myeloid leukemia (CML)."( [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
Luo, Y; Pan, J; Shi, JM, 2007)		0.34
" Mycophenolate mofetil combined with cyclosporin A and methotrexate was used for the prevention of acute GVHD."( [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
Luo, Y; Pan, J; Shi, JM, 2007)		0.34
"The treatment of CML consisting of myeloablative Allo-SCT combined with Gleevec before and after transplantation is an effective and safe method for CML."( [Clinical observation of Gleevec combined with myeloablative allogeneic stem cells transplantation in treatment of chronic myeloid leukemia].
Luo, Y; Pan, J; Shi, JM, 2007)		0.34
" Here we examined the growth inhibitory effect of (-)gossypol and its combination with imatinib in K562 cells."( (-)Gossypol and its combination with imatinib induce apoptosis in human chronic myeloid leukemic cells.
Chen, X; Fu, J; Li, H; Li, J; Li, Y; Liu, H; Liu, Y; Meng, Y, 2007)		0.34
" We treated four children with imatinib in combination with conventional chemotherapy (CT) before stem cell transplantation (SCT)."( Imatinib mesylate in combination with chemotherapy in four children with de novo and advanced stage Philadelphia chromosome-positive acute lymphoblastic leukemia.
Bermúdez, M; Calle, D; Fuster, JL; Galera, A; Llinares, ME; Ortuño, FJ, 2007)		1.78
" Many new drugs including targeted therapy are combined with antineoplastic agents safely."( Bleomycin, etoposide and cisplatin (BEP) combination with concurrent imatinib mesylate (GLEEVEC) in chronic myeloid leukemia (CML) patient with mesenchymal tumor.
Alanoğlu, G; Coşkun, HS; Göksu, SS; Sahin, M, 2008)		0.58
" Proliferation assays were performed with single agent Imatinib or combined with Paclitaxel and Carboplatin."( Novel treatment of ovarian cancer cell lines with Imatinib mesylate combined with Paclitaxel and Carboplatin leads to receptor-mediated antiproliferative effects.
Bauerschlag, DO; Hilpert, F; Jonat, W; Maass, N; Meinhold-Heerlein, I; Mundhenke, C; Roesel, F; Schem, C; Sturner, KH; Weigel, MT, 2008)		0.6
" This study was conducted to determine the activity of imatinib in combination with docetaxel in patients with recurrent, platinum-resistant epithelial ovarian cancer (EOC)."( Imatinib mesylate in combination with docetaxel for the treatment of patients with advanced, platinum-resistant ovarian cancer and primary peritoneal carcinomatosis : a Hoosier Oncology Group trial.
Baldridge, LA; Breen, T; Emerson, RE; Johnson, CS; Matei, D; McClean, J; Menning, N; Schilder, J; Stephens, D; Sutton, G; Whalen, C, 2008)		1.79
"To study the safety, tolerability, and pharmacokinetics of the selective tyrosine kinase inhibitor nilotinib as a single agent or in combination with imatinib in patients with advanced imatinib-resistant gastrointestinal stromal tumors."( A phase I study of single-agent nilotinib or in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors.
Bailey, SM; Bertulli, R; Blay, JY; Borghaei, H; Casali, PG; Cassier, P; Cheung, W; Davey, M; Debiec-Rychter, M; Demetri, GD; Fumagalli, E; Morgan, JA; Pink, D; Ray-Coquard, I; Reichardt, A; Reichardt, P; Veronese, ML; von Mehren, M, 2009)		0.35
"Nilotinib alone or in combination with imatinib was well tolerated overall and showed clinical activity in imatinib-resistant gastrointestinal stromal tumor patients."( A phase I study of single-agent nilotinib or in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors.
Bailey, SM; Bertulli, R; Blay, JY; Borghaei, H; Casali, PG; Cassier, P; Cheung, W; Davey, M; Debiec-Rychter, M; Demetri, GD; Fumagalli, E; Morgan, JA; Pink, D; Ray-Coquard, I; Reichardt, A; Reichardt, P; Veronese, ML; von Mehren, M, 2009)		0.35
"Having reported feasibility previously, we hereby report the efficacy of escalated imatinib (200 mg, 400 mg, 600 mg or 800 mg) in combination with two cycles of intravenous cytarabine (200 mg/m(2) or 1000 mg/m(2) days 1 to 7) in 162 patients with chronic myeloid leukemia."( Efficacy of escalated imatinib combined with cytarabine in newly diagnosed patients with chronic myeloid leukemia.
Beverloo, HB; Cornelissen, JJ; Daenen, SM; Deenik, W; Ferrant, A; Janssen, JJ; Kersten, MJ; Löwenberg, B; Ossenkoppele, GJ; Schattenberg, AV; Smit, WM; Sonneveld, P; Valk, PJ; van der Holt, B; van Marwijk Kooy, M; Verdonck, LF; Verhoef, GE; Wijermans, PW; Willemze, R; Wittebol, S, 2010)		0.36
"The study was purposed to explore the efficacy of allogeneic hematopoietic stem cell transplantation (allo-HSCT) combined with Imatinib for treatment of Philadelphia chromosome positive acute lymphoblastic leukemia (Ph(+)ALL) patients."( [Allogeneic hematopoietic stem cell transplantation combined with imatinib for treatment of Philadelphia chromosome positive acute lymphoblastic leukemia].
Bo, J; Cai, B; Ding, Y; Gao, CJ; Gao, L; Huang, WR; Li, HH; Sun, JF; Wang, LL; Yu, L, 2010)		0.36
" Moreover, honikiol exhibited schedule-dependent synergy in combination with imatinib and sequential administration of imatinib followed by honokiol could be the optimal sequence to combine these two drugs in K562 cells."( Honokiol induces paraptosis and apoptosis and exhibits schedule-dependent synergy in combination with imatinib in human leukemia cells.
Wang, Y; Yang, Z; Zhao, X, 2010)		0.36
" Imatinib mesylate, a recently introduced specific tyrosine kinase inhibitor of BCR-ABL, in combination with chemotherapy, resulted in more than 90% hematologic CR in adult Ph-positive ALL, including molecular CR in more than 50% of patients."( Treatment of Philadelphia-chromosome-positive acute lymphoblastic leukemia with imatinib in combination with chemotherapy.
Ohno, R, 2006)		1.24
" We conducted a Phase 1 study of the c-kit inhibitor, imatinib mesylate (IM), in combination with cytarabine and daunorubicin (7+3) in c-kit+ relapsed AML."( A Phase 1 study of imatinib mesylate in combination with cytarabine and daunorubicin for c-kit positive relapsed acute myeloid leukemia.
Advani, AS; Bates, J; Copelan, EA; Cotta, CV; Egorin, MJ; Howard, M; Hsi, E; Jin, T; Kalaycio, M; Lim, K; Maciejewski, J; Noon, E; Price, C; Rush, ML; Salvado, A; Saunthararajah, Y; Sekeres, MA; Sobecks, R; Tiu, R; Tripp, B, 2010)		0.94
" We aimed to clarify the safety and effects of WT1 peptide vaccination in combination with imatinib therapy for a CML patient."( WT1 peptide vaccination in combination with imatinib therapy for a patient with CML in the chronic phase.
Aizawa, Y; Furukawa, T; Fuse, I; Kawakami, M; Kitajima, T; Kurasaki, T; Masuko, M; Narita, M; Oka, Y; Saitoh, A; Sugiyama, H; Takahashi, M; Takenouchi, S; Toba, K; Watanabe, N, 2010)		0.36
" Treatment with HDACis combined with IM effectively induced apoptosis in quiescent CML progenitors resistant to elimination by IM alone, and eliminated CML stem cells capable of engrafting immunodeficient mice."( Effective targeting of quiescent chronic myelogenous leukemia stem cells by histone deacetylase inhibitors in combination with imatinib mesylate.
Bhatia, R; Chu, S; Ho, Y; Holyoake, T; Huettner, CS; Li, M; Shiang, KD; Shultz, L; Snyder, DS; Strauss, AC; Zhang, B, 2010)		0.57
"In phase I, patients received imatinib (600/800 mg/day) combined with weekly (20 mg) or daily (2."( A phase I-II study of everolimus (RAD001) in combination with imatinib in patients with imatinib-resistant gastrointestinal stromal tumors.
Blay, JY; Demetri, GD; Dumez, H; Hollaender, N; Jappe, A; Morgan, JA; Ray-Coquard, I; Reichardt, P; Schöffski, P, 2010)		0.36
" The STI571 combined with As₂O₃ can enhance these two effects, increase the expression of caspase-3 mRNA and decrease the expression of bcl-xL mRNA."( [Effects of STI571 combined with As₂O₃ on proliferation, apoptosis and caspase 3, Bcl-xL expression of K562 cells].
Chen, NY; Wang, J; Wang, XM; Wang, YM; Yan, B; Yan, ZY; Zhang, HX; Zhang, S, 2010)		0.36
" Therefore, they are regularly co-administered along with treatments at risk of drug-drug interactions."( Drug interactions with the tyrosine kinase inhibitors imatinib, dasatinib, and nilotinib.
Buclin, T; Decosterd, LA; Duchosal, MA; Haouala, A; Montemurro, M; Widmer, N, 2011)		0.37
"These findings suggest that surgical intervention in combination with imatinib treatment is more effective than imatinib alone against GIST liver metastases, with minimal complications and side effects."( Resection combined with imatinib therapy for liver metastases of gastrointestinal stromal tumors.
Ji, L; Li, X; Wu, XT; Xia, L; Zhang, MM, 2010)		0.36
" To evaluate this effect in vivo, we performed a phase I study of chlorambucil combined with imatinib in relapsed CLL patients."( A phase I study of imatinib mesylate in combination with chlorambucil in previously treated chronic lymphocytic leukemia patients.
Aloyz, R; Amrein, L; Assouline, S; Caplan, S; Desjardins, P; Egorin, MJ; Hebb, J; Panasci, L; Rousseau, C, 2011)		0.7
"A phase II trial to evaluate Im in combination with D in patients with recurrent NSCLC was conducted."( Potential role of platelet-derived growth factor receptor inhibition using imatinib in combination with docetaxel in the treatment of recurrent non-small cell lung cancer.
Allen, A; Hsueh, CT; Huang, CH; Kelly, K; Mayo, M; Smith, H; Tawfik, O; Uypeckcuat, AM; Van Veldhuizen, PJ; Wick, J; Williamson, SK, 2011)		0.37
"Im in combination with D did not achieve its primary objective of improving response rate in patients with recurrent NSCLC."( Potential role of platelet-derived growth factor receptor inhibition using imatinib in combination with docetaxel in the treatment of recurrent non-small cell lung cancer.
Allen, A; Hsueh, CT; Huang, CH; Kelly, K; Mayo, M; Smith, H; Tawfik, O; Uypeckcuat, AM; Van Veldhuizen, PJ; Wick, J; Williamson, SK, 2011)		0.37
"To evaluat the efficacy and safety of myeloablative allogeneic hematopoietic stem cell transplantation (allo-HSCT) combined with imatinib for advanced chronic myeloid leukemia (CML), 15 patients with accelerated phase (n=6) or blast crisis (n=9) were enrolled in this study."( Imatinib combined with myeloablative allogeneic hematopoietic stem cell transplantation for advanced phases of chronic myeloid leukemia.
Cai, Z; Han, X; He, J; Huang, H; Li, L; Lin, M; Luo, Y; Shi, J; Tan, Y; Xie, W; Ye, X; Zhao, Y; Zheng, Y, 2011)		0.37
" In addition, nilotinib combined with the MEK1/2 inhibitor selumetinib (AZD6244) at low concentrations displayed stronger efficiency toward tumor growth inhibition, compared with nilotinib alone."( Nilotinib alone or in combination with selumetinib is a drug candidate for neurofibromatosis type 2.
Ammoun, S; Hanemann, CO; Manley, P; Schmid, MC; Triner, J, 2011)		0.37
" This study aimed to define safe doses of gemcitabine plus oxaliplatin when combined with imatinib (potent PDGFR-β inhibitor) in patients with advanced gemcitabine-refractory pancreatic cancer (PC)."( A dose escalation study of gemcitabine plus oxaliplatin in combination with imatinib for gemcitabine-refractory advanced pancreatic adenocarcinoma.
Barbachano, Y; Brown, G; Chau, I; Cunningham, D; Hawkes, EA; Oates, J; Starling, N; Thomas, J; Thomas, K; Watkins, D; Webb, J, 2012)		0.38
"In gemcitabine-refractory PC, gemcitabine (1000 mg/m(2)) and oxaliplatin (85 mg/m(2)) can be safely combined with imatinib given on a 7 days on and 7 days off intermittent schedule."( A dose escalation study of gemcitabine plus oxaliplatin in combination with imatinib for gemcitabine-refractory advanced pancreatic adenocarcinoma.
Barbachano, Y; Brown, G; Chau, I; Cunningham, D; Hawkes, EA; Oates, J; Starling, N; Thomas, J; Thomas, K; Watkins, D; Webb, J, 2012)		0.38
"To explore the effect of trichostatin A (TSA) alone and combination with imatinib on the proliferation and apoptosis of K562R cells."( [Effect of trichostatin alone and combination with imatinb on the proliferation and apoptosis of the K562R cells].
Chen, F; Chen, S; He, Q; Liu, Y; Zeng, H; Zhao, X, 2011)		0.37
" Combined with imatinib, the effect of proliferation inhibition was better."( [Effect of trichostatin alone and combination with imatinb on the proliferation and apoptosis of the K562R cells].
Chen, F; Chen, S; He, Q; Liu, Y; Zeng, H; Zhao, X, 2011)		0.37
"TSA combined with imatinib can inhibit the proliferation of K562R cells and induce its apopotosis."( [Effect of trichostatin alone and combination with imatinb on the proliferation and apoptosis of the K562R cells].
Chen, F; Chen, S; He, Q; Liu, Y; Zeng, H; Zhao, X, 2011)		0.37
" Both patients received initial IM therapy combined with daunorubicin-based chemotherapy followed by allogeneic hematopoietic stem cell transplantation (allo-HSCT) and IM maintenance treatment after allo-HSCT."( Prolonged survival with imatinib mesylate combined with chemotherapy and allogeneic stem cell transplantation in de novo Ph+ acute myeloid leukemia.
Allan, DS; Huang, H; Luo, Y; Sun, J; Tan, Y; Wang, Z, 2012)		0.69
"Our cases indicate that IM combined with daunorubicin-based chemotherapy followed by allo-HSCT and IM maintenance treatment is associated with a favorable outcome for de novo Ph+ AML, especially when IM is used in an early phase of AML."( Prolonged survival with imatinib mesylate combined with chemotherapy and allogeneic stem cell transplantation in de novo Ph+ acute myeloid leukemia.
Allan, DS; Huang, H; Luo, Y; Sun, J; Tan, Y; Wang, Z, 2012)		0.69
" All patients received IM combined with standard VDCP ± L as induction therapy then intensive consolidation with modified Hyper-CVAD/MA regimen plus IM, and followed by allo-SCT in CR1."( [Imatinib combined with modified hyper-CVAD/MA followed by allogeneic hematopoietic stem cell transplantation in CR1 as the front-line therapy for adult Ph(+) acute lymphoblastic leukemia].
Fu, MW; Huang, J; Li, ZJ; Qi, JY; Qiu, LG; Xu, Y; Zhao, YZ; Zou, DH, 2011)		0.37
"IM combined with intensive chemotherapy significantly increased the CR rate and improved the quality of CR, which prepared the feasibility of allo-SCT in CR1."( [Imatinib combined with modified hyper-CVAD/MA followed by allogeneic hematopoietic stem cell transplantation in CR1 as the front-line therapy for adult Ph(+) acute lymphoblastic leukemia].
Fu, MW; Huang, J; Li, ZJ; Qi, JY; Qiu, LG; Xu, Y; Zhao, YZ; Zou, DH, 2011)		0.37
" SIRT1 effects were enhanced in combination with the BCR-ABL TKI imatinib."( Activation of p53 by SIRT1 inhibition enhances elimination of CML leukemia stem cells in combination with imatinib.
Bhatia, R; Chen, W; Ho, Y; Holyoake, TL; Li, L; McDonald, T; Wang, L; Wang, Z, 2012)		0.38
"To investigate the impact of 5-aza-2'-deoxycytidine(5-aza-CdR) combined with imatinib on the proliferation, motility, invasion, and apoptosis of gastrointestinal stromal tumors(GIST) cells in vitro."( [Therapeutic effect of in vitro 5-aza-2'-deoxycytidine combined with imatinib on gastrointestinal stromal tumor].
Liang, G; Liang, JF; Wu, LN; Xiao, H; Zhao, YZ; Zheng, HX, 2012)		0.38
" Cyclosporine had an additive or synergistic effect on T-cell proliferation when combined with dasatinib and imatinib for 3 of the 4 methods of stimulating T-cell proliferation."( Drug-interaction studies evaluating T-cell proliferation reveal distinct activity of dasatinib and imatinib in combination with cyclosporine A.
Blake, SJ; Hughes, TP; Lyons, AB, 2012)		0.38
" This phase I study aimed to assess the maximal tolerated dose (MTD) of imatinib in combination with mFOLFOX6-bevacizumab in patients with advanced colorectal cancer and to identify pharmacokinetic (PK) interactions and toxicities."( A phase I trial of imatinib in combination with mFOLFOX6-bevacizumab in patients with advanced colorectal cancer.
Copeman, M; Gibbs, P; Gouillou, M; Jefford, M; Lipton, L; Lynch, K; McArthur, G; Michael, M; Tebbutt, NC; Zalcberg, J, 2013)		0.39
"Leukemia, breast and cervical cancer cell lines were exposed to D3CLP-alone or in combination with imatinib, tamoxifen or cisplatin, respectively."( Synergistic anticancer activity of Thiazolo[5,4-b]quinoline derivative D3CLP in combination with cisplatin in human cervical cancer cells.
Cerbón, MA; Coronel-Cruz, C; González-Sánchez, I; Lira-Rocha, A; Loza-Mejía, MA; Mendoza-Rodríguez, CA; Navarrete, A, 2012)		0.38
"Antiproliferative activity results indicate that D3CLP in combination with antineoplastic drugs induced a synergistic effect, at 3:1 and 1:1 ratios for D3CLP plus imatinib in K-562 leukemia cells, and at a 3:1 ratio for D3CLP with cisplatin in HeLa cells, as determined by their combination index."( Synergistic anticancer activity of Thiazolo[5,4-b]quinoline derivative D3CLP in combination with cisplatin in human cervical cancer cells.
Cerbón, MA; Coronel-Cruz, C; González-Sánchez, I; Lira-Rocha, A; Loza-Mejía, MA; Mendoza-Rodríguez, CA; Navarrete, A, 2012)		0.38
" These findings suggest that RIC allo-HSCT combined with short-term imatinib mesylate does not necessarily have profound effects on female fertility."( Twin pregnancy and childbirth after reduced-intensity conditioning allogeneic haematopoietic stem cell transplantation combined with imatinib mesylate for chronic myeloid leukaemia: case report and literature review.
Hu, YX; Huang, H; Lai, XY; Liu, LZ; Luo, Y; Tan, YM; Wu, KN; Zhao, YM, 2012)		0.82
"To describe 12-month rates and patterns of coprescription of drugs that potentially create drug-drug interactions (DDIs) through shared metabolic or transport pathways for 9 enzyme-targeted kinase inhibitor oral antineoplastic drugs (OADs)."( Twelve-month frequency of drug-metabolizing enzyme and transporter-based drug-drug interaction potential in patients receiving oral enzyme-targeted kinase inhibitor antineoplastic agents.
Bowlin, SJ; Robinson, KD; Stanek, EJ; Wang, W; Xia, F, 2013)		0.39
" One hundred nine patients aged 18-65 years were randomly assigned to either imatinib 800 mg (n = 55) or to imatinib 800 mg in combination with two successive cycles of cytarabine 200 mg/m(2) for 7 days (n = 54)."( High-dose imatinib versus high-dose imatinib in combination with intermediate-dose cytarabine in patients with first chronic phase myeloid leukemia: a randomized phase III trial of the Dutch-Belgian HOVON study group.
Ammerlaan, RA; Chu, IW; Cornelissen, JJ; Deenik, W; Falkenburg, JH; Janssen, JJ; Kersten, MJ; Ossenkoppele, GJ; Schattenberg, A; Schipperus, M; Sinnige, HA; Smit, WM; Sonneveld, P; Thielen, N; Valk, PJ; van der Holt, B; van Marwijk Kooy, R; Verhoef, GE, 2013)		0.39
" NVP-BEZ235 in combination with nilotinib also inhibited tumor growth in a xenograft model and inhibited the growth of primary T315I mutant cells and ponatinib-resistant cells."( Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with nilotinib against BCR-ABL-positive leukemia cells involves the ABL kinase domain mutation.
Kimura, S; Kitahara, T; Maekawa, T; Ohyashiki, K; Okabe, S; Tanaka, Y; Tauchi, T, 2014)		0.4
"The pegylated form of interferon-α-2a (PegIFNa2a) in combination with imatinib has demonstrated a molecular improvement in patients with chronic-phase chronic myeloid leukemia."( Tolerability and efficacy of pegylated interferon-α-2a in combination with imatinib for patients with chronic-phase chronic myeloid leukemia.
Guilhot, F; Guilhot, J; Johnson-Ansah, H; Legros, L; Mahon, FX; Nicolini, FE; Preudhomme, C; Rea, D; Rigal-Huguet, F; Rousselot, P, 2013)		0.39
"The results of the current study demonstrate that in combination with imatinib, the efficient dose of PegIFNa2a appears to be 45 μg/week."( Tolerability and efficacy of pegylated interferon-α-2a in combination with imatinib for patients with chronic-phase chronic myeloid leukemia.
Guilhot, F; Guilhot, J; Johnson-Ansah, H; Legros, L; Mahon, FX; Nicolini, FE; Preudhomme, C; Rea, D; Rigal-Huguet, F; Rousselot, P, 2013)		0.39
"Allo-SCT has a satisfactory outcome when combined with 2nd-generation TKI, which could provide a good quality of remission before transplantation and prevent relapse after transplantation."( Second-generation tyrosine kinase inhibitors combined with stem cell transplantation in patients with imatinib-refractory chronic myeloid leukemia.
Cai, Z; Huang, H; Luo, Y; Shi, J; Zhao, Y, 2014)		0.4
"Conventional induction chemotherapy in combination with imatinib in the first induction therapy of adult Ph⁺ ALL, not only improved the rate of hematologic remission, also the rate of molecular response."( [Imatinib in combination with allogeneic hematopoietic stem cell transplantation improved the outcome of adult Philadelphia chromosome-positive acute lymphoblastic leukemia].
Chen, F; Chen, G; Cheng, Z; Fu, C; Jin, Z; Qiu, H; Sun, A; Tang, X; Wu, D; Xue, S; Zhao, L, 2014)		0.4
" Therefore, we focused on the comparison of the efficacy between imatinib and nilotinib in combination with IL-2 in a murine B16F10 melanoma model."( Nilotinib combined with interleukin-2 mediates antitumor and immunological effects in a B16 melanoma model.
Bauer, R; Geisler, K; Jacobs, B; Kroeger, I; Mackensen, A; Meinhardt, K; Reischer, A; Ryffel, B; Ullrich, E, 2014)		0.4
"The aim of this study was to investigate the effect of the p15 gene combined with Bcr-abl-specific siRNA and STI571 on the proliferation, cell cycle and apoptosis of K562 chronic myeloid leukemia cells."( Study on the treatment of the p15 gene combined with Bcr-abl-specific siRNA and STI571 for chronic myeloid leukemia.
Du, Y; Li, NN; Lin, GQ; Lv, FF; Wang, W, 2014)		0.4
" In this study, we identified eleven candidate anti-leukemic drugs that might be combined with imatinib, using three approaches: a kinase inhibitor library screen, a gene expression correlation analysis, and literature analysis."( Identification of drug combinations containing imatinib for treatment of BCR-ABL+ leukemias.
Hodges, A; Kang, Y; Ong, E; Paternostro, G; Piermarocchi, C; Roberts, W, 2014)		0.4
" We therefore investigated the antiproliferative effects of nilotinib in combination with drugs that are usually used for conditioning: the alkylating agents mafosfamide, treosulfan, and busulfan."( In vitro testing of drug combinations employing nilotinib and alkylating agents with regard to pretransplant conditioning treatment of advanced-phase chronic myeloid leukemia.
Dreger, P; Fruehauf, S; Ho, AD; Jens Zeller, W; Luft, T; Radujkovic, A; Topaly, J, 2014)		0.4
"Treatment of imatinib-sensitive, BCR-ABL-positive K562 and LAMA84 cells with nilotinib in combination with mafosfamide, treosulfan, or busulfan resulted in synergistic (CI < 1), additive (CI ~ 1), and predominantly antagonistic (CI > 1) effects, respectively."( In vitro testing of drug combinations employing nilotinib and alkylating agents with regard to pretransplant conditioning treatment of advanced-phase chronic myeloid leukemia.
Dreger, P; Fruehauf, S; Ho, AD; Jens Zeller, W; Luft, T; Radujkovic, A; Topaly, J, 2014)		0.4
" Categorization of GIST based on KIT genotype and PI3K/PTEN genomic status combined with dose optimization is suggested for patient selection for clinical trials exploring such combinations."( Phosphoinositide 3-kinase inhibitors combined with imatinib in patient-derived xenograft models of gastrointestinal stromal tumors: rationale and efficacy.
Debiec-Rychter, M; Fletcher, JA; Floris, G; Li, H; Manley, PW; Schöffski, P; Sciot, R; Van Looy, T; Vanleeuw, U; Wellens, J; Wozniak, A, 2014)		0.4
"In this study, we randomly compared high doses of the tyrosine kinase inhibitor imatinib combined with reduced-intensity chemotherapy (arm A) to standard imatinib/hyperCVAD (cyclophosphamide/vincristine/doxorubicin/dexamethasone) therapy (arm B) in 268 adults (median age, 47 years) with Philadelphia chromosome-positive (Ph+) acute lymphoblastic leukemia (ALL)."( Randomized study of reduced-intensity chemotherapy combined with imatinib in adults with Ph-positive acute lymphoblastic leukemia.
Abbal, C; Berthon, C; Cayuela, JM; Chalandon, Y; Chevret, S; Dombret, H; Escoffre-Barbe, M; Hayette, S; Huguet, F; Ifrah, N; Lafage-Pochitaloff, M; Lambert, JF; Leguay, T; Lepretre, S; Lhéritier, V; Maury, S; Raffoux, E; Rousselot, P; Tavernier, E; Thomas, X, 2015)		0.42
" These predictions were in good agreement with clinical single dose drug-drug interaction studies, but not with reports of imatinib interactions at steady-state."( Human hepatocyte assessment of imatinib drug-drug interactions - complexities in clinical translation.
Beumer, JH; Christner, SM; Kiesel, BF; Parise, RA; Pillai, VC; Rudek, MA; Venkataramanan, R, 2015)		0.42
" We examined the effects of the MDM2 inhibitor nutlin3a and its combination with the dual Bcl-2 and Bcl-xL inhibitor ABT-737, and the Bcr-Abl inhibitor nilotinib on BC CML patient samples."( Synergistic effects of p53 activation via MDM2 inhibition in combination with inhibition of Bcl-2 or Bcr-Abl in CD34+ proliferating and quiescent chronic myeloid leukemia blast crisis cells.
Andreeff, M; Carter, BZ; Champlin, RE; Cortes, J; Kantarjian, HM; Konopleva, M; Mak, DH; Mak, PY; McQueen, T; Ruvolo, VR; Schober, W, 2015)		0.42
"To investigate the inductive therapeutic effects of imatinib combined with VP low dose regiment on adult patients with Ph-positive acute lymphoblastic leukemia (Ph(+) ALL)."( [Imatinib Combined with VP Low Dose Regiment for Treating Newly Diagnosed Adult Patients with Ph-positive ALL].
Gao, XN; Guo, YL; Han, XP; Jin, XS; Jing, Y; Liu, K; Yao, ZL; Yu, L; Zhang, R, 2015)		0.42
" Patients could be treated with imatinib combined with chemotherapy for consolidation and maintenance therapy or were treated with allogeneic hematopoietic stem cell transplantation after complete remission."( [Imatinib Combined with VP Low Dose Regiment for Treating Newly Diagnosed Adult Patients with Ph-positive ALL].
Gao, XN; Guo, YL; Han, XP; Jin, XS; Jing, Y; Liu, K; Yao, ZL; Yu, L; Zhang, R, 2015)		0.42
"In the period of tyrosine kinase inhibitor (TKI), inductive chemotherapy combined with imatinib and low dose VP can obtaine satisfactory CR rate and decrease the toxicity of the traditional drugs."( [Imatinib Combined with VP Low Dose Regiment for Treating Newly Diagnosed Adult Patients with Ph-positive ALL].
Gao, XN; Guo, YL; Han, XP; Jin, XS; Jing, Y; Liu, K; Yao, ZL; Yu, L; Zhang, R, 2015)		0.42
" In this study, we investigated the effectiveness of CX and its combination with anticancer agent IM on human colorectal cancer HT-29 cell and their probable molecular targets."( The effect of celecoxib and its combination with imatinib on human HT-29 colorectal cancer cells: Involvement of COX-2, Caspase-3, VEGF and NF-κB genes expression.
Atari-Hajipirloo, S; Heydari, A; Kheradmand, F; Nikanfar, S; Noori, F, 2016)		0.43
"Many patients treated with imatinib, used in cancer treatment, are using several other drugs that could interact with imatinib."( Drug-drug interactions with imatinib: An observational study.
Bondon-Guitton, E; Bourrel, R; Chebane, L; Despas, F; Lapeyre-Mestre, M; Montastruc, JL; Récoché, I; Rousseau, V, 2016)		0.43
"To investigate the efficacy of targeted therapy combined with surgery in the treatment of recurrent and metastatic gastrointestinal stromal tumor(GIST)."( [Efficacy analysis of targeted therapy combined with surgery in the treatment of recurrent and metastatic gastrointestinal stromal tumor].
Fang, Y; Gao, X; Hou, Y; Li, H; Ling, J; Qin, J; Qin, X; Shen, K; Shu, P; Sun, Y; Wang, L; Xue, A, 2016)		0.43
" According to different treatment methods, the patients were divided into four groups: surgery group (operation alone, 44 cases), target therapy group (imatinib alone, 108 cases), target therapy combined with surgery group (imatinib plus operation, 139 cases), other therapy group (chemotherapy, Chinese medicine and others, 27 cases)."( [Efficacy analysis of targeted therapy combined with surgery in the treatment of recurrent and metastatic gastrointestinal stromal tumor].
Fang, Y; Gao, X; Hou, Y; Li, H; Ling, J; Qin, J; Qin, X; Shen, K; Shu, P; Sun, Y; Wang, L; Xue, A, 2016)		0.43
"Target therapy combined with surgery can prolong the survival of recurrent and metastatic GIST patients."( [Efficacy analysis of targeted therapy combined with surgery in the treatment of recurrent and metastatic gastrointestinal stromal tumor].
Fang, Y; Gao, X; Hou, Y; Li, H; Ling, J; Qin, J; Qin, X; Shen, K; Shu, P; Sun, Y; Wang, L; Xue, A, 2016)		0.43
"To explore the effects of homoharringtonine (HHT) alone or combined with imatinib (IM) on K562 cell proliferation and apoptosis, as well as the mRNA and protein expression of BCL6."( [Effects of Homoharringtonine Combined with Imatinib on K562 Cell Apoptosis and BCL6 expression].
Ding, W; Ding, YH; Li, YF; Wang, Q; Wu, JJ, 2016)		0.43
" The effect of drug combination showed that BCL6 protein significantly down-regulated(P<0."( [Effects of Homoharringtonine Combined with Imatinib on K562 Cell Apoptosis and BCL6 expression].
Ding, W; Ding, YH; Li, YF; Wang, Q; Wu, JJ, 2016)		0.43
"To explore the effect of homoharringtonine(HHT) combined with imatinib(IM) on proliferation and apoptosis of K562/G01 cells and its potential mechanism."( [Effect of Homoharringtonine Combined with Imatinib on the K562/G01 Cells and Its Mechanism].
Deng, ZK; Ding, YH; Li, YF; Lu, XY; Shi, YY; Wu, JJ, 2017)		0.46
"HHT combined with IM can synergistically inhibit proliferation and induce apoptosis of K562/G01 cells by suppressing the p210 expression and its kinase activity."( [Effect of Homoharringtonine Combined with Imatinib on the K562/G01 Cells and Its Mechanism].
Deng, ZK; Ding, YH; Li, YF; Lu, XY; Shi, YY; Wu, JJ, 2017)		0.46
" We report the single most extensive analysis of data from China to evaluate the feasibility and safety of the procedure combined with neoadjuvant imatinib therapy to treat patients with rectal GISTs."( A Novel Curative Treatment Strategy for Patients with Lower Grade Rectal Gastrointestinal Stromal Tumor: Chemoreduction Combined with Transanal Endoscopic Microsurgery.
Han, X; Lin, G; Qiu, H; Xu, J, 2017)		0.46
" NVP-BEZ235 in combination with imatinib was also used to reveal the effect on proliferation and apoptosis."( Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with imatinib mesylate against chronic myelogenous leukemia cell lines.
Huang, Y; Li, C; Peng, Q; Xiao, H; Xin, P; Zheng, Y; Zhu, X, 2017)		0.68
" Moreover, imatinib in combination with NVP-BEZ235 induced a more pronounced colony growth inhibition than imatinib alone."( Efficacy of the dual PI3K and mTOR inhibitor NVP-BEZ235 in combination with imatinib mesylate against chronic myelogenous leukemia cell lines.
Huang, Y; Li, C; Peng, Q; Xiao, H; Xin, P; Zheng, Y; Zhu, X, 2017)		0.68
" After demonstrating the safety and feasibility in a phase I study, we conducted a phase II clinical study of CLAG (cladribine, cytarabine, granulocyte colony-stimulating factor) regimen combined with IM for patients with RR-AML."( A Phase II Study of CLAG Regimen Combined With Imatinib Mesylate for Relapsed or Refractory Acute Myeloid Leukemia.
Cubitt, C; Komrokji, RS; Lancet, JE; List, AF; Mirza, AS; Nardelli, L; Padron, E; Pinilla-Ibarz, J; Sweet, K, 2017)		0.71
" Vitamin D compounds have been shown to exert synergistic effects when used in combination with different agents used in anticancer therapies in different cancer models."( Vitamin D derivatives potentiate the anticancer and anti-angiogenic activity of tyrosine kinase inhibitors in combination with cytostatic drugs in an A549 non-small cell lung cancer model.
Filip-Psurska, B; Kutner, A; Maj, E; Milczarek, M; Psurski, M; Wietrzyk, J, 2018)		0.48
"In the present study, we evaluate the in vitro cytotoxicity of fucoxanthin (Fx) on two human leukemia cell lines, K562 and TK6, alone and in combination with the conventional anticancer drugs imatinib (Imat) and doxorubicin (Dox)."( Cytotoxic activity of fucoxanthin, alone and in combination with the cancer drugs imatinib and doxorubicin, in CML cell lines.
Almeida, TP; Azqueta, A; Ferreira, J; Ramos, AA; Rocha, E; Vettorazzi, A, 2018)		0.48
" To investigate the effect and mechanism of PD alone or combined with imatinib (IM) in inhibiting CML imatinib resistant cell line K562/R, the cell proliferation was examined by CCK8 assay to reveal the effect of PD on the inhibitory function of imatinib."( [Inhibitory effect and mechanism of platycodin D combined with imatinib on K562/R].
Dai, Q; Ge, YQ, 2018)		0.48
" In FGF stimulated GIST cell lines, BGJ398, a pan-FGFR kinase inhibitor in combination with imatinib, was cytotoxic and superior to imatinib therapy alone."( A phase Ib study of BGJ398, a pan-FGFR kinase inhibitor in combination with imatinib in patients with advanced gastrointestinal stromal tumor.
Antonescu, CR; Chi, P; D'Angelo, SP; DeMatteo, RP; Dickson, MA; Francis, JH; Gounder, MM; Heinemann, MH; Hwang, S; Kelly, CM; Keohan, ML; Mcfadyen, C; Qin, LX; Shoushtari, AN; Singer, S; Sjoberg, A; Tap, WD, 2019)		0.51
"This Phase 1b, multicentre, open-label study aimed to determine the maximum tolerated dose (MTD) and/or a recommended Phase 2 dose of buparlisib in combination with 400 mg of imatinib through a dose-escalation part and a dose-expansion part, and also evaluated the clinical profile of the combination."( Imatinib in combination with phosphoinositol kinase inhibitor buparlisib in patients with gastrointestinal stromal tumour who failed prior therapy with imatinib and sunitinib: a Phase 1b, multicentre study.
Aimone, P; Benson, C; Brandt, U; Doi, T; Gelderblom, H; George, S; Hertle, S; Jones, RL; Le Cesne, A; Leahy, M; Renouf, DJ; Schӧffski, P; Valverde Morales, C, 2020)		0.56
"Buparlisib in combination with imatinib provided no additional benefit compared with currently available therapies."( Imatinib in combination with phosphoinositol kinase inhibitor buparlisib in patients with gastrointestinal stromal tumour who failed prior therapy with imatinib and sunitinib: a Phase 1b, multicentre study.
Aimone, P; Benson, C; Brandt, U; Doi, T; Gelderblom, H; George, S; Hertle, S; Jones, RL; Le Cesne, A; Leahy, M; Renouf, DJ; Schӧffski, P; Valverde Morales, C, 2020)		0.56
"To investigate the curative efficacy of first generation TKI in the treatment of CML-CP combined with vPh and genetic characteristics."( [Curative Efficacy of First Generation TKI in the Treatment of CML-CP Combined with vPh and Analysis of Its Genetic Characteristics].
Liu, L; Tan, L; Xie, Y; Yang, J, 2020)		0.56
"60 patients with CML-CP combined with vPh from January 2010 to May 2017 in the First Affiliated Hospital of Kunming Medical University were chosen as CML-CP-vPh group, and 107 patients with CML-CP combined with typical Ph chromosome at the same time were chosen as control group."( [Curative Efficacy of First Generation TKI in the Treatment of CML-CP Combined with vPh and Analysis of Its Genetic Characteristics].
Liu, L; Tan, L; Xie, Y; Yang, J, 2020)		0.56
"Patients with CML-CP combined with vPh possess higher primary drug-resistance rate and primary hematological drug-resistance rate for the first generation TKI, while second-generation TKI can efficiently improve long-term survival, its efficacy is similar to efficacy for patients with typical Ph chromosomes."( [Curative Efficacy of First Generation TKI in the Treatment of CML-CP Combined with vPh and Analysis of Its Genetic Characteristics].
Liu, L; Tan, L; Xie, Y; Yang, J, 2020)		0.56
"We treated T-ALL cell lines in vitro and T-ALL patient-derived xenograft (PDX) models in vivo with MRK-560 alone or in combination with other targeted inhibitors (ruxolitinib, imatinib or KPT-8602/eltanexor)."( PSEN1-selective gamma-secretase inhibition in combination with kinase or XPO-1 inhibitors effectively targets T cell acute lymphoblastic leukemia.
Boeckx, N; Cools, J; De Keersmaecker, K; Gielen, O; Govaerts, I; Jacobs, K; Maertens, J; Nittner, D; Prieto, C; Provost, S; Segers, H; Vandersmissen, C, 2021)		0.62
"All NOTCH1-signaling-dependent T-ALL cell lines were sensitive to MRK-560 and its combination with ruxolitinib or imatinib in JAK1- or ABL1-dependent cell lines synergistically inhibited leukemia proliferation."( PSEN1-selective gamma-secretase inhibition in combination with kinase or XPO-1 inhibitors effectively targets T cell acute lymphoblastic leukemia.
Boeckx, N; Cools, J; De Keersmaecker, K; Gielen, O; Govaerts, I; Jacobs, K; Maertens, J; Nittner, D; Prieto, C; Provost, S; Segers, H; Vandersmissen, C, 2021)		0.62
" The aim of this study was to assess the potential P-gp-mediated drug-drug interactions between 11 tyrosine kinase inhibitors (TKIs) with apixaban and rivaroxaban."( Tyrosine kinase inhibitors and direct oral anticoagulants: In vitro evaluation of drug-drug interaction mediated by P-glycoprotein.
Bertoletti, L; Bin, V; Delavenne, X; Hodin, S; Lafaie, L; Saïb, S, 2022)		0.72
" This study investigated the safety, tolerability and efficacy of alpelisib, a phosphatidylinositol 3-kinase inhibitor, used in combination with imatinib in patients with advanced GIST who had failed prior therapy with both imatinib and sunitinib."( A multicenter, dose-finding, phase 1b study of imatinib in combination with alpelisib as third-line treatment in patients with advanced gastrointestinal stromal tumor.
Bauer, S; Berhanu, G; Brandt, U; Gelderblom, H; Grignani, G; Heinrich, MC; Italiano, A; Pantaleo, MA; Reichardt, P; Reyners, AKL; Schöffski, P; Stark, D; Stefanelli, T; Valverde, C, 2022)		0.72
" These were combined with 400 mg QD imatinib until maximum tolerated dose (MTD) and/or a recommended phase 2 dose (RP2D) of alpelisib in combination with imatinib was determined."( A multicenter, dose-finding, phase 1b study of imatinib in combination with alpelisib as third-line treatment in patients with advanced gastrointestinal stromal tumor.
Bauer, S; Berhanu, G; Brandt, U; Gelderblom, H; Grignani, G; Heinrich, MC; Italiano, A; Pantaleo, MA; Reichardt, P; Reyners, AKL; Schöffski, P; Stark, D; Stefanelli, T; Valverde, C, 2022)		0.72
" The MTD of alpelisib given with imatinib was determined as 350 mg QD."( A multicenter, dose-finding, phase 1b study of imatinib in combination with alpelisib as third-line treatment in patients with advanced gastrointestinal stromal tumor.
Bauer, S; Berhanu, G; Brandt, U; Gelderblom, H; Grignani, G; Heinrich, MC; Italiano, A; Pantaleo, MA; Reichardt, P; Reyners, AKL; Schöffski, P; Stark, D; Stefanelli, T; Valverde, C, 2022)		0.72
"The MTD of alpelisib was estimated as 350 mg QD when used in combination with imatinib 400 mg QD after oral administration in patients with advanced GIST."( A multicenter, dose-finding, phase 1b study of imatinib in combination with alpelisib as third-line treatment in patients with advanced gastrointestinal stromal tumor.
Bauer, S; Berhanu, G; Brandt, U; Gelderblom, H; Grignani, G; Heinrich, MC; Italiano, A; Pantaleo, MA; Reichardt, P; Reyners, AKL; Schöffski, P; Stark, D; Stefanelli, T; Valverde, C, 2022)		0.72
"The study intended to explore the effects and molecular mechanisms of imatinib combined with everolimus on AtT-20 cells in AtT-20 mouse pituitary tumors."( Effects of Imatinib Combined With Everolimus on Mouse Pituitary Tumor Cell AtT-20.
Lin, Y; Meng, L; Qu, X; Wang, W; Yang, J, 2023)		0.91
"Imatinib combined with everolimus can affect the AtT-20 cell cycle through the signaling pathway of the phosphatidylin-ositol-3-kinase (PI3K)/Akt/ protein kinase A (PKA) system and can inhibit cell proliferation and induce cell apoptosis."( Effects of Imatinib Combined With Everolimus on Mouse Pituitary Tumor Cell AtT-20.
Lin, Y; Meng, L; Qu, X; Wang, W; Yang, J, 2023)		0.91
" Here, we show that ISR inhibition combined with imatinib treatment sensitized and more effectively eradicated leukemic cells both in vitro and in vivo compared to treatment with single agents."( Targeting integrated stress response with ISRIB combined with imatinib treatment attenuates RAS/RAF/MAPK and STAT5 signaling and eradicates chronic myeloid leukemia cells.
Brewinska-Olchowik, M; Dudka, W; Hoser, G; Klejman, A; Kominek, A; Kusio-Kobialka, M; Machnicki, MM; Mondal, SS; Piwocka, K; Seferynska, I; Stoklosa, T; Swatler, J; Turos-Korgul, L; Wiech, M; Wołczyk, M, 2022)		0.72
" The impact of drug-drug interaction (DDI) also differs between drugs with low or high oral bioavailability."( Considering the Oral Bioavailability of Protein Kinase Inhibitors: Essential in Assessing the Extent of Drug-Drug Interaction and Improving Clinical Practice.
Chatelut, E; Le Louedec, F; Puisset, F; Tod, M, 2023)		0.91
"The introduction of protein kinase inhibitors (PKIs) for chronic myeloid leukaemia (CML) has considerably improved prognosis of the disease but has also demonstrated a great potential for drug-drug interactions."( Drug-drug interactions of protein kinase inhibitors in chronic myeloid leukaemia patients: A study using the French health insurance database.
Despas, F; Lapeyre-Mestre, M; Pajiep, M, 2023)		0.91
"Chronic oral anticancer therapies, are increasingly prescribed and present new challenges including the enhanced risk of overlooked drug-drug interactions (DDIs)."( The use of therapeutic drug monitoring to highlight an over-looked drug-drug interaction leading to imatinib treatment failure.
Buonadonna, A; Canil, G; Cecchin, E; Dalle Fratte, C; Gagno, S; Guardascione, M; Orleni, M; Posocco, B; Roncato, R; Toffoli, G; Zanchetta, M, 2023)		0.91
" Drug-drug interactions were evaluated though Lexicomp."( The use of therapeutic drug monitoring to highlight an over-looked drug-drug interaction leading to imatinib treatment failure.
Buonadonna, A; Canil, G; Cecchin, E; Dalle Fratte, C; Gagno, S; Guardascione, M; Orleni, M; Posocco, B; Roncato, R; Toffoli, G; Zanchetta, M, 2023)		0.91
"Tyrosine kinase inhibitors combined with conventional chemotherapy (CC) in treating Philadelphia chromosome-positive acute lymphoblastic leukemia (Ph-positive ALL) has achieved promising efficacy and safety outcomes."( Cost-effectiveness analysis of imatinib versus dasatinib in the treatment of pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia when combined with conventional chemotherapy in China.
Chen, M; Lin, Y; Liu, L; Lu, X; Ni, J; Yang, H; Zhang, L, 2023)		0.91
"A Markov model was established to simulate a hypothetical cohort of pediatric Ph-positive ALL patients receiving imatinib or dasatinib, combined with CC."( Cost-effectiveness analysis of imatinib versus dasatinib in the treatment of pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia when combined with conventional chemotherapy in China.
Chen, M; Lin, Y; Liu, L; Lu, X; Ni, J; Yang, H; Zhang, L, 2023)		0.91
" The probabilistic sensitivity analysis indicated that treatment with dasatinib combined with CC achieved a 96."( Cost-effectiveness analysis of imatinib versus dasatinib in the treatment of pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia when combined with conventional chemotherapy in China.
Chen, M; Lin, Y; Liu, L; Lu, X; Ni, J; Yang, H; Zhang, L, 2023)		0.91
"Dasatinib combined with CC is likely to be a cost-effective strategy compared to imatinib combination therapy for pediatric Ph-positive ALL in China at a WTP threshold of $37,765/QALY."( Cost-effectiveness analysis of imatinib versus dasatinib in the treatment of pediatric Philadelphia chromosome-positive acute lymphoblastic leukemia when combined with conventional chemotherapy in China.
Chen, M; Lin, Y; Liu, L; Lu, X; Ni, J; Yang, H; Zhang, L, 2023)		0.91

Bioavailability

Imatinib mesylate (IMS) is an anti-cancer drug. Its bioavailability is more than 97%. The exact gastrointestinal site of its absorption is unknown.

ExcerptReferenceRelevance
" STI 571 is highly bioavailable in oral form and produced minimal toxicities in phase I studies."( Tyrosine kinase inhibitors: a cure for chronic myeloid leukemia?
Zitella, L, )		0.13
"Imatinib (Gleevec) (formerly STI571) is an orally bioavailable rationally developed inhibitor of the tyrosine kinases Bcr-Abl, Kit, and platelet-derived growth factor receptor (PDGFR)."( Imatinib: a targeted clinical drug development.
Capdeville, R; Silberman, S, 2003)		0.32
"The purpose of this study was to investigate the absolute bioavailability of a single oral dose of imatinib (Glivec), 400 mg (capsules vs."( Absolute bioavailability of imatinib (Glivec) orally versus intravenous infusion.
Ben-Am, M; Capdeville, R; Dutreix, C; Hayes, MJ; Lloyd, P; Mehring, G; Peng, B; Pokorny, R; Seiberling, M, 2004)		0.32
" BMS-354825 is an orally bioavailable ABL kinase inhibitor with two-log increased potency relative to imatinib that retains activity against 14 of 15 imatinib-resistant BCR-ABL mutants."( Overriding imatinib resistance with a novel ABL kinase inhibitor.
Chen, P; Lee, FY; Norris, D; Sawyers, CL; Shah, NP; Tran, C, 2004)		0.32
" Finally, alterations of drug transporters or drug-metabolizing pathways may block the bioavailability of the tyrosine kinase inhibitors (drug-dependent resistance)."( Mechanisms of clinical resistance to small molecule tyrosine kinase inhibitors targeting oncogenic tyrosine kinases.
Aulitzky, WE; Oetzel, C; Schwab, M; van der Kuip, H; Wohlbold, L, 2005)		0.33
" Both ABCG2 and ABCB1 are normally expressed in the gastrointestinal tract and it might be anticipated that drug-induced upregulation of these intestinal pumps could reduce the oral bioavailability of imatinib, representing a novel mechanism of acquired pharmacokinetic drug resistance in cancer patients that are chronically treated with imatinib."( Chronic imatinib mesylate exposure leads to reduced intracellular drug accumulation by induction of the ABCG2 (BCRP) and ABCB1 (MDR1) drug transport pumps.
Brok, M; Burger, H; de Boeck, G; de Bruijn, EA; Guetens, G; Nooter, K; Sparreboom, A; van Tol, H; Verweij, J; Wiemer, EA, 2005)		0.76
" AMN107 is a novel, orally bioavailable ATP-competitive inhibitor of Bcr-Abl."( AMN107, a novel aminopyrimidine inhibitor of Bcr-Abl, has in vitro activity against imatinib-resistant chronic myeloid leukemia.
Alland, L; Arlinghaus, RB; Beran, M; Cortes, J; Dugan, M; Giles, F; Golemovic, M; Griffin, JD; Kantarjian, H; Manley, PW; Manshouri, T; Mestan, J; Sun, T; Verstovsek, S, 2005)		0.33
" Pharmacokinetic studies of imatinib in healthy volunteers and patients with CML, GIST and other cancers show that orally administered imatinib is well absorbed, and has an absolute bioavailability of 98% irrespective of oral dosage form (solution, capsule, tablet) or dosage strength (100 mg, 400 mg)."( Clinical pharmacokinetics of imatinib.
Lloyd, P; Peng, B; Schran, H, 2005)		0.33
" Dasatinib (BMS-354825) is a novel orally bioavailable SRC/ABL inhibitor that has activity against multiple imatinib-resistant BCR-ABL isoforms in vitro that is presently showing considerable promise in early-phase clinical trials of chronic myeloid leukemia (CML)."( Dasatinib (BMS-354825) inhibits KITD816V, an imatinib-resistant activating mutation that triggers neoplastic growth in most patients with systemic mastocytosis.
Akin, C; Donker, M; Jiang, Y; Lee, FY; Luo, R; Shah, NP, 2006)		0.33
" BMS-354825 is an orally bioavailable dual Src/Bcr-Abl tyrosine kinase inhibitor currently undergoing clinical trials in cancer patients."( Potent inhibition of platelet-derived growth factor-induced responses in vascular smooth muscle cells by BMS-354825 (dasatinib).
Bhalla, KN; Chen, Z; Lee, FY; Wu, J, 2006)		0.33
" An extensive search for molecules to block the aberrant BCR-ABL1 protein resulted in the development of IM as an orally bioavailable agent with remarkable efficacy in producing hematologic, cytogenetic, and molecular remissions."( Imatinib resistance: obstacles and opportunities.
Litzow, MR, 2006)		0.33
" Although the bioavailability of imatinib mesylate is more than 97%, the exact gastrointestinal site of its absorption is unknown."( Disposition of imatinib and its metabolite CGP74588 in a patient with chronic myelogenous leukemia and short-bowel syndrome.
Beumer, JH; Egorin, MJ; Lagattuta, TF; Natale, JJ; Raptis, A, 2006)		0.62
" When ciclosporin (10 mg kg(-1)) was orally administered, the time course, area under the curve, bioavailability and peak blood concentration of ciclosporin were significantly increased in rats that had been treated with imatinib mesilate 2 h before ciclosporin administration as compared with the control."( Effect of imatinib mesilate on the disposition kinetics of ciclosporin in rats.
Fujii, Y; Higashi, Y; Imamura, M; Kajita, T; Maida, C; Miyamoto, E; Yamamoto, I, 2006)		0.33
" This agent is also orally bioavailable and has been found to be effective in clinical trials."( Mechanisms of resistance to imatinib in CML patients: a paradigm for the advantages and pitfalls of molecularly targeted therapy.
Nichols, G; Ritchie, E, 2006)		0.33
" This orally bioavailable drug has a low toxicity profile."( [STI571: a summary of targeted therapy].
Czyz, M; Jakubowska, J, 2006)		0.33
"Lonafarnib is an orally bioavailable nonpetidomimetic farnesyl transferase inhibitor with significant activity against BCR-ABL-positive cell lines and primary human chronic myeloid leukemia (CML) cells."( Phase 1 study of lonafarnib (SCH 66336) and imatinib mesylate in patients with chronic myeloid leukemia who have failed prior single-agent therapy with imatinib.
Cortes, J; Daley, GQ; Ferrajoli, A; Jabbour, E; Kantarjian, H; Koller, C; O'Brien, S; Statkevich, P; Verstovsek, S; Zhu, Y, 2007)		0.6
"The tolerability and efficacy of the combination of tipifarnib, an orally bioavailable nonpeptidomimetic farnesyl transferase inhibitor, and imatinib was investigated in patients with chronic myelogenous leukemia in chronic phase who had failed imatinib."( Phase 1 study of tipifarnib in combination with imatinib for patients with chronic myelogenous leukemia in chronic phase after imatinib failure.
Cortes, J; Ebarb, T; Faderl, S; Garcia-Manero, G; Giles, F; Jones, D; Kantarjian, H; O'Brien, S; Quintás-Cardama, A; Thomas, D, 2007)		0.34
" In this study, we show that carboxyamidotriazole (CAI), an orally bioavailable calcium influx and signal transduction inhibitor, is equally effective in inhibiting the proliferation and bcr-abl dependent- and independent-signaling pathways in imatinib-resistant CML cells."( Effects of carboxyamidotriazole on in vitro models of imatinib-resistant chronic myeloid leukemia.
Alessandro, R; Colomba, P; Corrado, C; De Leo, G; Flugy, AM; Fontana, S; Giordano, M; Kohn, EC; Santoro, A, 2008)		0.35
" More recently, attention has turned to the relative roles of drug bioavailability and drug efflux and drug influx proteins in the development of resistance to imatinib."( Part I: mechanisms of resistance to imatinib in chronic myeloid leukaemia.
Apperley, JF, 2007)		0.34
" A population analysis done in NONMEM with a time-dependent covariate confirmed that ritonavir did not influence the clearance or bioavailability of imatinib."( Influence of CYP3A4 inhibition on the steady-state pharmacokinetics of imatinib.
Baker, SD; Gelderblom, H; Guchelaar, HJ; Karlsson, MO; Li, J; Nortier, JW; Ouwerkerk, J; Sparreboom, A; van Erp, NP; Zhao, M, 2007)		0.34
"Besides affecting the systemic bioavailability of the parent drug, drug metabolizing enzymes (DMEs) may produce bioactive and/or toxic metabolites of clinical interest."( Imatinib metabolite profiling in parallel to imatinib quantification in plasma of treated patients using liquid chromatography-mass spectrometry.
Biollaz, J; Décosterd, LA; Fayet, A; Lahrichi, SL; Pesse, B; Rochat, B; Widmer, N, 2008)		0.35
" bioavailability and brain penetration of chemotherapy drugs in animal models, we sought to examine the effect of sunitinib on the ATP-binding cassette (ABC) drug transporters P-glycoprotein (P-gp, ABCB1), the multidrug resistance-associated protein 1 (ABCC1), and ABCG2, which are known to transport a wide variety of anticancer drugs."( Sunitinib (Sutent, SU11248), a small-molecule receptor tyrosine kinase inhibitor, blocks function of the ATP-binding cassette (ABC) transporters P-glycoprotein (ABCB1) and ABCG2.
Ambudkar, SV; Bates, SE; Robey, RW; Shukla, S, 2009)		0.35
" As a complementary approach, cell-based, target-driven secondary screens may help predict in vivo compound potency and specificity as well as evaluate bioavailability and toxicity."( Cell treatment and lysis in 96-well filter-bottom plates for screening Bcr-Abl activity and inhibition in whole-cell extracts.
Kron, SJ; Mand, MR; Veach, DR; Wu, D, 2010)		0.36
" Ketoconazole and primaquine affect imatinib clearance, bioavailability and distribution pattern, which could improve the treatment of renal and brain tumors, but also increase toxicity."( Differential effects of ketoconazole and primaquine on the pharmacokinetics and tissue distribution of imatinib in mice.
Bukhari, NI; Chay, G; Kan, E; Law, JH; Lim, WY; Segarra, I; Soo, GW; Tan, SY, 2010)		0.36
" Major gastrectomy decreased the bioavailability of nilotinib and, in some patients, lowered its clinical activity."( Nilotinib in patients with GIST who failed imatinib and sunitinib: importance of prior surgery on drug bioavailability.
Beck, MY; Chang, HM; Choi, DR; Kang, YK; Kim, KP; Kim, TW; Lee, JL; Ryoo, BY; Ryu, MH; Yoo, C, 2011)		0.37
"The bioavailability of orally administered imatinib is >90%, although the drug is monocationic under the acidic conditions in the duodenum."( Environmental and genetic factors affecting transport of imatinib by OATP1A2.
Boere, I; Eechoute, K; Franke, RM; Gurney, H; Kim, RB; Loos, WJ; Mathijssen, RH; Scherkenbach, LA; Sparreboom, A; Tirona, RG; Verweij, J, 2011)		0.37
" The bioavailability of intraperitoneally administered imatinib-ULS-lysozyme was 100%."( Imatinib-ULS-lysozyme: a proximal tubular cell-targeted conjugate of imatinib for the treatment of renal diseases.
Dolman, ME; Hennink, WE; Kok, RJ; Lacombe, M; Pato, J; Pieters, EH; Storm, G; van Dorenmalen, KM, 2012)		0.38
" In conclusion, saquinavir and imatinib are both drugs utilized for long-term therapies, with good oral bioavailability and a well-known toxicity profile."( In vitro anti-neuroblastoma activity of saquinavir and its association with imatinib.
Cordero di Montezemolo, L; Crescenzio, N; Doria, A; Fagioli, F; Foglia, L; Pagliano, S; Ricotti, E; Timeus, F; Tovo, PA, 2012)		0.38
" Carboxyamidotriazole-orotate (CTO) is the orotate salt form of carboxyamidotriazole (CAI), an orally bioavailable signal transduction inhibitor that in vitro has been shown to possess antileukaemic activities."( Carboxyamidotriazole-orotate inhibits the growth of imatinib-resistant chronic myeloid leukaemia cells and modulates exosomes-stimulated angiogenesis.
Alessandro, R; Corrado, C; De Leo, G; Flugy, AM; Guggino, G; Karmali, R; Raimondo, S; Taverna, S, 2012)		0.38
" Herein, we report GZD824 (10a) as a novel orally bioavailable inhibitor against a broad spectrum of Bcr-Abl mutants including T315I."( Identification of GZD824 as an orally bioavailable inhibitor that targets phosphorylated and nonphosphorylated breakpoint cluster region-Abelson (Bcr-Abl) kinase and overcomes clinically acquired mutation-induced resistance against imatinib.
Bai, Y; Ding, K; Feng, Y; Lang, X; Leng, F; Li, Y; Liu, J; Long, H; Lu, X; Luo, J; Pan, J; Pan, X; Ren, X; She, M; Tu, Z; Wang, D; Wen, D; Zhang, F; Zhang, Z; Zhuang, X, 2013)		0.39
"Given that the validated method has proved to be linear, accurate, precise, and robust, it is suitable for pharmacokinetic assays, such as bioavailability and bioequivalence, and is being successfully applied in routine therapeutic drug monitoring in the hospital service."( Quantification of imatinib in human serum: validation of a high-performance liquid chromatography-mass spectrometry method for therapeutic drug monitoring and pharmacokinetic assays.
Bendit, I; de Alencar Fisher Chamone, D; Novaes, MM; Rezende, VM; Rivellis, A, 2013)		0.39
" The results show that the good bioavailability of imatinib is highly likely achieved by its active absorption from the intestine and that its active elimination through the intestinal mucosa is mediated by a synergistic activity of organic cation transporter 1 in the basolateral membrane and the added activity of two efflux proteins (P-glycoprotein and breast cancer resistant protein) in the apical membrane of enterocytes of the rat ileum."( Absorption and elimination of imatinib through the rat intestine in vitro.
Cernelč, P; Kralj, E; Kristl, A; Roškar, R; Trontelj, J; Zakelj, S, 2014)		0.4
" Indeed, the Supreme Court stated that even if the bioavailability of the drug was improved, it did not demonstrate enhanced efficacy and that Glivec was not patentable."( "To patent or not to patent? the case of Novartis' cancer drug Glivec in India".
Gabble, R; Kohler, JC, 2014)		0.4
" We have examined the biological effects of a highly selective, orally bioavailable JAK2 inhibitor, BMS-911543, in combination with TKIs on CD34+ treatment-naïve IM-nonresponder cells."( Selective JAK2/ABL dual inhibition therapy effectively eliminates TKI-insensitive CML stem/progenitor cells.
Chen, M; Jiang, X; Lin, H; Lorenzi, MV; Rothe, K; Woolfson, A, 2014)		0.4
" ABCB1 single nucleotide polymorphisms (SNPs) have been reported as modulators of ABCB1-mediated transport, affecting IM's bioavailability and consequently the treatment outcome of IM therapy."( ABCB1 haplotypes but not individual SNPs predict for optimal response/failure in Egyptian patients with chronic-phase chronic myeloid leukemia receiving imatinib mesylate.
Ali, MA; Elsalakawy, WA, 2014)		0.6
"The aim of the study was to investigate the bioavailability of a generic product of 100 mg and 400 mg imatinib film-coated tablets (test) as compared to that of a branded product (reference) at the same strength to determine bioequivalence."( Bioequivalence study of 400 and 100 mg imatinib film-coated tablets in healthy volunteers.
Boguradzki, P; Mikołajczak, PL; Ostrowicz, A; Wierzbicka, M, )		0.13
" IMT-NLC displayed sustained IMT release in vitro, significantly enhanced in vivo bioavailability of IMT after intravenous and oral administration, and greater in vitro cytotoxicity on NCI-H727 cells, compared with free IMT."( Modulation of Pharmacokinetic and Cytotoxicity Profile of Imatinib Base by Employing Optimized Nanostructured Lipid Carriers.
Cho, HJ; Choi, HG; Gupta, B; Jeong, JH; Kim, JO; Poudel, BK; Pradhan, R; Shin, BS; Tran, TH; Yong, CS, 2015)		0.42
" Doubts on the bioequivalence and bioavailability of emerging generic compounds have been expressed."( Comparison of Branded and Generic Imatinib Plasma Concentrations in Patients With Chronic Myelogenous Leukemia: Unicentric Study.
Basic-Kinda, S; Granic, P; Matic, N; Nemet, D; Ostojic, A; Peric, Z; Radman, I; Roncevic, P; Sertic, D; Serventi-Seiwerth, R; Zadro, R, 2016)		0.43
" However, a minority of patients fail to achieve optimal response due to impaired bioavailability of IM."( hOCT1 gene expression predict for optimal response to Imatinib in Tunisian patients with chronic myeloid leukemia.
Abbes, S; Amouri, H; Bellaaj, H; Ben Hadj Othman, H; Ben Hassine, I; Farrah, A; Gharbi, H; Lakhal, RB; Menif, S; Romdhane, NB; Soltani, I; Teber, M, 2017)		0.46
" Whole blood count, ethnicity, CYP3A5*3, and ABCB1 C3435T were found to have significant influence on the apparent clearance, while the interindividual variability in clearance and interoccasion variability in bioavailability were 17."( Population Pharmacokinetics of Imatinib in Nigerians With Chronic Myeloid Leukemia: Clinical Implications for Dosing and Resistance.
Adeagbo, BA; Bolaji, OO; Bolarinwa, RA; Durosinmi, MA; Ogungbenro, K; Olugbade, TA, 2017)		0.46
" Results from permeability studies evidenced that SYA did not impact Imatinib's permeability across membranes while suggesting improved bioavailability through higher kinetic solubility at the biological barriers."( Bioinspired co-crystals of Imatinib providing enhanced kinetic solubility.
Dix, I; Galli, B; Gutmann, M; Harlacher, C; Holzgrabe, U; Meinel, L; Müller-Buschbaum, K; Piechon, P; Reggane, M; Saedtler, M; Wiest, J; Zottnick, SH, 2018)		0.48
"32-fold, and the bioavailability was greatly decreased about 30."( Effects of aprepitant on the pharmacokinetics of imatinib and its main metabolite in rats.
Darbalaei, S; Han, X; Lu, Y; Qin, Y; Rang, Y; Wang, N; Zhai, X; Zhang, X, 2018)		0.48
"Marked inter-species variability in PK parameters and resulting oral bioavailability was observed."( Preclinical pharmacokinetic evaluation to facilitate repurposing of tyrosine kinase inhibitors nilotinib and imatinib as antiviral agents.
Ananthula, HK; Buller, RM; Damon, IK; Desai, PB; Gallardo-Romero, N; Kalman, D; Moir-Savitz, T; Olson, V; Parker, S; Patel, G; Sallans, L; Salzer, JS; Sherwin, CM; Touchette, E; Werner, MH, 2018)		0.48
" N-oleoyl-D-galactosamine was synthesized for fabricating biomimetic galactose-modified nanoparticles (GNPs) in an attempt to improve the oral bioavailability of IMT."( Oral delivery of imatinib through galactosylated polymeric nanoparticles to explore the contribution of a saccharide ligand to absorption.
Li, Y; Yang, B; Zhang, X, 2019)		0.51
"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
"Here we describe the development and validation of an LC-MS/MS method for the quantification of imatinib and imatinib-d8 in plasma for the support of a clinical absolute bioavailability microdosing trial."( Development and validation of an LC-MS/MS method for the quantification of imatinib and imatinib-d8 in human plasma for the support of an absolute bioavailability microdose trial.
Beijnen, JH; Lucas, L; Roosendaal, J; Rosing, H; Venekamp, N, 2020)		0.56
"The aim of this study was to ascertain whether the absolute bioavailability of oral imatinib (Glivec®) during steady state plasma pharmacokinetics in cancer patients could be determined through a concomitant intravenous administration of a single 100 μg microdose of deuterium labeled imatinib (imatinib-d8)."( Determination of the absolute bioavailability of oral imatinib using a stable isotopically labeled intravenous imatinib-d8 microdose.
Beijnen, JH; Groenland, SL; Huitema, ADR; Lucas, L; Nuijen, B; Roosendaal, J; Rosing, H; Steeghs, N; Venekamp, N, 2020)		0.56
" The absolute bioavailability was calculated by comparing the dose-normalized exposure with unlabeled and stable isotopically labeled imatinib in plasma."( Determination of the absolute bioavailability of oral imatinib using a stable isotopically labeled intravenous imatinib-d8 microdose.
Beijnen, JH; Groenland, SL; Huitema, ADR; Lucas, L; Nuijen, B; Roosendaal, J; Rosing, H; Steeghs, N; Venekamp, N, 2020)		0.56
" The median absolute bioavailability of oral imatinib at steady state was 76% (range 44-106%)."( Determination of the absolute bioavailability of oral imatinib using a stable isotopically labeled intravenous imatinib-d8 microdose.
Beijnen, JH; Groenland, SL; Huitema, ADR; Lucas, L; Nuijen, B; Roosendaal, J; Rosing, H; Steeghs, N; Venekamp, N, 2020)		0.56
"The absolute bioavailability of imatinib was successfully estimated at steady state plasma pharmacokinetics using the stable isotopically labeled microdose trial design."( Determination of the absolute bioavailability of oral imatinib using a stable isotopically labeled intravenous imatinib-d8 microdose.
Beijnen, JH; Groenland, SL; Huitema, ADR; Lucas, L; Nuijen, B; Roosendaal, J; Rosing, H; Steeghs, N; Venekamp, N, 2020)		0.56
" Previous reports have ascertained the antiproliferative activity of imatinib mesylate (IMS) against diverse types of carcinomas, but limited bioavailability has also been reported."( Fabrication of Imatinib Mesylate-Loaded Lactoferrin-Modified PEGylated Liquid Crystalline Nanoparticles for Mitochondrial-Dependent Apoptosis in Hepatocellular Carcinoma.
Guleria, A; Kumar, P; Kumar, U; Maurya, P; Mishra, N; Nisha, R; Saha, S; Saraf, SA; Singh, P; Singh, S, 2021)		1.21
" However, the drug has severe side effects, poor brain bioavailability which may hinder effective treatment of Alzheimer's disease."( Development of Imatinib Mesylate-Loaded Liposomes for Nose to Brain Delivery: In Vitro and In Vivo Evaluation.
Chella, N; Khan, W; Saka, R, 2021)		0.97
" According to the results of these theoretical studies, it can be said that the bioavailability and bioactivity of these compounds may be high."( Synthesis and biological evaluation of thiosemicarbazone derivatives.
Budak, Y; Ceylan, M; Doğan, M; Gürdere, MB; Koçyiğit, ÜM, 2022)		0.72
" However, their oral bioavailability differs."( Considering the Oral Bioavailability of Protein Kinase Inhibitors: Essential in Assessing the Extent of Drug-Drug Interaction and Improving Clinical Practice.
Chatelut, E; Le Louedec, F; Puisset, F; Tod, M, 2023)		0.91

Dosage Studied

Two patients with stage 5 chronic kidney disease and NSF were treated with oral imatinib mesylate at a dosage of 400 mg/day. Skin biopsies performed both before and after initial dosing of that patient revealed less fibrosis and less staining for type I procollagen.

ExcerptRelevanceReference
"We present here provisional indications for the use of imatinib in CML patients and give details of the dosage regimens we have used and side-effects we have encountered."( The use of imatinib (STI571) in chronic myelod leukemia: some practical considerations.
Apperley, JF; Armstrong, L; Bua, M; Goldman, JM; Marin, D; Marktel, S; Olavarria, E, 2002)		0.31
" Serious adverse effects requiring dosage decreases and/or therapy termination are edema, hepatotoxicity, and hematologic toxicity."( Imatinib mesylate, the first molecularly targeted gene suppressor.
Pindolia, VK; Zarowitz, BJ, 2002)		1.76
" We present a CML patient in megakaryoblastic crisis with severe myelofibrosis, who was treated with imatinib at a dosage of 400 mg/day and achieved complete remission together with a marked regression of myelofibrosis after 1 month."( Successful treatment with imatinib mesylate of a CML patient in megakaryoblastic crisis with severe fibrosis.
Hirose, Y; Ito, M; Iwai, M; Kiyoi, H; Naoe, T; Yokozawa, T, 2002)		0.61
" These cells displayed high levels of immunoreactivity with pSTAT5 probes that could be inhibited uniformly with imatinib mesylate in a dose-response and time-dependent manner."( Immunoreactivity of Stat5 phosphorylated on tyrosine as a cell-based measure of Bcr/Abl kinase activity.
Frisa, PS; Goolsby, CL; Gottlieb, MA; Hedley, DW; Jacobberger, JW; Paniagua, M; Shankey, TV; Smith, BL; Sramkoski, RM; Ye, PP, 2003)		0.53
" Ph(+)-ANLL patients were infused with HHT over 6-24 hours daily at the doses of 1-2 mg intravenously and Ara-C 30-50 mg daily subcutaneously for 10-14 days; 3 patients with Ph(+)-ALL received HOAP or DOP combination treatment regimens (One cycle consists of HA with the same dosage described above for Ph(+)-ANLL patients for 7 days, daunorubicin at the dose of 40 mg/d intravenously for 3 days, vincristine at the dose of 2 mg/wk for two weeks, and prednisone at the doses of 60-80 mg/d for 14 days)."( [Glivec in combination with HA regimen for treatment of 20 patients with Ph chromosome positive acute leukemia].
Huang, F; Liu, XL; Meng, FY; Song, LL; Xu, B; Zhang, Y; Zheng, WY, 2003)		0.32
" Treatment was interrupted or dosage reduced in a few patients."( [Relationship between cytopenia and cytogenetic response in imatinib mesylate treated Ph-positive chronic myeloid leukemia in chronic phase patients].
Chen, S; Huang, X; Jiang, B; Jiang, H; Jiang, Q; Lu, D; Lu, Y, 2003)		0.56
" Complete hematologic, cytogenetic and molecular responses were attained 5 weeks after readministration of regularly dosed imatinib and two-step nested RT-PCR confirmed molecular remission throughout a 6 month follow-up period."( Durable molecular response to imatinib mesylate following nonmyeloablative allogeneic stem-cell transplantation for persisting myeloid blast crisis in chronic myeloid leukemia.
Brezinschek, R; Linkesch, W; Neumeister, P; Sill, H; Staber, PB, 2003)		0.61
" The dosage of imatinib is 400 mg/day for CP patients and 600 mg/day for AP and BC patients."( [The early efficacy of imatinib in the treatment of 54 cases of chronic myeloid leukemia].
Lou, FD; Lu, XC, 2003)		0.32
" In patients with CML in blastic phase, AGP levels could reflect pharmacological resistance to imatinib, suggesting that increased dosage of imatinib or the use of a competitor to drug binding should be recommended to optimize the therapeutic effect of the drug."( Relationship between elevated levels of the alpha 1 acid glycoprotein in chronic myelogenous leukemia in blast crisis and pharmacological resistance to imatinib (Gleevec) in vitro and in vivo.
Bastie, JN; Berthaud, P; Calvo, F; Chomienne, C; Degos, L; Larghero, J; Leguay, T; Madelaine-Chambrin, I; Mahon, FX; Marolleau, JP; Mourah, S; Raffoux, E; Rousselot, P; Taksin, AL, 2003)		0.32
" Imatinib pharmacokinetics were determined up to 96 h after dosing on day 1 (no induction) and on days 15-18 (during concomitant rifampicin)."( Effect of rifampicin on the pharmacokinetics of imatinib mesylate (Gleevec, STI571) in healthy subjects.
Bolton, AE; Capdeville, R; Hubert, M; Keller, U; Krebs-Brown, A; Peng, B; Seiberling, M, 2004)		0.58
"Once-weekly administration of imatinib allowed imatinib therapy to continue, and this dosing schedule appeared safe."( Overcoming recurrent cutaneous reactions from imatinib using once-weekly dosing.
Nand, S; Tanvetyanon, T, 2003)		0.32
"In a patient with recurrent cutaneous reactions due to imatinib, a once-weekly dosing schedule was safe, well tolerated, and associated with eventual disappearance of the reaction."( Overcoming recurrent cutaneous reactions from imatinib using once-weekly dosing.
Nand, S; Tanvetyanon, T, 2003)		0.32
" The recommended daily dosage of 400-600 mg requires simultaneous intake of up to six of the current 100-mg capsules."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
" These events showed no clustering by type of dosage form and were of little to no clinical significance."( Bioequivalence, safety, and tolerability of imatinib tablets compared with capsules.
Capdeville, R; Ho, YY; Hubert, M; Keller, U; Nikolova, Z; Peng, B; Schran, H; Sieberling, M, 2004)		0.32
" To prevent resistance, early diagnosis and prompt treatment with appropriate initial dosing is essential."( Imatinib therapy in chronic myelogenous leukemia: strategies to avoid and overcome resistance.
Hochhaus, A; La Rosée, P, 2004)		0.32
" A maximum tolerated dosage was not defined."( Imatinib mesylate (STI571) for treatment of children with Philadelphia chromosome-positive leukemia: results from a Children's Oncology Group phase 1 study.
Bernstein, M; Blaney, SM; Capdeville, R; Champagne, MA; Krailo, M; Peng, B; Qu, W; Rosamilia, M; Therrien, M; Zoellner, U, 2004)		1.77
"Studies with imatinib are underway in pediatrics, but whether pediatric dosing schemes will lead to outcomes similar to adults is unknown."( Treatment of CML in pediatric patients: should imatinib mesylate (STI-571, Gleevec) or allogeneic hematopoietic cell transplant be front-line therapy?
Pulsipher, MA, 2004)		0.58
" Maintaining dosing of imatinib in the face of isolated sites of disease progression is also important, as other metastatic sites may still be sensitive."( Cerebral relapse of metastatic gastrointestinal stromal tumor during treatment with imatinib mesylate: case report.
Beshay, V; Chong, G; Goldstein, D; Hughes, B; Waring, P; Yip, D, 2004)		0.55
" Although 29 of 39 patients required an adjustment of dosing because of grade 3 or 4 adverse events, most of the events were reversible, and 25 of the 29 patients were able to resume therapy."( Efficacy and safety of imatinib mesylate for patients in the first chronic phase of chronic myeloid leukemia: results of a Japanese phase II clinical study.
Bessho, M; Chiba, S; Emi, N; Fujimoto, M; Hirai, H; Hirano, M; Jinnai, I; Kawai, Y; Mizoguchi, H; Morishima, Y; Nakao, S; Nishimura, M; Ogura, M; Ohnishi, K; Ohno, R; Shimazaki, C; Taguchi, H; Takahashi, M; Tauchi, T; Urabe, A; Yazaki, F; Yokozawa, T, 2004)		0.63
" However, hematological toxicity often occurs and requires dosage reduction or discontinuation of imatinib treatment."( [Imatinib mesylate plus G-CSF therapy for chronic myelogenous leukemia in the blastic crisis].
Asaka, M; Dazai, M; Hashino, S; Imamura, M; Izumiyama, K; Kobayashi, S; Kondo, T; Morita, R; Onozawa, M; Ota, S; Sogabe, S, 2004)		1.23
" dosing for up to 3 weeks with a >100 mg/kg concentration of this agent is well tolerated in rodents, without any hematotoxicity."( A non-ATP-competitive inhibitor of BCR-ABL overrides imatinib resistance.
Baker, SJ; Cosenza, SC; Gumireddy, K; John, P; Kang, AD; Reddy, EP; Reddy, MV; Robell, KA, 2005)		0.33
" Recent data have also suggested benefit with metronomic scheduling of cytotoxic agents at lower doses at more frequent dosing intervals, in combination with other targeted therapies."( Imatinib mesylate and its potential implications for gynecologic cancers.
Dushkin, H; Schilder, RJ, 2005)		1.77
" The dosage of sHHT was escalated by adding one day of treatment every two days."( Phase I/II trial of adding semisynthetic homoharringtonine in chronic myeloid leukemia patients who have achieved partial or complete cytogenetic response on imatinib.
Andreasson, C; Apperley, JF; Bua, M; Goldman, JM; Kaeda, JS; Marin, D; Olavarria, E; Saunders, SM, 2005)		0.33
" drug dosage and selection."( Role of cytochrome P450 activity in the fate of anticancer agents and in drug resistance: focus on tamoxifen, paclitaxel and imatinib metabolism.
Rochat, B, 2005)		0.33
"The aim of this study was to identify factors predicting initial and late resistance of GI stromal tumor (GIST) patients to imatinib and to document the dose-response relationship in the prognostic subgroups."( Initial and late resistance to imatinib in advanced gastrointestinal stromal tumors are predicted by different prognostic factors: a European Organisation for Research and Treatment of Cancer-Italian Sarcoma Group-Australasian Gastrointestinal Trials Grou
Bertulli, R; Brown, M; Casali, PG; Goldstein, D; Hogendoorn, PC; Hohenberger, P; Judson, IR; Le Cesne, A; Ray-Coquard, I; Schlemmer, M; Sciot, R; Van Glabbeke, M; van Oosterom, AT; Verweij, J, 2005)		0.33
" Pharmacokinetic studies of imatinib in healthy volunteers and patients with CML, GIST and other cancers show that orally administered imatinib is well absorbed, and has an absolute bioavailability of 98% irrespective of oral dosage form (solution, capsule, tablet) or dosage strength (100 mg, 400 mg)."( Clinical pharmacokinetics of imatinib.
Lloyd, P; Peng, B; Schran, H, 2005)		0.33
" Due to the low frequency of adverse effects, further evaluation of imatinib is ongoing at a dosage of 10 mg/kg PO q24h."( A phase I clinical trial evaluating imatinib mesylate (Gleevec) in tumor-bearing cats.
Brodsky, E; Lachowicz, JL; Post, GS, )		0.41
" However, imatinib mesylate was effective independently of the dosing regime."( Pharmacologic differentiation of inflammation and fibrosis in the rat bleomycin model.
Chaudhary, NI; Park, JE; Schnapp, A, 2006)		0.74
" Finally, we provide genetic evidence in the mouse that E2A gene dosage can influence the development of pre-B cells during the phase of Igkappa gene activation."( E2A and IRF-4/Pip promote chromatin modification and transcription of the immunoglobulin kappa locus in pre-B cells.
Lazorchak, AS; Schlissel, MS; Zhuang, Y, 2006)		0.33
" However, in all studies imatinib dosage was tapered to 400-600 mg per day."( High-dose imatinib mesylate combined with vincristine and dexamethasone (DIV regimen) as induction therapy in patients with resistant Philadelphia-positive acute lymphoblastic leukemia and lymphoid blast crisis of chronic myeloid leukemia.
Choufi, B; Dombret, H; Dupriez, B; Huguet, F; Legros, L; Maury, S; Ojeda-Uribe, M; Pigneux, A; Raffoux, E; Rea, D; Recher, C; Reman, O; Rousselot, P; Royer, B; Stéphane, D; Thomas, X; Turlure, P; Vigier, M, 2006)		0.74
" Daily dosing of imatinib with concurrent administration of cytotoxic chemotherapy (either gemcitabine or doxorubicin) at standard doses was associated with toxicity that was clinically unacceptable."( Selective kinase inhibition with daily imatinib intensifies toxicity of chemotherapy in patients with solid tumours.
Appleman, LJ; Demetri, GD; Desai, J; George, S; Manola, J; Paul Eder, J; Ryan, DP, 2006)		0.33
" IFN dosage was reduced to 5 MIU, alternate days, in June 2001 and a cytogenetic relapse occurred 3 months later."( Durable molecular complete remission induced by low-dose imatinib plus low-dose interferon alpha in a patient with chronic myelogenous leukaemia.
Hatta, Y; Miura, K; Sawada, U; Takeuchi, J, )		0.13
" This study introduced a novel approach using intermittent dosage of IM in order to avoid prolonged interruptions in therapy, to allow spontaneous recovery in blood count and, simultaneously, to achieve intermittently therapeutic plasma drug levels."( Intermittent dosage of imatinib mesylate in CML patients with a history of significant hematologic toxicity after standard dosing.
Divoký, V; Egorin, MJ; Faber, E; Holzerová, M; Indrák, K; Jarosová, M; Maresová, I; Nausová, J; Rozmanová, S, 2006)		0.64
" A series of four resistant K562 sublines was established with different imatinib dosage (200, 400, 600 and 800 nM) and analyzed using microarray technology."( Gene expression signatures associated with the resistance to imatinib.
Chung, YJ; Ha, SA; Kang, HM; Kim, DW; Kim, HK; Kim, JH; Kim, JW; Kim, S; Kim, TM; Lee, YJ; Namkoong, H; Shin, SM, 2006)		0.33
" The proposed developed HPTLC method can be applied for identification and quantitative determination of imatinib mesylate in bulk drug and dosage forms."( Stability-indicating HPTLC determination of imatinib mesylate in bulk drug and pharmaceutical dosage form.
Musmade, P; Subramanian, G; Vadera, N, 2007)		0.81
" In this study, we investigated the influence of dosing time on the ability of imatinib to inhibit tumor growth in mice."( Basis for dosing time-dependent change in the anti-tumor effect of imatinib in mice.
Aramaki, H; Furuyama, A; Higuchi, S; Koyanagi, S; Nakagawa, H; Nakamura, M; Ohdo, S; Takiguchi, T, 2006)		0.33
" However, the synergistic dose-response relationship found for the combination of imatinib and HI was restricted to Bcr-Abl-positive cells."( Hypusination of eukaryotic initiation factor 5A (eIF5A): a novel therapeutic target in BCR-ABL-positive leukemias identified by a proteomics approach.
Balabanov, S; Bokemeyer, C; Brassat, U; Brümmendorf, TH; Copland, M; Gontarewicz, A; Hartmann, U; Hauber, I; Hauber, J; Holyoake, TL; Kammer, W; Kanz, L; Nordheim, A; Priemer, M; Schwarz, G; Wilhelm, T; Ziegler, P, 2007)		0.34
" Future clinical studies need to focus on how imatinib can be incorporated into chemotherapy more effectively by determining the optimal dosage of imatinib, the optimal combinational schedule, and the role of allogeneic HSCT."( Imatinib combined chemotherapy for Philadelphia chromosome-positive acute lymphoblastic leukemia: major challenges in current practice.
Naoe, T; Yanada, M, 2006)		0.33
" Some patients become resistant or intolerant to imatinib therapy; management strategies to overcome these problems include dosage adjustment, other treatments, or combination therapy with imatinib and other agents."( Imatinib: a review of its use in chronic myeloid leukaemia.
McKeage, K; Moen, MD; Plosker, GL; Siddiqui, MA, 2007)		0.34
" Therefore, further research on the efficacy of imatinib should be carried out as well as the most effective dosage needs to he worked out."( [Imatinib mesylate in treatment of childhood chronic myeloid leukaemia. Preliminary report].
Jankowska, K; Kurylak, A; Pogorzała, M; Styczyński, J; Wysocki, M, )		1.04
" Imatinib dosages higher than 400 mg/day (up to 800 mg/day) may improve progression-free survival, with an increase in dosage benefiting some patients who show disease progression at the lower dosage, particularly in those with exon 9 mutation; however, there is also a dose-related increase in imatinib toxicity."( Imatinib: a review of its use in the management of gastrointestinal stromal tumours.
Scott, LJ; Siddiqui, MA, 2007)		0.34
" Twenty-two patients with gastrointestinal stromal tumor or chronic myeloid leukemia initially received imatinib 600 mg daily with dosage subsequently toxicity adjusted."( Imatinib disposition and ABCB1 (MDR1, P-glycoprotein) genotype.
Balleine, RL; Clarke, CL; Collins, M; Delforce, SE; Gurney, H; Hoskins, JM; Lynch, K; Mann, GJ; McLachlan, AJ; Rivory, LP; Schran, H; Wilcken, N; Wong, M, 2007)		0.34
" IM dosage was increased up to 300 mg/day."( PDGFRalpha/FIP1L1-positive chronic eosinophilic leukemia presenting with retro-orbital localization: efficacy of imatinib treatment.
Armentano, A; Bisconte, MG; Gentile, C; Gentile, M; Lucia, E; Martinelli, G; Mazzone, C; Morabito, F; Ottaviani, E; Rondoni, M; Vigna, E, 2008)		0.35
"In the present report, we address the question if the reduction of standard dosage of imatinib mesylate (IM) in imatinib-intolerant chronic myeloid leukemia (CML) patients with undetectable residual disease may impair their outcome."( Durable responses in chronic myeloid leukemia patients maintained with lower doses of imatinib mesylate after achieving molecular remission.
Carella, AM; Lerma, E, 2007)		0.79
" Patients taking 600mg or higher dosage of imatinib had more gastrointestinal side effects."( Imatinib mesylate in the treatment of chronic myeloid leukemia: a local experience.
Bee, PC; Gan, GG; Haris, AR; Teh, A, 2006)		1.78
" Reinitiation of therapy at the prior effective dose led to molecular remission in all 5 patients, although 2 patients subsequently required increased dosing to maintain remission."( Relapse following discontinuation of imatinib mesylate therapy for FIP1L1/PDGFRA-positive chronic eosinophilic leukemia: implications for optimal dosing.
Dunbar, CE; Fay, MP; Fu, W; Hartsell, M; Klion, AD; Law, MA; Lemery, S; Maric, I; Noel, P; Nutman, TB; Robyn, J; Schmid, L; Talar-Williams, C, 2007)		0.61
" Various strategies have been tried to overcome the resistance to this drug including using newer combinations, higher dosage of Imatinib and development of newer compounds."( Strategies for overcoming imatinib mesylate resistance in chronic myelogenous leukemia.
Casson, C; Singh, T, )		0.43
" This suggests that patient-tailored dosing may be more rational than a fixed dose for all."( Measurement of in vivo BCR-ABL kinase inhibition to monitor imatinib-induced target blockade and predict response in chronic myeloid leukemia.
Arthur, C; Filshie, R; Grigg, A; Hughes, T; Leahy, MF; Lynch, K; Saunders, V; To, LB; White, D, 2007)		0.34
"The addition of intermittently dosed IM to GEM at low to full dose was associated with broad antitumor activity and little increase in toxicity."( Phase I and pharmacokinetic study of imatinib mesylate (Gleevec) and gemcitabine in patients with refractory solid tumors.
Ali, Y; Egorin, MJ; Gharibo, MM; Gounder, MK; Lagattuta, TF; Lin, Y; Poplin, EA; Rubin, EH; Stein, MN, 2007)		0.61
" In many cases, imatinib dosage can be briefly halted or lowered while the toxicity is managed."( Targeted chronic myeloid leukemia therapy: seeking a cure.
Fausel, C, 2007)		0.34
" Subtherapeutic dosing is highly likely to result in the selection of a resistant clone; thus, it is of paramount importance to ensure the imatinib dose is sufficient."( New strategies in controlling drug resistance.
Frame, D, 2007)		0.34
"New clinical data are beginning to supply us with effective dosing and monitoring parameters for imatinib and dasatinib treatment of CML."( New strategies in controlling drug resistance.
Frame, D, 2007)		0.34
" We report a case of unresectable duodenal GIST, which we were able to resect with curative intent after down-staging treatment with a dosage of imatinib 400 mg daily for 8 months."( Successful resection of an advanced duodenal gastrointestinal stromal tumor after down-staging with imatinib: report of a case.
Bergenfeldt, M; Krarup-Hansen, A; Ludvigsen, L; Mahdi, B; Toxvaerd, A, 2007)		0.34
"We show here that, consistent with our previous in vitro studies, gemcitabine inhibited tumor growth, whereas pemetrexed was ineffective, even at the highest dosage tested."( Imatinib mesylate enhances therapeutic effects of gemcitabine in human malignant mesothelioma xenografts.
Bertino, P; Cilli, M; Favoni, R; Gaudino, G; Mutti, L; Piccardi, F; Porta, C, 2008)		1.79
"Imatinib therapy for unresectable or metastatic gastrointestinal stromal tumour (GIST) is typically initiated at a dosage of 400mg/d."( Optimizing the dose of imatinib for treatment of gastrointestinal stromal tumours: lessons from the phase 3 trials.
Patel, S; Zalcberg, JR, 2008)		0.35
"To develop dosing guidelines and to evaluate the pharmacokinetics of imatinib in patients with liver dysfunction (LD)."( Phase I and pharmacokinetic study of imatinib mesylate in patients with advanced malignancies and varying degrees of liver dysfunction: a study by the National Cancer Institute Organ Dysfunction Working Group.
Belani, CP; Doroshow, JH; Egorin, MJ; Grem, JL; Hamilton, A; Hayes, MJ; Ivy, SP; LoRusso, PA; Mulkerin, DL; Murgo, AJ; Peng, B; Potter, DM; Ramanathan, RK; Remick, SC; Takimoto, CH, 2008)		0.62
" Dosing guidelines for patients with moderate and severe LD remain undetermined."( Phase I and pharmacokinetic study of imatinib mesylate in patients with advanced malignancies and varying degrees of liver dysfunction: a study by the National Cancer Institute Organ Dysfunction Working Group.
Belani, CP; Doroshow, JH; Egorin, MJ; Grem, JL; Hamilton, A; Hayes, MJ; Ivy, SP; LoRusso, PA; Mulkerin, DL; Murgo, AJ; Peng, B; Potter, DM; Ramanathan, RK; Remick, SC; Takimoto, CH, 2008)		0.62
"This study was undertaken to determine the safety, dose-limiting toxicities (DLT), maximum-tolerated dose (MTD), and pharmacokinetics of imatinib in cancer patients with renal impairment and to develop dosing guidelines for imatinib in such patients."( Phase I and pharmacokinetic study of imatinib mesylate in patients with advanced malignancies and varying degrees of renal dysfunction: a study by the National Cancer Institute Organ Dysfunction Working Group.
Egorin, MJ; Flick, SM; Fu, P; Gibbons, J; Grem, JL; Ivy, SP; Lagattuta, TF; Lenz, HJ; LoRusso, PA; Mani, S; Mulkerin, DL; Murgo, AJ; Parise, RA; Pavlick, A; Ramanathan, RK; Remick, SC; Reynolds, S; Shibata, S; Takimoto, CH; Wang, Y, 2008)		0.62
" However, dosage reduction of imatinib may be required to avoid its potential toxicity."( Evaluation of neoadjuvant inhibition of aromatase activity and signal transduction in breast cancer.
Chow, LW; Loo, WT; Toi, M; Yip, AY, 2008)		0.35
" Imatinib doses up to 1,000 mg/day for 8 consecutive days are well tolerated when combined with standard TMZ dosing for MG patients."( Safety and pharmacokinetics of dose-intensive imatinib mesylate plus temozolomide: phase 1 trial in adults with malignant glioma.
Desjardins, A; Egorin, MJ; Friedman, AH; Friedman, HS; Gururangan, S; Herndon, JE; Lagattuta, TF; McLendon, R; Quinn, JA; Reardon, DA; Rich, JN; Salvado, AJ; Sathornsumetee, S; Vredenburgh, JJ, 2008)		0.6
" Monitoring the actual BCR-ABL inhibition in nilotinib treated patients using pCRKL as a surrogate is a means to establish effective dosing and to characterize resistance mechanisms against nilotinib."( Phospho-CRKL monitoring for the assessment of BCR-ABL activity in imatinib-resistant chronic myeloid leukemia or Ph+ acute lymphoblastic leukemia patients treated with nilotinib.
Binckebanck, A; Debatin, J; Dugan, M; Erben, P; Ernst, T; Härtel, N; Hehlmann, R; Hochhaus, A; Holm-Eriksen, S; Konig, H; La Rosée, P; Mueller, MC; Ottmann, OG; Shou, Y; Wunderle, L, 2008)		0.35
" Blood samples were drawn prior to dosing and over 24-48 h on days 1 and 8 of the studies."( Population pharmacokinetics of imatinib mesylate and its metabolite in children and young adults.
Barrett, JS; Bernstein, M; Blaney, SM; Bond, M; Champagne, M; Fossler, MJ; Jayaraman, B; Menon-Andersen, D; Mondick, JT; Thompson, PA, 2009)		0.64
"Current imatinib dosing guidelines in pediatrics is based on the achievement of exposures consistent with doses known to be safe and efficacious in adults."( Population pharmacokinetics of imatinib mesylate and its metabolite in children and young adults.
Barrett, JS; Bernstein, M; Blaney, SM; Bond, M; Champagne, M; Fossler, MJ; Jayaraman, B; Menon-Andersen, D; Mondick, JT; Thompson, PA, 2009)		0.64
" administration, whereas the AUC after oral dosing was unaltered."( The effect of P-gp (Mdr1a/1b), BCRP (Bcrp1) and P-gp/BCRP inhibitors on the in vivo absorption, distribution, metabolism and excretion of imatinib.
Beijnen, JH; Buckle, T; Oostendorp, RL; Schellens, JH; van Tellingen, O, 2009)		0.35
" We retrospectively studied hematologic and immunological parameters in 72 chronic myeloid leukemia and 15 gastrointestinal stromal tumor patients treated with imatinib at standard dosage and in 20 chronic myeloid leukemia patients treated before the introduction of imatinib in clinical practice."( Development of hypogammaglobulinemia in patients treated with imatinib for chronic myeloid leukemia or gastrointestinal stromal tumor.
Alfieri, P; Arcari, A; Ferrari, A; Leonardi, G; Longo, G; Luppi, G; Maffei, R; Marasca, R; Martinelli, S; Piacentini, F; Santachiara, R; Torelli, G; Trabacchi, E; Vallisa, D, 2008)		0.35
"Two patients with stage 5 chronic kidney disease and NSF were treated with oral imatinib mesylate at a dosage of 400 mg/day."( Imatinib mesylate treatment of nephrogenic systemic fibrosis.
High, WA; Kay, J, 2008)		2.02
" Skin biopsies performed both before and after initial dosing of that patient revealed less fibrosis and less staining for type I procollagen after imatinib mesylate treatment, but essentially unchanged tissue gadolinium content."( Imatinib mesylate treatment of nephrogenic systemic fibrosis.
High, WA; Kay, J, 2008)		1.99
" However, despite its relative tolerability, some patients require a lower dosage or temporary cessation of treatment because of severe adverse events."( Efficacy of low-dose imatinib in chronic-phase chronic myelogenous leukemia patients.
Kimura, F; Kobayashi, A; Kobayashi, S; Motoyoshi, K; Sato, K, 2009)		0.35
"A patient with recurrent and initially unresectable but non-metastatic DFSP of the scalp received Imatinib over 3 months with increasing dosage from 400 mg/day to 800 mg/day orally."( Remission with Imatinib mesylate treatment in a patient with initially unresectable dermatofibrosarcoma protuberans--a case report.
Aklan, T; Hoeffken, K; Lemm, D; Mentzel, T; Muegge, LO; Schultze-Mosgau, S; Thorwarth, M, 2008)		0.7
" Fluid restriction and imatinib dosage reduction (to 600 mg/day) restored sodium levels."( Syndrome of inappropriate secretion of antidiuretic hormone associated with imatinib.
Apostolidis, J; Charitaki, E; Harhalakis, N; Liapis, K; Nikiforakis, E; Panitsas, F, 2008)		0.35
" Due to her uncontrolled thrombocytosis after 3 years of interferon-alpha treatment, the patient received imatinib at a dosage of 400 mg/day."( Imatinib mesylate resistance in a chronic myeloid leukemia patient with a novel e8a2 BCR-ABL transcript variant.
Chen, SS; Huang, XJ; Jiang, B; Jiang, H; Jiang, Q; Li, JL; Li, LD; Liu, YR; Qin, YZ; Zhang, Y; Zhu, HH, 2008)		1.79
" Imatinib dosing was escalated to 600 mg/day in 12 patients, then to 800 mg/day in four patients."( Dose escalation of imatinib after failure of standard dose in Korean patients with metastatic or unresectable gastrointestinal stromal tumor.
Chang, HM; Jang, G; Kang, YK; Kim, TW; Lee, H; Lee, JL; Lee, SS; Park, I; Ryu, MH; Sym, SJ, 2009)		0.35
"The BCR-ABL inhibitor dasatinib achieves clinical remissions in chronic myeloid leukemia (CML) patients using a dosing schedule that achieves potent but transient BCR-ABL inhibition."( Transient potent BCR-ABL inhibition is sufficient to commit chronic myeloid leukemia cells irreversibly to apoptosis.
Balbas, M; Bleickardt, E; Kasap, C; Nicaise, C; Nicoll, JM; Sawyers, CL; Shah, NP; Weier, C, 2008)		0.35
" Routinely, avoiding single doses lower than 300 mg and continuous daily dosing has been recommended."( Has the time come for induction and maintenance imatinib therapy in chronic myeloid leukemia?
Faber, E, 2009)		0.35
" In addition, this application also provides evidence to support a change in the label to allow for an escalation of imatinib dosing to 800 mg/day for patients with progressive disease on a lower dose."( Approval summary: imatinib mesylate in the treatment of metastatic and/or unresectable malignant gastrointestinal stromal tumors.
Cohen, MH; Farrell, A; Justice, R; Pazdur, R, 2009)		0.69
" Phase 1 and 2 trials have shown a dose-response effect and high-dose imatinib trials in early CP CML showed better results compared with standard dose."( Results of high-dose imatinib mesylate in intermediate Sokal risk chronic myeloid leukemia patients in early chronic phase: a phase 2 trial of the GIMEMA CML Working Party.
Alimena, G; Amabile, M; Baccarani, M; Breccia, M; Castagnetti, F; Galieni, P; Iacobucci, I; Iuliano, F; Luatti, S; Martinelli, G; Palandri, F; Pane, F; Rege Cambrin, G; Rosti, G; Saglio, G; Soverini, S; Specchia, G; Stagno, F; Testoni, N, 2009)		0.67
" Imatinib was dosed at 400 mg per day for patients not taking enzyme-inducing antiepileptic drugs (EIAEDs; stratum A) and at 500 mg twice-a-day for patients taking EIAEDs (stratum B)."( Phase I pharmacokinetic study of the vascular endothelial growth factor receptor tyrosine kinase inhibitor vatalanib (PTK787) plus imatinib and hydroxyurea for malignant glioma.
Beumer, JH; Desjardins, A; Egorin, MJ; Friedman, HS; Gururangan, S; Herndon, JE; Lagattuta, TF; Reardon, DA; Salvado, AJ; Vredenburgh, JJ, 2009)		0.35
" Recent clinical trial developments raise questions regarding the proper dosage and schedule of these newer agents as well as the timing of their use in the treatment of patients with CML."( Efficacy of various doses and schedules of second-generation tyrosine kinase inhibitors.
Bixby, DL; Talpaz, M, 2008)		0.35
"To assess the antitumour activity, safety, pharmacokinetics and pharmacodynamics of continuous daily sunitinib dosing in patients with imatinib-resistant/intolerant gastrointestinal stromal tumour (GIST) and to assess morning dosing versus evening dosing."( Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure.
Blay, JY; Casali, PG; Cohen, DP; Demetri, GD; Deprimo, SE; George, S; Harmon, CS; Law, CN; Le Cesne, A; Morgan, JA; Ray-Coquard, I; Stephenson, P; Tassell, V, 2009)		0.35
"In this open-label phase II study, patients were randomised to receive morning or evening dosing of sunitinib 37."( Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure.
Blay, JY; Casali, PG; Cohen, DP; Demetri, GD; Deprimo, SE; George, S; Harmon, CS; Law, CN; Le Cesne, A; Morgan, JA; Ray-Coquard, I; Stephenson, P; Tassell, V, 2009)		0.35
"Sixty of 61 planned patients received treatment (30 per dosing group); 26 completed the study."( Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure.
Blay, JY; Casali, PG; Cohen, DP; Demetri, GD; Deprimo, SE; George, S; Harmon, CS; Law, CN; Le Cesne, A; Morgan, JA; Ray-Coquard, I; Stephenson, P; Tassell, V, 2009)		0.35
"For patients with imatinib-resistant/intolerant GIST, continuous daily sunitinib dosing appears to be an active alternative dosing strategy with acceptable safety."( Clinical evaluation of continuous daily dosing of sunitinib malate in patients with advanced gastrointestinal stromal tumour after imatinib failure.
Blay, JY; Casali, PG; Cohen, DP; Demetri, GD; Deprimo, SE; George, S; Harmon, CS; Law, CN; Le Cesne, A; Morgan, JA; Ray-Coquard, I; Stephenson, P; Tassell, V, 2009)		0.35
"To discuss the new dasatinib dosing regimen for the treatment of chronic phase chronic myelogenous leukemia (CP CML) in patients who failed or were intolerant to imatinib therapy."( Once-daily dasatinib for treatment of patients with chronic myeloid leukemia.
Tyler, T, 2009)		0.35
" Dasatinib was approved for the treatment of imatinib-resistant/intolerant patients with CML or Philadelphia chromosome-positive acute lymphoblastic leukemia at the dosage of 70 mg twice daily."( Once-daily dasatinib for treatment of patients with chronic myeloid leukemia.
Tyler, T, 2009)		0.35
" Continuous and adequate dosing is essential for optimal outcomes and with imatinib treatment possibly being lifelong, patient adherence is critical."( Prevalence, determinants, and outcomes of nonadherence to imatinib therapy in patients with chronic myeloid leukemia: the ADAGIO study.
Abraham, I; Albrecht, T; Berneman, Z; De Bock, R; De Geest, S; MacDonald, K; Martiat, P; Mineur, P; Noens, L; Van Eygen, K; van Lierde, MA; Verhoef, G; Zachée, P, 2009)		0.35
" However, the development of molecular targeted therapies with highly specific mechanisms of action has raised questions about the paradigm of dosing at the MTD."( Maximum tolerated dose: clinical endpoint for a bygone era?
Takimoto, CH, 2009)		0.35
" However, plasma exposure to the drug from a given dosing regimen can vary widely among patients."( Pharmacokinetic/pharmacodynamic correlation and blood-level testing in imatinib therapy for chronic myeloid leukemia.
Cortes, JE; Egorin, MJ; Guilhot, F; Mahon, FX; Molimard, M, 2009)		0.35
" We found that STI571 had synergistic effects with cisplatin in BT-549 and to some extent in MDA-MB-468 cells; synergized with camptothecin using an alternate dosing regimen in MDA-MB-231 cells; and STI571 synergistically sensitized MDA-MB-468 cells to paclitaxel and to high doses of 5-fluorouracil."( STI571 sensitizes breast cancer cells to 5-fluorouracil, cisplatin and camptothecin in a cell type-specific manner.
Fiore, LS; Ganguly, S; Holler, CJ; Park, ES; Plattner, R; Sims, JT, 2009)		0.35
"This study suggests that intentional inhibition of ABCB1 and ABCG2 function at the blood-brain barrier is unlikely to significantly improve clinical outcome of imatinib with currently used dosing regimens."( Influence of the dual ABCB1 and ABCG2 inhibitor tariquidar on the disposition of oral imatinib in mice.
Figg, WD; Gardner, ER; Smith, NF; Sparreboom, A, 2009)		0.35
" The importance of imatinib dosing and plasma levels is likely due to their impact on intracellular concentrations of the drug."( Clinical strategies to achieve an early and successful response to tyrosine kinase inhibitor therapy.
Hochhaus, A; Hughes, T, 2009)		0.35
" Mean AUCs from time 0 to the end of the dosing interval tau (AUC(0-tau)) were 5076."( Nilotinib for imatinib-resistant or -intolerant chronic myeloid leukemia in chronic phase, accelerated phase, or blast crisis: a single- and multiple-dose, open-label pharmacokinetic study in Chinese patients.
Hu, P; Meng, F; Shen, Z; Wang, J; Wang, Y; Wei, Y; Yin, O; Zhou, L, 2009)		0.35
" In the elimination phase the concentration of IM (C(t)) follows a mono-exponential decline, and the standardized trough concentration (C(min,std) = C(tau)) can be described by a simple algorithm C(min,std) = C(t)* exp(k(e) x Delta t), where Delta t = t - tau, and tau is 24 hours for qd or 12 hours for bid dosing and k(e) is the elimination rate constant."( A therapeutic drug monitoring algorithm for refining the imatinib trough level obtained at different sampling times.
Chia, YL; Mahon, FX; Molimard, M; Nedelman, J; Schran, H; Wang, Y, 2009)		0.35
"By using the algorithm, the pharmacokinetic sampling window can be extended to a wider window to make the trough sampling easy to implement in the clinical setting, provided that the sampling time and dosing time are accurately recorded."( A therapeutic drug monitoring algorithm for refining the imatinib trough level obtained at different sampling times.
Chia, YL; Mahon, FX; Molimard, M; Nedelman, J; Schran, H; Wang, Y, 2009)		0.35
"To establish a recommended sunitinib dosing schedule in Japanese patients with imatinib-resistant/intolerant gastrointestinal stromal tumor (GIST) and to evaluate the efficacy, safety/tolerability, pharmacokinetics, and pharmacodynamics of sunitinib using this schedule."( Phase I/II study of sunitinib malate in Japanese patients with gastrointestinal stromal tumor after failure of prior treatment with imatinib mesylate.
Doi, T; Komatsu, Y; Li, Y; Muro, K; Nishida, T; Ohtsu, A; Shirao, K; Ueda, E, 2010)		0.56
" Discordant responses could be related to drug dosage variations and unknown BCR-ABL independent mechanisms."( BCR-ABL mutational studies for predicting the response of patients with chronic myeloid leukaemia to second-generation tyrosine kinase inhibitors after imatinib failure.
Chan, YY; Kwan, TK; Lie, AK; Liu, HS; Ma, ES; Sim, JP; Wan, TS; Yeung, YM; Yip, SF, 2009)		0.35
" The higher imatinib dosing in cohort 5 appears to improve survival by having an impact on the outcome of children with a higher burden of minimal residual disease after induction."( Improved early event-free survival with imatinib in Philadelphia chromosome-positive acute lymphoblastic leukemia: a children's oncology group study.
Aledo, A; Borowitz, MJ; Bowman, WP; Burden, L; Camitta, B; Carroll, A; Carroll, WL; Davies, SM; Devidas, M; Gaynon, PS; Heerema, NA; Hunger, SP; Jorstad, D; Rutledge, R; Sather, H; Schultz, KR; Slayton, WB; Trigg, M; Wang, C; Winick, N, 2009)		0.35
" For the minority of patients who are judged to have failed initial treatment with imatinib at standard dosage or increased dosage, the use of second-generation TKI or allogeneic stem cell transplantation must be considered."( Treatment strategies for CML.
Goldman, JM, 2009)		0.35
" We recommend IM dosing for patients (1) who are not responding to IM as well as expected, (2) who are suspected to be poorly compliant to their IM regimen, (3) who experience adverse events that are unusually severe for the prescribed dosage and (4) when a drug-drug interaction is suspected."( Pharmacologic monitoring and determinants of intracytoplasmic drug levels.
Mahon, FX, 2009)		0.35
"We report a case of a large gastric gastrointestinal stromal tumor (GIST), which we were able to curatively resect after treatment with a daily dosage of 400 mg imatinib for 3 months."( [Successful resection of an advanced gastrointestinal stromal tumor by neoadjuvant chemotherapy with imatinib- a case report].
Kadokawa, Y; Kawabe, A; Nakajima, S; Sonoda, K; Yamamoto, T, 2009)		0.35
" This is consistent with the results of other observational studies where dose-response was not the primary research objective."( Integrating pharmacogenetics and therapeutic drug monitoring: optimal dosing of imatinib as a case-example.
Craddock, C; Farndon, P; Griffiths, M; Li-Wan-Po, A, 2010)		0.36
" In patients with chronic-phase chronic myelogenous leukemia, once-daily dosing has similar efficacy with improved safety, compared with twice-daily dosing."( Dasatinib 140 mg once daily versus 70 mg twice daily in patients with Ph-positive acute lymphoblastic leukemia who failed imatinib: Results from a phase 3 study.
Brigid Bradley-Garelik, M; Bullorsky, E; Charbonnier, A; Dombret, H; Ehninger, G; Larson, RA; Lilly, MB; Martinelli, G; Müller, MC; Ottmann, OG; Reiffers, JJ; Shah, NP; Zhu, C, 2010)		0.36
" The mean imatinib dosage administered in the three phases patients did not differ significantly."( [Overview of chronic myelogenous leukemia and its current diagnosis and treatment patterns in 15 hospitals in China.].
Chen, FY; Chen, XQ; Guo, T; Hou, M; Hu, JD; Hu, Y; Huang, HH; Huang, XJ; Ji, CY; Jiang, B; Jiao, L; Li, Y; Liu, T; Liu, TB; Lü, XY; Meng, FY; Qiu, LG; Ren, HY; Song, XM; Sun, AN; Wang, JM; Wang, JX; Wang, SJ; Wu, DP; Xu, D; Yu, L; Zhu, HL, 2009)		0.35
" In light of the potential role of NK cells in the immunesurveillance of residual leukemia and for future combinatory immunotherapeutic approaches, our data indicate that choice and dosing of the most suitable BCR/ABL-inhibitor for a given patient require careful consideration."( The BCR/ABL-inhibitors imatinib, nilotinib and dasatinib differentially affect NK cell reactivity.
Grünebach, F; Hilpert, J; Krusch, M; Placke, T; Salih, HR; Salih, J; Steinle, A, 2010)		0.36
" Twice-daily dosing also was evaluated."( Phase 1 study of INNO-406, a dual Abl/Lyn kinase inhibitor, in Philadelphia chromosome-positive leukemias after imatinib resistance or intolerance.
Cortes, J; Hochhaus, A; Kantarjian, H; Kimura, S; le Coutre, P; Nagler, A; Ottmann, O; Pinilla-Ibarz, J, 2010)		0.36
" We propose that OA could be used to individualize dosage strategies for patients with CML to maximize molecular response and optimize long-term outcome."( Functional activity of the OCT-1 protein is predictive of long-term outcome in patients with chronic-phase chronic myeloid leukemia treated with imatinib.
Dang, P; Engler, J; Frede, A; Hughes, TP; Manley, PW; Osborn, M; Saunders, VA; White, DL; Zrim, S, 2010)		0.36
" Imatinib is remarkably effective as treatment for CML in the chronic phase (at a dosage of 400 mg/d) and the accelerated phase (at 600 mg/d)."( Update on practical aspects of the treatment of chronic myeloid leukemia with imatinib mesylate.
Schiffer, CA; Zonder, JA, 2006)		0.56
" A prospective trial is underway to evaluate whether modification of imatinib dose to achieve a target imatinib plasma level will impact patient outcome when compared with standard imatinib dosing (www."( Personalized cancer therapy for gastrointestinal stromal tumor: synergizing tumor genotyping with imatinib plasma levels.
George, S; Marrari, A; Trent, JC, 2010)		0.36
" Although laboratory and clinical studies had led to the prevailing view that continual inhibition of the BCR-ABL kinase was required for optimal efficacy, recent data on dasatinib have upended this notion and have led to a change in the recommended dosing schedule."( How much and how long: tyrosine kinase inhibitor therapy in chronic myeloid leukemia.
Deininger, MW; Traer, E, 2010)		0.36
" We report a case of unresectable primary GIST of the ampulla of Vater, which we were able to completely resect after treatment with a dosage of imatinib 400 mg daily for 5 months."( [Successful resection of locally advanced gastrointestinal stromal tumor of the ampulla of Vater after treatment with imatinib].
Chang, R; Chang, YW; Cho, KH; Dong, SH; Jang, JY; Kim, BH; Kim, HJ; Park, JE, 2010)		0.36
" To overcome this problem, future trials concerning best dosage in this subset of patients could be useful."( "Real-life" results of front-line treatment with Imatinib in older patients (≥ 65 years) with newly diagnosed chronic myelogenous leukemia.
Alimena, G; Breccia, M; Cannella, L; Carmosino, I; De Cuia, R; Diverio, D; Frustaci, A; Latagliata, R; Loglisci, G; Mancini, M; Santopietro, M; Stefanizzi, C; Volpicelli, P; Vozella, F, 2010)		0.36
" Treatment continued without obvious side effects, and PDL dosage was tapered to 10 mg/day."( [Complete response achieved in a case of gastric gastrointestinal stromal tumor by administration of imatinib mesilate with concurrent relatively high-dose steroid therapy to control side effects].
Kishimoto, H; Nakamura, M; Otagiri, N; Sasahara, K; Tauchi, K; Tsukada, Y; Yoshifuku, S, 2010)		0.36
" The different dosing requirements of dasatinib (once daily with or without food) and nilotinib (twice daily with fasting) may be an additional factor in selecting frontline agents."( First-line treatment for chronic myeloid leukemia: dasatinib, nilotinib, or imatinib.
Liu, D; Rafiyath, S; Wei, G, 2010)		0.36
" A prospective trial is underway in order to evaluate whether modification of imatinib dose to achieve a target imatinib plasma level will impact patient outcome when compared to standard imatinib dosing in GIST ( http://www."( The role of imatinib plasma level testing in gastrointestinal stromal tumor.
George, S; Trent, JC, 2011)		0.37
" On the other hand, imatinib sometimes causes leucopenia and it is hard to maintain a dosage of 400 mg/day."( [Usefulness of low-dose and long-term administration of imatinib in patients with liver metastases of rectal GIST and GIST of stomach].
Hamazoe, R; Hisamitsu, K; Kimura, O; Yamamoto, O; Yamane, N, 2010)		0.36
" However, it seems that assuming the correct patient's eligibility criteria and proper dosage schedule, possible in combination with chemotherapy, imatinib may become safe and effective treatment modality."( [Expression of c-kit and PDGFR and possibility of tyrosine kinase inhibitor employment in treatment of neuroblastoma in children].
Balwierz, W; Wieczorek, A, 2010)		0.36
" Twice-daily vatalanib dosing improved tolerability and ease of full-dose administration."( A phase I trial to determine the safety of imatinib in combination with vatalanib in patients with advanced malignancies.
Burris, H; Doss, H; Greco, FA; Hainsworth, J; Infante, J; Jones, S; Spigel, D; Thompson, D, 2011)		0.37
"To achieve successful therapeutic outcomes in chronic myeloid leukemia (CML), continuous and adequate imatinib (Gleevec(®), Glivec(®), Novartis Pharmaceuticals, Basel, Switzerland) dosing is essential."( Patient counseling program to improve the compliance to imatinib in chronic myeloid leukemia patients.
Cheong, JW; Jung, CW; Kim, DH; Kim, HJ; Kim, IH; Kim, JS; Kim, SN; Kim, YK; Min, YH; Moon, JH; Park, SY; Sohn, SK; Yoon, SS, 2012)		0.38
" Knowledge of the ABCG2 421 genotype could be useful when making dosing decisions aimed at achieving the optimal imatinib exposure."( Therapeutic drug monitoring of imatinib for chronic myeloid leukemia patients in the chronic phase.
Miura, M; Takahashi, N, 2011)		0.37
"We tested ex vivo blasts from 42 acute leukemias (14 Philadelphia-negative and 14 Philadelphia-positive B acute lymphoid leukemias, Ph-/Ph+B-ALL; 14 acute myeloid leukemias, AML) for their sensitivity to α-bisabolol in 24-hour dose-response assays."( Pro-apoptotic activity of α-bisabolol in preclinical models of primary human acute leukemia cells.
Bergamini, C; Bonifacio, M; Carcereri de Prati, A; Cavalieri, E; Fato, R; Guardalben, E; Pizzolo, G; Rigo, A; Suzuki, H; Vinante, F, 2011)		0.37
" The whole kidney of an animal dosed with imatinib was measured at 35 μm spatial resolution."( Mass spectrometry imaging with high resolution in mass and space (HR(2) MSI) for reliable investigation of drug compound distributions on the cellular level.
Guenther, S; Römpp, A; Spengler, B; Takats, Z, 2011)		0.37
" In addition, it can be applied for the extraction, quantification and clinical assessments of metabolites of Imatinib and other basic pharmaceutical drug molecules in biological fluids or pharmaceutical dosage forms."( A method for quantitative analysis of an anticancer drug in human plasma with CE-ESI-TOF-MS.
Bergquist, J; Elhamili, A, 2011)		0.37
" No significant difference of imatinib level between blood and bone marrow in IM-treated patients dosed to steady state was observed."( Analysis of imatinib in bone marrow and plasma samples of chronic myeloid leukaemia patients using solid phase extraction LC-ESI-MS.
Elliott, M; Holyoake, T; Iqbal, Z; Jørgensen, H; Watson, DG, 2011)		0.37
" Most patients achieved planned dosing of 400 mg twice daily and maintained the dose >12 months."( Expanding Nilotinib Access in Clinical Trials (ENACT): an open-label, multicenter study of oral nilotinib in adult patients with imatinib-resistant or imatinib-intolerant Philadelphia chromosome-positive chronic myeloid leukemia in the chronic phase.
De Souza, C; Gallagher, N; Jootar, S; le Coutre, P; Nicolini, FE; Powell, BL; Shen, ZX; Szczudlo, T; Turkina, A; Zheng, M, 2012)		0.38
" Mice were divided into six treatment groups and dosed orally for 15 days as follows: (i) control group, sterile water; (ii) IMA alone; (iii) SUN alone; (iv) IPI-493 alone; (v) IPI-493+IMA; and (vi) IPI-493+SUN."( The Novel HSP90 inhibitor, IPI-493, is highly effective in human gastrostrointestinal stromal tumor xenografts carrying heterogeneous KIT mutations.
Debiec-Rychter, M; Faa, G; Floris, G; Normant, E; Schöffski, P; Sciot, R; Van Looy, T; Wellens, J; Wozniak, A, 2011)		0.37
" The mean ± SD dosage of imatinib was 445 ± 125 mg/day."( A one-year, phase I/IIa, open-label pilot trial of imatinib mesylate in the treatment of systemic sclerosis-associated active interstitial lung disease.
Abtin, F; Assassi, S; Clements, PJ; Furst, DE; Khanna, D; Maranian, P; Mayes, MD; Saggar, R; Singh, RR, 2011)		0.62
" Most side effects occurred within the first week of treatment, and even when imatinib was reintroduced at a lower dosage (200 mg daily), it was poorly tolerated."( Imatinib in active diffuse cutaneous systemic sclerosis: Results of a six-month, randomized, double-blind, placebo-controlled, proof-of-concept pilot study at a single center.
de Leon, F; McBain, D; Petrlich, L; Pope, J; Seney, S; Summers, K; Vanderhoek, L; Watson, S, 2011)		0.37
" Nude mice were grafted with human GIST carrying KIT exon 13 (GIST-882; n = 59) or exon 11 (GIST-PSW; n = 44) mutations and dosed with imatinib (50 mg/kg twice daily), sunitinib (40 mg/kg once daily), IPI-504 (100 mg/kg 3 times per week), IPI-504 + imatinib, or IPI-504 + sunitinib."( The heat shock protein 90 inhibitor IPI-504 induces KIT degradation, tumor shrinkage, and cell proliferation arrest in xenograft models of gastrointestinal stromal tumors.
Debiec-Rychter, M; Faa, G; Floris, G; Machiels, K; Normant, E; Schöffski, P; Sciot, R; Stefan, C; Vanleeuw, U; Wozniak, A, 2011)		0.37
" Although imatinib mesylate (IM) is usually ineffective for the treatment of HES/CEL with negative-F/P fusion gene, in the present case it led to the remission of HES/CEL and UC at a higher drug dosage level (400 mg/day)."( Successful treatment of ulcerative colitis associated with hypereosinophilic syndrome/chronic eosinophilic leukemia.
Awano, N; Kitamura, S; Ryu, T; Takazoe, M; Tanaka, M; Yoshimura, N, 2011)		0.77
" Of 156 total samples from 68 adult CML patients and 127 total samples from 42 adult GIST, only 48 samples from 22 CML patients and 40 samples from 20 GIST patients were trough samples with adequate dosing and collection information."( Use of total and unbound imatinib and metabolite LC-MS/MS assay to understand individual responses in CML and GIST patients.
Armbrust, T; Binder, L; Brandhorst, G; Braulke, F; Cameron, S; Haase, D; Hafke, A; Oellerich, M; Ramadori, G; Streit, F; Walson, P, 2011)		0.37
"The liquid-chromatography tandem-mass-spectrometry methods developed provided information useful to understand individual responses to therapy even though necessary sampling and dosing information was often not available."( Use of total and unbound imatinib and metabolite LC-MS/MS assay to understand individual responses in CML and GIST patients.
Armbrust, T; Binder, L; Brandhorst, G; Braulke, F; Cameron, S; Haase, D; Hafke, A; Oellerich, M; Ramadori, G; Streit, F; Walson, P, 2011)		0.37
" We used flow cytometry to analyze the populations and generate high-resolution, nearly continuous Ras dose-response curves."( Quantitative assessment of Ras over-expression via shotgun deployment of vectors utilizing synthetic promoters.
Ferreira, JP; Lawhorn, IE; Peacock, RW; Wang, CL, 2012)		0.38
" Ultimately, decreasing both the cyclosporine and imatinib dosing was associated with stabilized renal function (serum creatinine 150-186 μmol/L) and cyclosporine concentrations (53-97 μg/L)."( Renal dysfunction in a renal transplant patient treated concurrently with cyclosporine and imatinib.
Egorin, MJ; Mulder, KE; Sawyer, MB, 2012)		0.38
" Because continuous and adequate dosing is important to achieve this outcome, it is important to understand treatment adherence as part of managing long-term CML therapy."( Adherence to treatment with second-line therapies, dasatinib and nilotinib, in patients with chronic myeloid leukemia.
Cziraky, M; Davis, C; Hamdan, M; Hirji, I; Oliveria, SA; Yood, MU, 2012)		0.38
" The first set consisted of 241 samples taken 24 ± 2 h after dosing in 54 patients, and the second one consisted of 329 samples taken 24 ± 4 h after imatinib ingestion in 84 patients."( Imatinib trough plasma levels do not correlate with the response to therapy in patients with chronic myeloid leukemia in routine clinical setting.
Adam, T; Divoká, M; Faber, E; Friedecký, D; Indrák, K; Jarošová, M; Mičová, K; Rožmanová, S, 2012)		0.38
" However, high-dose imatinib brought patients more toxic effect and more dosage adjustment for down regulation was made for these patients with severe toxic effect."( Efficacy evaluation of imatinib in the treatment of patients with gastrointestinal stromal tumors.
Chen, P; Shi, L; Zhao, W; Zong, L, 2011)		0.37
" Higher dosage (> 600 mg) and smaller body size (< 60 kg) were risk factors for haematological side effects."( An update on imatinib mesylate therapy in chronic myeloid leukaemia patients in a teaching hospital in Malaysia.
Bee, PC; Chin, E; Gan, GG; Haris, AR; Tai, YT; Veera, SN, 2012)		0.75
" Because imatinib dosage was reduced in many patients due mainly to adverse events, subgroup analysis was performed according to the mean daily dose during the first 24 months of treatment: ≥360 mg (400-mg group; n = 294), 270-359 mg (300-mg group; n = 90) and <270 mg (200-mg group; n = 67)."( Long-term outcome following imatinib therapy for chronic myelogenous leukemia, with assessment of dosage and blood levels: the JALSG CML202 study.
Fujisawa, S; Imai, K; Kiyoi, H; Maeda, Y; Miyamura, K; Miyazaki, Y; Mori, N; Nagai, T; Nakaseko, C; Naoe, T; Ohnishi, K; Ohtake, S; Takeuchi, J; Tauchi, T; Usui, N; Yagasaki, F; Yamazaki, H, 2012)		0.38
" No definite guidelines currently exist regarding the exact dosing and duration of imatinib therapy for these patients."( Congenital and childhood myeloproliferative disorders with eosinophilia responsive to imatinib.
Abraham, S; Fluchel, M; Hancock, J; Jacobsen, J; Salama, M, 2012)		0.38
" The method is also suitable for the assay determination of IMM in pharmaceutical dosage forms."( Stability-indicating UPLC method for determination of Imatinib Mesylate and their degradation products in active pharmaceutical ingredient and pharmaceutical dosage forms.
Mukkanti, K; Nageswari, A; Reddy, KV, 2012)		0.63
" Most of the patients responded to standard dosage of imatinib, and the response was maintained in the time in those patients with a follow-up higher than 9 years."( Incidence and clinical characteristics of myeloproliferative neoplasms displaying a PDGFRB rearrangement.
Arefi, M; de las Heras, N; García, JL; Giraldo, P; Gutiérrez, NC; Hermosín, L; Hernández-Rivas, JM; López-Corral, L; Megido, M; Peñarrubia, MJ; Queizán, JA; Vanegas, RJ, 2012)		0.38
"5 mg/day continuous daily dose sunitinib dosing schedule appears to be the optimal choice for Chinese patients due to a decreased incidence of adverse events."( Efficacy and safety of sunitinib in Chinese patients with imatinib-resistant or -intolerant gastrointestinal stromal tumors.
Gao, J; Hong, J; Li, J; Shen, L, 2012)		0.38
" Moreover, daily doses calculated based on refill records may not reflect accurate dosing regimens."( A retrospective analysis of therapy adherence in imatinib resistant or intolerant patients with chronic myeloid leukemia receiving nilotinib or dasatinib in a real-world setting.
Chen, L; Griffin, JD; Guérin, A; Ponce de Leon, D; Wu, EQ, 2012)		0.38
" However, achieving maximum benefit with these drugs may require optimal dosing and adherence to therapy."( Simultaneous measurement of imatinib, nilotinib and dasatinib in dried blood spot by ultra high performance liquid chromatography tandem mass spectrometry.
Kralj, E; Kristl, A; Pajič, T; Trontelj, J, 2012)		0.38
" However, the newer targeted anticancer therapies have different pharmacokinetic (PK) and dosing characteristics compared with traditional cytotoxic drugs, making it possible to estimate the steady-state drug exposure with a single trough-level measurement."( Evidence for therapeutic drug monitoring of targeted anticancer therapies.
Balakrishnar, B; Clements, A; Gao, B; Gurney, H; Wong, M; Yeap, S, 2012)		0.38
" After 3 months of treatment with a maximum dosage of 400 mg/day sorafenib, there was an improvement in the patient's New York Heart Association (NYHA) functional class from IV to III."( Sorafenib is effective in the treatment of pulmonary veno-occlusive disease.
Fukuda, K; Kataoka, M; Satoh, T; Yanagisawa, R; Yoshino, H, 2012)		0.38
" Sorafenib dosage was reduced in a third of patients, but this did not have an impact on progression-free survival (PFS) (p=0."( Sorafenib as third- or fourth-line treatment of advanced gastrointestinal stromal tumour and pretreatment including both imatinib and sunitinib, and nilotinib: A retrospective analysis.
Bauer, S; Bitz, U; Blay, JY; Duffaud, F; Gelderblom, H; Joensuu, H; Montemurro, M; Pink, D; Rutkowski, P; Schütte, J; Trent, J, 2013)		0.39
" Mice were orally dosed over four weeks, grouped as follows: (A) control; (B) GDC-0941; (C) imatinib, and (D) GDC+IMA treatments."( A potent combination of the novel PI3K Inhibitor, GDC-0941, with imatinib in gastrointestinal stromal tumor xenografts: long-lasting responses after treatment withdrawal.
Debiec-Rychter, M; Deroose, CM; Fletcher, JA; Floris, G; Friedman, L; Li, H; Schöffski, P; Sciot, R; Van Looy, T; Vermaelen, P; Wellens, J; Wozniak, A, 2013)		0.39
" The patient consequently received imatinib treatment at a dosage of 100 mg daily."( A case of nonleukemic myeloid sarcoma with FIP1L1-PDGFRA rearrangement: an unusual presentation of a rare disease.
Bachanova, V; Begna, KH; Chen, D; Hanson, CA; Ketterling, RP; Viswanatha, DS, 2013)		0.39
" Therapeutic drug monitoring-guided dosage adjustment seems justified for imatinib, but a formal predictive therapeutic range remains difficult to propose in the absence of prospective target concentration intervention trials."( Systematic review of population pharmacokinetic analyses of imatinib and relationships with treatment outcomes.
Buclin, T; Csajka, C; Gotta, V; Widmer, N, 2013)		0.39
" After 400 mg/d imatinib treatment failure, sunitinib should be prescribed instead of increased dosage of imatinib."( [Efficacy and safety of sunitinib on patients with imatinib-resistant gastrointestinal stromal tumor].
Chen, ZF; Chi, P; Guan, GX; Jiang, WZ; Liu, X; Lu, HS, 2013)		0.39
" However, clinical responses seen in patients treated with the ABL TKI dasatinib despite its much shorter plasma half-life and the apparent rapid restoration of BCR-ABL signaling activity following once-daily dosing suggested acute, potent inhibition of kinase activity may be sufficient to irrevocably commit CML cells to apoptosis."( Threshold levels of ABL tyrosine kinase inhibitors retained in chronic myeloid leukemia cells determine their commitment to apoptosis.
Adrian, LT; Agarwal, A; Apgar, J; Deininger, MW; Druker, BJ; Eide, CA; Johnson, KJ; Koop, DR; Latocha, DH; Luo, J; Mackenzie, RJ; Marks, BD; O'Hare, T; Riddle, SM; Tyner, JW; Vogel, KW; You, H; Zabriskie, MS, 2013)		0.39
" These toxicities seem to be due to a high imatinib plasmatic concentration and are frequently controlled by a discontinuation or a dosage reduction of the drug."( [Imatinib plasma levels in the management of cutaneous side effects induced by imatinib (Glivec®): 2 case reports].
Daghfous, R; El Aïdli, S; Gaïes, E; Klouz, A; Lakhal, M; Sahnoun, R; Sraïri, S; Trabelsi, S, )		0.13
"Intermittent dosing of dasatinib with a once daily regimen has been shown to reduce side effects while preserving clinical efficacy in early and advanced phase chronic myeloid leukemia (CML)."( Improved tolerability by a modified intermittent treatment schedule of dasatinib for patients with chronic myeloid leukemia resistant or intolerant to imatinib.
Erben, P; Hochhaus, A; Klag, T; La Rosée, P; Leitner, A; Martiat, P; Müller, MC; Saussele, S; Schenk, T, 2013)		0.39
" Furthermore, individualisation of dosing based on the directly measured targeted drug delivery could be possible."( Monitoring of imatinib targeted delivery in human leukocytes.
Černelč, P; Kralj, E; Kristl, A; Marc, J; Ostanek, B; Pajič, T; Preložnik Zupan, I; Trontelj, J; Žakelj, S, 2013)		0.39
"Dasatinib 60 mg/m(2) and 80 mg/m(2) once-daily dosing were selected for phase II studies in children with Ph-positive leukemias."( Dasatinib in children and adolescents with relapsed or refractory leukemia: results of the CA180-018 phase I dose-escalation study of the Innovative Therapies for Children with Cancer Consortium.
Agrawal, S; Baruchel, A; Beverloo, BB; den Boer, ML; Dworzak, M; Kearns, PR; Lancaster, DL; Lehrnbecher, T; Manos, G; Mechinaud, F; Pieters, R; Reinhardt, D; Rizzari, C; Rosenberg, J; Strauss, L; van der Velden, VH; Zwaan, CM, 2013)		0.39
" Adjusting imatinib dosage by plasma level monitoring may facilitate management of patients who experience intolerable toxicities due to overexposure to the drug."( Imatinib plasma monitoring-guided dose modification for managing imatinib-related toxicities in gastrointestinal stromal tumor patients.
Beck, MY; Kang, YK; Ryoo, BY; Ryu, MH; Yoo, C; Yoon, S, 2013)		0.39
" We used Hill's equation for in vitro response of Ba/F3 cells transduced with various BCR-ABL mutants to determine IC(50) and the slope of the dose-response curve."( Integrating in vitro sensitivity and dose-response slope is predictive of clinical response to ABL kinase inhibitors in chronic myeloid leukemia.
Druker, BJ; Eide, CA; O'Hare, T; Shukron, O; Vainstein, V, 2013)		0.39
" Common concerns include how to best select therapy based upon patient-specific comorbidities, monitoring and interpretation of treatment outcomes, and optimization of dosing when side effects occur."( BCR-ABL inhibitors: updates in the management of patients with chronic-phase chronic myeloid leukemia.
Bixby, DL; Khan, AM, 2014)		0.4
" However, clinically relevant dosing of these adenosine triphosphate-mimetic agents in humans leads to inhibition of numerous tyrosine kinases beyond those touted by drug manufacturers and studied in landmark clinical trials."( Off-Target Effects of BCR-ABL and JAK2 Inhibitors.
Fancher, KM; Green, MR; Newton, MD, 2016)		0.43
"The issue of tailored dosing adjusted according to a range of patient-specific factors other than bodyweight or body surface area is of large and increasing clinical and financial concern."( A new frontier in haematology - combining pharmacokinetic with pharmacodynamic factors to improve choice and dose of drug.
Arpon, DR; Gandhi, MK; Martin, JH, 2014)		0.4
" Correlative studies in this trial may help to optimise dosing schedules in GIST."( Phase I study of panobinostat and imatinib in patients with treatment-refractory metastatic gastrointestinal stromal tumors.
Ahrens, M; Bauer, S; Bock, E; Grabellus, F; Grunewald, S; Hilger, RA; Hoiczyk, M; Mühlenberg, T; Nagarajah, J; Pink, D; Pustowka, A; Reichardt, A; Reichardt, P; Scheulen, ME; Schuler, M, 2014)		0.4
" These results also support using imatinib as a clinical depigmentation agent when dosage being carefully determined."( Inhibitory effects of imatinib mesylate on human epidermal melanocytes.
Cao, W; Fu, H; Hu, Y; Huang, H; Liu, L; Luo, Y; Wang, Y; Wu, K; Xiao, H; Xu, Y; Zhang, L; Zhao, Y, 2014)		0.72
"Plasma concentrations from a randomized controlled trial consist of 61 patients who received oral imatinib at doses ranged between 300 and 800 mg in various dosing interval, which were quantified using a validated reversed-phase high-performance liquid chromatographic method with UV detection method on different occasions at SS and evaluated using PPK model."( Population pharmacokinetics of imatinib in Iranian patients with chronic-phase chronic myeloid leukemia.
Alimoghaddam, K; Dinan, NM; Ghavamzadeh, A; Golabchifar, AA; Rezaee, S; Rouini, MR, 2014)		0.4
" Nonetheless, these observational results strongly suggest that a subgroup of patients could benefit from early dosage optimization assisted by TDM, because of lower imatinib concentrations and lower response rates."( Large-scale imatinib dose-concentration-effect study in CML patients under routine care conditions.
Bouchet, S; Buclin, T; Csajka, C; Decosterd, LA; Gotta, V; Mahon, FX; Molimard, M; Schuld, P; Widmer, N, 2014)		0.4
" Having calibrated the model against dose-response curves of these drugs acting as single agents on Bcr-Abl-transformed cells in vitro, the model was used to predict effects of the agents in combination."( A pharmacodynamic model of Bcr-Abl signalling in chronic myeloid leukaemia.
Jackson, RC; Radivoyevitch, T, 2014)		0.4
" The dosage of TKI Imatinib was 400 mg/d for chronic phase, 600 mg/d for accelerated and blast phase respectively."( [Efficacy of tyrosine kinase inhibitor in treatment of chronic myeloid leukemia patients].
Li, XL; Liu, HY; Liu, T; Lü, SJ; Niu, T; Wu, Y; Zheng, SP; Zhu, HL, 2014)		0.4
"This study assessed whether a cycle of "routine" therapeutic drug monitoring (TDM) for imatinib dosage individualization, targeting an imatinib trough plasma concentration (C min) of 1,000 ng/ml (tolerance: 750-1,500 ng/ml), could improve clinical outcomes in chronic myelogenous leukemia (CML) patients, compared with TDM use only in case of problems ("rescue" TDM)."( Clinical usefulness of therapeutic concentration monitoring for imatinib dosage individualization: results from a randomized controlled trial.
Baerlocher, GM; Benz, R; Buclin, T; Chalandon, Y; Csajka, C; Decosterd, LA; Duchosal, MA; Gotta, V; Gregor, M; Heim, D; Leoncini-Franscini, L; Widmer, N, 2014)		0.4
" In the "routine TDM" arm, dosage recommendations were correctly adopted in 14 patients (median C min: 895 ng/ml), who had fewer unfavorable events (28 %) than the 13 not receiving the advised dosage (77 %; P = 0."( Clinical usefulness of therapeutic concentration monitoring for imatinib dosage individualization: results from a randomized controlled trial.
Baerlocher, GM; Benz, R; Buclin, T; Chalandon, Y; Csajka, C; Decosterd, LA; Duchosal, MA; Gotta, V; Gregor, M; Heim, D; Leoncini-Franscini, L; Widmer, N, 2014)		0.4
"This first target concentration intervention trial could not formally demonstrate a benefit of "routine TDM" because of small patient number and surprisingly limited prescriber's adherence to dosage recommendations."( Clinical usefulness of therapeutic concentration monitoring for imatinib dosage individualization: results from a randomized controlled trial.
Baerlocher, GM; Benz, R; Buclin, T; Chalandon, Y; Csajka, C; Decosterd, LA; Duchosal, MA; Gotta, V; Gregor, M; Heim, D; Leoncini-Franscini, L; Widmer, N, 2014)		0.4
" Animals were dosed orally for two weeks as follows: control group (untreated); imatinib (IMA); PI3Ki (BKM120-buparlisib, BEZ235, or BYL719) or combinations of imatinib with a PI3Ki."( Phosphoinositide 3-kinase inhibitors combined with imatinib in patient-derived xenograft models of gastrointestinal stromal tumors: rationale and efficacy.
Debiec-Rychter, M; Fletcher, JA; Floris, G; Li, H; Manley, PW; Schöffski, P; Sciot, R; Van Looy, T; Vanleeuw, U; Wellens, J; Wozniak, A, 2014)		0.4
"To investigate whether imatinib dosage correlated with effective plasma levels and clinical characteristics for Japanese patients undergoing long-term (≥2 years) imatinib therapy for GISTs."( Imatinib plasma levels during successful long-term treatment of metastatic-gastrointestinal stromal tumors.
Hayashi, K; Hirai, T; Inaba, K; Kanie, H; Nomura, S; Okawaki, M; Orito, E; Sawaki, A; Yamada, T; Yamaguchi, Y; Yamamura, M, 2014)		0.4
" Imatinib dosage was significantly correlated with history of gastrectomy."( Imatinib plasma levels during successful long-term treatment of metastatic-gastrointestinal stromal tumors.
Hayashi, K; Hirai, T; Inaba, K; Kanie, H; Nomura, S; Okawaki, M; Orito, E; Sawaki, A; Yamada, T; Yamaguchi, Y; Yamamura, M, 2014)		0.4
" Our results suggest that imatinib dosage of 400 mg/day is recommended for a patient with a large BSA (≥1."( Imatinib plasma levels during successful long-term treatment of metastatic-gastrointestinal stromal tumors.
Hayashi, K; Hirai, T; Inaba, K; Kanie, H; Nomura, S; Okawaki, M; Orito, E; Sawaki, A; Yamada, T; Yamaguchi, Y; Yamamura, M, 2014)		0.4
"Via multivariate analysis, the IM dosage divided by the body surface area (BSA) was an important index, presupposing a complete cytogenetic response at 12 months (CCyR12)."( Imatinib Mesylate Dose Adjustment Based on Body Surface Area for CML Chronic Phase Patients Intolerant to Standard Dosage.
Choi, CW; Choi, IK; Kim, BS; Kim, HJ; Lee, SR; Park, Y; Sung, HJ; Yhim, HY, 2015)		1.86
" Fixed dosing therapeutic regimens fail to respect known interindividual variability in pharmacokinetics of the drug and thus, some patients may not achieve sufficient plasma concentrations."( [Potential clinical benefit of therapeutic drug monitoring of imatinib in oncology].
Demlová, R; Juřica, J; Turjap, M, 2015)		0.42
" Two dosing schedules were studied: schedule A, in which danusertib was given by 3-hour intravenous infusion daily for 7 consecutive days (days 1-7) in a 14-day cycle, and schedule B, in which the danusertib was given by 3-hour intravenous infusion daily for 14 consecutive days (days 1-14) in a 21-day cycle."( A phase I study of danusertib (PHA-739358) in adult patients with accelerated or blastic phase chronic myeloid leukemia and Philadelphia chromosome-positive acute lymphoblastic leukemia resistant or intolerant to imatinib and/or other second generation c-
Boissel, N; Borthakur, G; Brummendorf, TH; Capolongo, L; Carpinelli, P; Cortes, JE; Davite, C; Dombret, H; Jabbour, E; Kantarjian, H; Mariani, M; Schafhausen, P, 2015)		0.42
" The most effective dosage of IM and its long-term efficacy in children are not well defined."( Long-term results of high-dose imatinib in children and adolescents with chronic myeloid leukaemia in chronic phase: the Italian experience.
Biondi, A; Burnelli, R; Consarino, C; Diverio, D; Foà, R; Giona, F; Gottardi, E; Iaria, G; Ladogana, S; Locatelli, F; Menna, G; Messina, C; Micalizzi, C; Moleti, ML; Nanni, M; Pession, A; Piciocchi, A; Putti, MC; Saglio, G; Santoro, N; Tucci, F; Varotto, S, 2015)		0.42
" In TKI therapy for CML patients, therapeutic drug monitoring is a new strategy for dosage optimization to obtain a faster and more effective clinical response."( Therapeutic drug monitoring of imatinib, nilotinib, and dasatinib for patients with chronic myeloid leukemia.
Miura, M, 2015)		0.42
" Animals were exposed to a standard and high imatinib dosage continuously and to the high imatinib dose intermittently."( Impact of long-term exposure to the tyrosine kinase inhibitor imatinib on the skeleton of growing rats.
Erben, RG; Gerdes, S; Glauche, I; Hofbauer, LC; Jung, R; Suttorp, M; Tauer, JT, 2015)		0.42
" The impact of HAART on imatinib may depend on whether it is being initiated or has already been dosed chronically in patients."( Human hepatocyte assessment of imatinib drug-drug interactions - complexities in clinical translation.
Beumer, JH; Christner, SM; Kiesel, BF; Parise, RA; Pillai, VC; Rudek, MA; Venkataramanan, R, 2015)		0.42
" Similar experimental conditions were used to establish a dose-response curve for the effects of Kit ligand and assess the effects of imatinib (small molecule inhibitor of the Kit receptor)."( Regulation of FOXO3 subcellular localization by Kit ligand in the neonatal mouse ovary.
Aloisio, GM; Baker, MD; Carr, BR; Castrillon, DH; Cuevas, I; Ezzati, MM; Nakada, Y; Pena, CG; Saatcioglu, HD, 2015)		0.42
" A dose-response curve for Kit ligand treatment showed that maximum effect was seen at 150 ng/mL."( Regulation of FOXO3 subcellular localization by Kit ligand in the neonatal mouse ovary.
Aloisio, GM; Baker, MD; Carr, BR; Castrillon, DH; Cuevas, I; Ezzati, MM; Nakada, Y; Pena, CG; Saatcioglu, HD, 2015)		0.42
" The objective of this study was to explore an optimal dosing regimen for a TKI, radotinib, to improve its safety profile."( Optimization of radotinib doses for the treatment of Asian patients with chronic myelogenous leukemia based on dose-response relationship analyses.
Cho, DJ; Kim, DW; Kim, SH; Lee, JI; Noh, H; Oh, SJ; Park, HL; Park, MS; Zang, DY, 2016)		0.43
" The relatively low prevalence rate of adverse reactions may be related to the low dosage of imatinib (400 mg/day) used to treat our patients and may have been affected by pharmacogenetic characteristics of our population."( Cutaneous adverse reactions of imatinib therapy in patients with chronic myeloid leukemia: A six-year follow up.
Akin Belli, A; Ayer, M; Barut, SG; Dervis, E, 2016)		0.43
" In the present article, we report our extensive experience with the management of imatinib therapy in a 'real' population, in particular in very elderly patients, discussing whether the use of personalized imatinib dosage could be a safe and advantageous option, enabling continuous administration, thus ensuring effective treatment."( Successful treatment with personalized dosage of imatinib in elderly patients with gastrointestinal stromal tumors.
Altimari, A; Biasco, G; Ceccarelli, C; Di Nunno, V; Di Scioscio, V; Fanti, S; Fiorentino, M; Gatto, L; Gruppioni, E; Nannini, M; Pantaleo, MA; Santini, D; Saponara, M; Tabacchi, E; Zompatori, M, 2016)		0.43
" Here, we study wild-type mice dosed with dasatinib and find that it causes the transient induction of proliferation of quiescent hematopoietic stem cells (HSCs)."( Dasatinib promotes the activation of quiescent hematopoietic stem cells in mice.
Dagger, SA; Duyvestyn, JM; Langdon, WY; Taylor, SJ, 2016)		0.43
" Based on measured drug concentrations, the CsA dosage needed to be reduced, on average, by 27 % after initiation of imatinib (p = 0."( A clinically relevant pharmacokinetic interaction between cyclosporine and imatinib.
Andrews, LM; Atiq, F; Broers, AE; Doorduijn, JK; Koch, BC; Van Gelder, T; Versmissen, J, 2016)		0.43
" Subsequently, we reduced the dosage to one level and regorafenib was continuously administered."( [A case of a gastrointestinal stromal tumor of the rectum effectively treated with continuously-administered regorafenib after failure of imatinib and sunitinib].
Ando, T; Hosokawa, A; Kajiura, S; Nakada, N; Nanjyo, S; Sugiyama, T, 2016)		0.43
"The combination of onalespib plus imatinib was well tolerated but exhibited limited antitumour activity as dosed in this TKI-resistant GIST patient population."( Dose-escalation study of a second-generation non-ansamycin HSP90 inhibitor, onalespib (AT13387), in combination with imatinib in patients with metastatic gastrointestinal stromal tumour.
Agulnik, M; Corless, CL; Demetri, GD; Heinrich, MC; Keer, H; Lyons, JF; Mahadevan, D; Oganesian, A; Riedel, RF; Trent, J; von Mehren, M; Wagner, AJ; Yule, M, 2016)		0.43
" Treatment history was subdivided into time periods for which treatment was given at constant dosage (total 483 time periods)."( 'Real-life' study of imatinib therapy in chronic phase-chronic myeloid leukemia: A novel retrospective observational longitudinal analysis.
Calvello, C; Cavigliano, P; Elena, C; Ferretti, V; Merante, S; Orlandi, E; Rocca, B; Zappatore, R, 2017)		0.46
" Considering the exacerbation of the cancer-related symptoms observed during the rest periods, further exploration of the continuous dosing schedule of regorafenib is warranted in future clinical trials."( Efficacy and Safety of Regorafenib in Korean Patients with Advanced Gastrointestinal Stromal Tumor after Failure of Imatinib and Sunitinib: A Multicenter Study Based on the Management Access Program.
Im, SA; Kang, YK; Kim, TY; Lee, SJ; Park, JO; Park, SR; Ryoo, BY; Ryu, MH; Son, MK, 2017)		0.46
" Further trials addressing the optimal dosage of imatinib and mTORi in kidney transplant recipients are recommended."( Gastrointestinal stromal tumors in kidney transplant recipients: Report of two cases and literature review.
Chan, CK; Chau, KF; Cheng, IK; Cheung, CY; Li, FK; Lo, SH, 2017)		0.46
"The stability of extemporaneously prepared erlotinib, lapatinib, and imatinib oral liquid dosage forms using two commercially available vehicles when stored at 4 and 25 °C was evaluated."( Stability of extemporaneous erlotinib, lapatinib, and imatinib oral suspensions.
Griffith, N; Kolli, S; Li, Q; Liu, Z; Poi, MJ; Wetz, K, 2016)		0.43
" Comparing patients exposed to polypharmacy to those without, no difference was observed pertaining to the dosage of imatinib, cytogenetic and molecular responses and hematological and extra-hematological toxicity."( Imatinib and polypharmacy in very old patients with chronic myeloid leukemia: effects on response rate, toxicity and outcome.
Abruzzese, E; Alimena, G; Annunziata, M; Avanzini, P; Binotto, G; Bocchia, M; Bonifacio, M; Breccia, M; Bucelli, C; Calistri, E; Castagnetti, F; Cattaneo, D; Cavazzini, F; Cedrone, M; Celesti, F; Cortelezzi, A; Cortesi, L; Crugnola, M; D'Addosio, AM; Falzetti, F; Fava, C; Ferrero, D; Galimberti, S; Giglio, G; Gozzini, A; Gugliotta, G; Isidori, A; Iurlo, A; Latagliata, R; Luciano, L; Mannucci, PM; Mansueto, G; Mauro, E; Montefusco, E; Nobili, A; Orlandi, EM; Pregno, P; Rege-Cambrin, G; Rossi, AR; Rosti, G; Russo, S; Saglio, G; Scaffidi, L; Sica, S; Sorà, F; Spadea, A; Stagno, F; Storti, S; Tettamanti, M; Tiribelli, M; Vigneri, P, 2016)		0.43
" The reintroduced imatinib dosage was stepped up every week starting from 10 mg/d and increasing to 25, 50, 75, 100, 150, 200, and 300 mg/d until the target dose of 400 mg/d was achieved."( Slow desensitization of imatinib-induced nonimmediate reactions and dynamic changes of drug-specific CD4
Buranapraditkun, S; Klaewsongkram, J; Mongkolpathumrat, P; Sodsai, P; Thantiworasit, P, 2016)		0.43
" For these patients, dosage of imatinib should be considered to increase in order to achieve effective plasma concentration."( [A Chinese multi-center study on the significance of monitoring imatinib plasma concentration in patients with gastrointestinal stromal tumor before and after administration].
Chen, H; Guan, W; Li, F; Li, G; Li, L; Ma, L; Miao, Y; Sun, L; Wang, B; Wang, J; Wang, Y; Xu, H; Xu, J; Xu, W; Xu, Z; Yang, L; Yu, J; Zhang, D; Zhi, X, 2016)		0.43
" Twenty patients with exon 11 mutation and 1 patient with wide type received imatinib treatment at a dose of 400 mg daily, and 3 patients with exon 9 mutation received the dosage of 600 mg per day."( [Efficacy observation on imatinib reintroduction in gastrointestinal stromal tumor with high recurrence risk after imatinib adjuvant therapy failure].
Dong, Z; Gao, J; Gong, J; Li, J; Li, Y; Shen, L; Wang, X, 2016)		0.43
" Therefore, while optimal asymptotic dosage might not be the best one at short time scales, our results raise interesting perspectives in terms of strategies for achieving and improving long-term deep response."( Long-term treatment effects in chronic myeloid leukemia.
Bernard, S; Besse, A; Lepoutre, T, 2017)		0.46
" Imatinib was initiated at a dosage of 200 mg, and after 10 months, the signal of the FIP1L1-PDGFRA fusion gene was undetectable in bone marrow sample."( [Clinical and genetic features of a patient with myeloid neoplasm in association with PDGFRA and EVI1 gene rearrangements].
Cen, L; Chao, H; Chen, S; Han, W; He, X; Lu, X; Zhou, M, 2017)		0.46
"Continuous diphenhydramine infusion can provide promising outcomes following the failure of intermittent antihistamine dosing in patients with severe mast cell activation syndrome."( Continuous diphenhydramine infusion and imatinib for KIT-D816V-negative mast cell activation syndrome: a case report.
Ali, N; Boigon, M; Fidler, C; Ghani, A; Hamid, M; Jafri, SIM; Malik, F, 2017)		0.46
"9%, 1-resistant GISTs) at a dosage of 100 mg/kg/day without exhibiting apparent toxicity."( Discovery of Potent, Selective Stem Cell Factor Receptor/Platelet Derived Growth Factor Receptor Alpha (c-KIT/PDGFRα) Dual Inhibitor for the Treatment of Imatinib-Resistant Gastrointestinal Stromal Tumors (GISTs).
Li, J; Li, X; Lu, Y; Mao, F; Wang, M; Xu, Q; Zheng, X; Zhu, J, 2017)		0.46
" Poor adherence can impact negatively on clinical outcomes, notably because most of these drugs are given as a standard non-individualized dosage despite marked inter-individual variabilities that can lead to toxic or inefficacious drug concentrations."( Effect of Adherence on Pharmacokinetic/Pharmacodynamic Relationships of Oral Targeted Anticancer Drugs.
Cardoso, E; Csajka, C; Schneider, MP; Widmer, N, 2018)		0.48
"Imatinib therapeutic drug monitoring only provides information on dosage adequacy and on short-term adherence; longer-term adherence cannot be assessed."( Women Administered Standard Dose Imatinib for Chronic Myeloid Leukemia Have Higher Dose-Adjusted Plasma Imatinib and Norimatinib Concentrations Than Men.
Belsey, SL; Bisquera, A; De Lavallade, H; Flanagan, RJ; Ho, A; Ireland, R; Kizilors, A; Lang, K; Mufti, GJ, 2017)		0.46
" Most patients commenced sunitinib in a 6-week cycle, however, dosing could be reduced, delayed, changed to (or initiated with) a continuous schedule."( Treatment of gastrointestinal stromal tumours in paediatric and young adult patients with sunitinib: a multicentre case series.
Benson, C; Chou, AJ; Magnan, H; Rutkowski, P, 2017)		0.46
"The tyrosine kinase inhibitors sorafenib and imatinib are important in the treatment of a range of cancers but adverse effects in some patients necessitate dosage modifications."( Differential effects of hepatic cirrhosis on the intrinsic clearances of sorafenib and imatinib by CYPs in human liver.
Edwards, RJ; Ghassabian, S; Gillani, TB; Murray, M; Rawling, T, 2018)		0.48
"A total of 54 patients were divided into two groups according to the dosage of nilotinib."( [Correlation of Serum Concentration of Nilotinib with Clinical Efficacy in Patients with Chronic Myeloid Leukemia].
Chen, XC; Gu, CH; Li, CX; Wang, P; Wang, T; Wu, DP; Yang, D; Zou, Q, 2018)		0.48
" The Cmins of nilotinib relate with the dosage and grade III-IV of adverse events."( [Correlation of Serum Concentration of Nilotinib with Clinical Efficacy in Patients with Chronic Myeloid Leukemia].
Chen, XC; Gu, CH; Li, CX; Wang, P; Wang, T; Wu, DP; Yang, D; Zou, Q, 2018)		0.48
" A phase I study determined suitable dosing for children with Philadelphia chromosome-positive (Ph+) leukemias."( Dasatinib in Pediatric Patients With Chronic Myeloid Leukemia in Chronic Phase: Results From a Phase II Trial.
Bertrand, Y; Cardos, RC; Chung, NG; de Martino, ML; De Souza, CA; Fagioli, F; Gore, L; Hijiya, N; Kearns, PR; Lancaster, D; Landman-Parker, J; Place, AE; Rabin, KR; Sacchi, M; Saikia, T; Seo, JJ; Stork, LC; Swanink, R; Zwaan, CM, 2018)		0.48
" A standard 3 + 3 dosing schema was utilized to determine the recommended phase II dose (RP2D)."( A phase Ib study of BGJ398, a pan-FGFR kinase inhibitor in combination with imatinib in patients with advanced gastrointestinal stromal tumor.
Antonescu, CR; Chi, P; D'Angelo, SP; DeMatteo, RP; Dickson, MA; Francis, JH; Gounder, MM; Heinemann, MH; Hwang, S; Kelly, CM; Keohan, ML; Mcfadyen, C; Qin, LX; Shoushtari, AN; Singer, S; Sjoberg, A; Tap, WD, 2019)		0.51
"We analyzed clinical, pathological, and molecular characteristics and long-term outcomes in patients with metastatic GIST treated with continuous daily dosing of frontline imatinib in a cohort of patients benefiting for ≥5 years."( Clinicopathological and Molecular Characterization of Metastatic Gastrointestinal Stromal Tumors with Prolonged Benefit to Frontline Imatinib.
Arribas, J; Carles, J; Díaz-Beveridge, R; Durán, J; Estival, A; García-Del-Muro, X; Hernández-Losa, J; Hindi, N; Jiménez, L; Landolfi, S; Lavernia, J; Manzano, A; Martínez-Marín, V; Pajares, I; Pericay, C; Rubió-Casadevall, J; Safont, MJ; Sebio, A; Serrano, C; Valverde, C; Vicente-Baz, D; Vivancos, A, 2019)		0.51
" The initial dosage of dasatinib for CML-CP and CML-AP patients were 100 mg once daily and 70 mg twice daily (total = 140 mg/ day), respectively."( Four-year follow-up of patients with imatinib-resistant or intolerant chronic myeloid leukemia receiving dasatinib: efficacy and safety.
Hu, J; Huang, X; Jiang, Q; Jin, J; Li, J; Liu, T; Meng, F; Shen, Z; Wang, J; Wu, D, 2019)		0.51
" PK of these agents following intravenous and oral dosing were evaluated in C57BL/6 mice, prairie dogs, guinea pigs and Cynomolgus monkeys."( Preclinical pharmacokinetic evaluation to facilitate repurposing of tyrosine kinase inhibitors nilotinib and imatinib as antiviral agents.
Ananthula, HK; Buller, RM; Damon, IK; Desai, PB; Gallardo-Romero, N; Kalman, D; Moir-Savitz, T; Olson, V; Parker, S; Patel, G; Sallans, L; Salzer, JS; Sherwin, CM; Touchette, E; Werner, MH, 2018)		0.48
"5 h), facilitated multiple dosing PK and safety assessment."( Preclinical pharmacokinetic evaluation to facilitate repurposing of tyrosine kinase inhibitors nilotinib and imatinib as antiviral agents.
Ananthula, HK; Buller, RM; Damon, IK; Desai, PB; Gallardo-Romero, N; Kalman, D; Moir-Savitz, T; Olson, V; Parker, S; Patel, G; Sallans, L; Salzer, JS; Sherwin, CM; Touchette, E; Werner, MH, 2018)		0.48
"Imatinib has shown to be highly efficacious in the treatment of chronic myeloid leukemia (CML) but continuous dosing and patient adherence is essential treatment success."( Prevalence and determinants of non-adherence to Imatinib in the first 3-months treatment among newly diagnosed Ethiopian's with chronic myeloid leukemia.
Engidawork, E; Gebremedhin, A; Mulu Fentie, A; Tadesse, F, 2019)		0.51
" Imatinib treatment is feasible in transplant recipients under immunosuppression, although immunosuppressive drugs metabolized by CYP3A4 should be used at a reduced dosage or withdrawn."( Small intestinal perforation due to a huge gastrointestinal stromal tumor in a kidney transplant recipient: a case report and literature review.
Akita, H; Asanuma, H; Hamamoto, Y; Ishida, T; Jinzaki, M; Kameyama, K; Kitaoka, S; Morita, S; Oya, M; Shinoda, K; Takahashi, R; Tamaki, S; Yoshida, T, 2019)		0.51
"Regorafenib at the standard intermittent dosing schedule proved effective in the GRID trial for refractory gastrointestinal stromal tumors (GISTs)."( Phase II Trial of Continuous Regorafenib Dosing in Patients with Gastrointestinal Stromal Tumors After Failure of Imatinib and Sunitinib.
Beck, MY; Kang, YK; Kim, JJ; Ma, JE; Ryu, MH; Yoo, C, 2019)		0.51
" With this fixed dosing regimen, only approximately 40% of patients reach adequate plasma levels within the therapeutic index."( Optimizing the dose in patients treated with imatinib as first line treatment for gastrointestinal stromal tumours: A cost-effectiveness study.
Desar, IME; Kievit, W; van Erp, NP; Zuidema, S, 2019)		0.51
"A survival model was created to simulate progression, mortality and treatment costs over a 5-year time horizon, comparing fixed dosing vs TDM-guided dosing."( Optimizing the dose in patients treated with imatinib as first line treatment for gastrointestinal stromal tumours: A cost-effectiveness study.
Desar, IME; Kievit, W; van Erp, NP; Zuidema, S, 2019)		0.51
"08 for fixed dosing vs TDM-guided dosing, respectively."( Optimizing the dose in patients treated with imatinib as first line treatment for gastrointestinal stromal tumours: A cost-effectiveness study.
Desar, IME; Kievit, W; van Erp, NP; Zuidema, S, 2019)		0.51
"Based on the currently available data, this analysis suggests that TDM-guided dosing may be a cost-effective intervention for patients with metastatic/unresectable GIST treated with imatinib which will be improved when imatinib losses its patency."( Optimizing the dose in patients treated with imatinib as first line treatment for gastrointestinal stromal tumours: A cost-effectiveness study.
Desar, IME; Kievit, W; van Erp, NP; Zuidema, S, 2019)		0.51
" However, even when treatment is started at the dosage indicated in the medical package insert, we have experienced many cases in which treatment had to be stopped early owing to the occurrence of serious side effects or an insufficient therapeutic effect."( [Toward Personalized Cancer Therapy with Oral Molecular-targeted Agents].
Arai, Y; Kawasaki, Y; Kikuchi, M; Mano, N; Takasaki, S; Yamaguchi, H, 2019)		0.51
" A 3+3 dosing schema was utilized to determine the recommended phase II dose (RP2D)."( Phase I Study of Rapid Alternation of Sunitinib and Regorafenib for the Treatment of Tyrosine Kinase Inhibitor Refractory Gastrointestinal Stromal Tumors.
Barysauskas, CM; Demetri, GD; Fletcher, JA; George, S; Kuang, Y; Leal, A; Mariño-Enríquez, A; Morgan, JA; Paweletz, CP; Phallen, J; Serrano, C; Triplett, O; Velculescu, VE; Wagner, AJ, 2019)		0.51
" Six out of 22 patients with CS late chronic anemia received subcutaneous recombinant alpha-erythropoietin (EPO) at the standard dosage of 40,000 IU weekly: all 6 patients achieved an erythroid response."( Incidence of Clinically Significant (≤10 g/dL) Late Anemia in Elderly Patients with Newly Diagnosed Chronic Myeloid Leukemia Treated with Imatinib.
Alimena, G; Breccia, M; Carmosino, I; Cesini, L; Colafigli, G; De Benedittis, D; De Luca, ML; Diverio, D; Foà, R; Latagliata, R; Loglisci, MG; Mancini, M; Mariggiò, E; Massaro, F; Mohamed, S; Molica, M; Rizzo, L; Scalzulli, E; Scamuffa, MC; Vozella, F, 2019)		0.51
" In this review, an overview of the current knowledge on TDM guided individualized dosing of imatinib, sunitinib and pazopanib for the treatment of solid tumours is presented."( Imatinib, sunitinib and pazopanib: From flat-fixed dosing towards a pharmacokinetically guided personalized dose.
Desar, IME; Steeghs, N; van der Graaf, WTA; van Erp, NP; Westerdijk, K, 2020)		0.56
"To determine whether dasatinib given at a daily dosage of 80 mg/m2 is more effective than imatinib mesylate at a daily dosage of 300 mg/m2 to improve event-free survival of children with Philadelphia chromosome-positive ALL in the context of intensive chemotherapy without prophylactic cranial irradiation."( Effect of Dasatinib vs Imatinib in the Treatment of Pediatric Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia: A Randomized Clinical Trial.
Cai, J; Chen, X; Cheng, C; Fang, Y; Gao, J; Hu, Q; Hu, S; Jeha, S; Jiang, H; Jin, R; Ju, X; Li, C; Li, CK; Liang, C; Pan, K; Pei, D; Pui, CH; Shen, S; Sun, L; Tang, J; Tian, X; Wang, N; Wu, X; Yang, JJ; Yang, M; Yu, J; Zhai, X; Zhang, H; Zhu, X; Zhu, Y, 2020)		0.78
"Intensive chemotherapy including dasatinib at a dosage of 80 mg/m2 per day yielded superior results in the treatment of Philadelphia chromosome-positive ALL compared with imatinib mesylate at a dosage of 300 mg/m2 per day and provided excellent control of central nervous system leukemia without the use of prophylactic cranial irradiation."( Effect of Dasatinib vs Imatinib in the Treatment of Pediatric Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia: A Randomized Clinical Trial.
Cai, J; Chen, X; Cheng, C; Fang, Y; Gao, J; Hu, Q; Hu, S; Jeha, S; Jiang, H; Jin, R; Ju, X; Li, C; Li, CK; Liang, C; Pan, K; Pei, D; Pui, CH; Shen, S; Sun, L; Tang, J; Tian, X; Wang, N; Wu, X; Yang, JJ; Yang, M; Yu, J; Zhai, X; Zhang, H; Zhu, X; Zhu, Y, 2020)		0.75
" Tumor development continued to be significantly inhibited after cessation of imatinib dosed at 50 and 100 mg/kg/day."( Early administration of imatinib mesylate reduces plexiform neurofibroma tumor burden with durable results after drug discontinuation in a mouse model of neurofibromatosis type 1.
Armstrong, AE; Bessler, W; Blakeley, JO; Chen, S; Clapp, DW; Ferguson, MJ; Ingram, DA; Jiang, L; Li, X; Rhodes, SD; Robertson, KA; Smith, A; Yang, FC; Yang, X; Yuan, J, 2020)		0.87
" After the nilotinib dosage was reduced to 400 mg, liver biopsy, also performed in 1996 + 20, revealed hypertrophy of renal small blood vessels and endothelial cells of the hepatic artery and loss of endothelial cells of the renal glomeruli, portal vein, and hepatic sinusoids."( Pathological findings suggesting vascular endothelial damage in multiple organs in chronic myelogenous leukemia patients on long-term tyrosine kinase inhibitor therapy.
Hasegawa, G; Koda, R; Morita, S; Nagano, O; Seki, Y, 2020)		0.56
"To achieve optimal clinical outcomes in patients with gastrointestinal stromal tumor (GIST), it is crucial to maintain sufficient dosing of imatinib."( Systemic Steroid Treatment for Imatinib-Associated Severe Skin Rash in Patients with Gastrointestinal Stromal Tumor: A Phase II Study.
Beck, MY; Kang, YK; Kim, EJ; Lee, MW; Lee, WJ; Park, SR; Ryu, MH, 2020)		0.56
" It is crucial to maintain sufficient dosing of imatinib to achieve optimal clinical outcomes."( Systemic Steroid Treatment for Imatinib-Associated Severe Skin Rash in Patients with Gastrointestinal Stromal Tumor: A Phase II Study.
Beck, MY; Kang, YK; Kim, EJ; Lee, MW; Lee, WJ; Park, SR; Ryu, MH, 2020)		0.56
" In the 150 days long-term engraftment model experiment, long intravenous dosing intervals of the NPs (every 4 or 8 days) exhibited much better survival and negligible toxicities as compared to daily oral administration of the inhibitor."( An ultra-long circulating nanoparticle for reviving a highly selective BCR-ABL inhibitor in long-term effective and safe treatment of chronic myeloid leukemia.
Fu, L; Liang, H; Liang, X; Liu, J; Liu, Q; Shi, J; Wang, B; Wang, J; Zou, F, 2020)		0.56
" In conclusion, although the patient's pemphigus was cleared with a single cycle of rituximab infusions while continuing imatinib therapy, the disease returned after imatinib dose was increased a year later, suggesting a dose-response relationship."( Pemphigus foliaceus in a patient with gastrointestinal stromal tumor treated with adjuvant imatinib mesylate.
Anadkat, MJ; Chen, DY; Lewis, HA; Picus, J; Rosman, IS, 2020)		0.78
" However, studies on the molecular biological traits of GIST have found that tumors respond differentially to imatinib dosage based on the KIT exon with variation."( Cost-effectiveness Analysis of Genetic Testing and Tailored First-Line Therapy for Patients With Metastatic Gastrointestinal Stromal Tumors.
Banerjee, S; Kumar, A; Lopez, N; Murphy, JD; Sicklick, JK; Tang, CM; Yebra, M; Yoon, H; Zhao, B, 2020)		0.56
"These findings suggest that using genetic testing to match treatment of KIT variations to imatinib dosing is a cost-effective approach compared with empirical imatinib."( Cost-effectiveness Analysis of Genetic Testing and Tailored First-Line Therapy for Patients With Metastatic Gastrointestinal Stromal Tumors.
Banerjee, S; Kumar, A; Lopez, N; Murphy, JD; Sicklick, JK; Tang, CM; Yebra, M; Yoon, H; Zhao, B, 2020)		0.56
" This study suggests the incorporation of these variables in to the imatinib dosing algorithm as predictive biomarkers of response to Imatinib therapy."( Plasma imatinib levels and ABCB1 polymorphism influences early molecular response and failure-free survival in newly diagnosed chronic phase CML patients.
Abraham, A; Anandan, S; Balasubramanian, P; Benjamin, ESB; Devasia, AJ; Fouzia, NA; Ganesan, S; George, B; Janet, NB; Karathedath, S; Korula, A; Kulkarni, UP; Lakshmi, KM; Mathews, V; Mohanan, E; Rajamani, BM; Ramachandran Velayudhan, S; Srivastava, A; Srivastava, VM; Varatharajan, S, 2020)		0.56
"Imatinib is a protein-tyrosine kinase inhibitor which is currently only commercially available as a tablet dosage form in the strength of 100mg and 400mg."( Design and stability of pediatric oral formulation of imatinib.
Annereau, M; Fleury, T; Gendron, A; Hinterlang, M; Rieutord, A; Schlatter, J; Vrana, A, 2022)		0.72
"The stability study showed that the imatinib oral solution at a concentration of 30 mg/mL provides an alternative option at the commercial tablet dosage forms for pediatric patients and patients who have difficulties to swallow."( Design and stability of pediatric oral formulation of imatinib.
Annereau, M; Fleury, T; Gendron, A; Hinterlang, M; Rieutord, A; Schlatter, J; Vrana, A, 2022)		0.72
" Per the trial protocol, 17 (38%) participants in the imatinib group required a temporary modification in drug dosing and six (13%) permanently discontinued imatinib due to adverse events; five (23%) participants in the placebo group had temporary modifications in dosing and none had a permanent discontinuation due to adverse events."( Imatinib therapy for patients with recent-onset type 1 diabetes: a multicentre, randomised, double-blind, placebo-controlled, phase 2 trial.
Blanchfield, JL; Bluestone, JA; Bundy, BN; DiMeglio, LA; Felner, EI; Ferrannini, E; Gaglia, JL; Gitelman, SE; Gottlieb, PA; Krischer, JP; Lim, N; Long, SA; Mari, A; Mirmira, RG; Raskin, P; Sanda, S; Tsalikian, E; Wentworth, JM; Willi, SM, 2021)		0.62
"5 mg of sunitinib (part 2e) continuously in 28-day dosing cycles until disease progression, treatment discontinuation, or withdrawal."( Association of Combination of Conformation-Specific KIT Inhibitors With Clinical Benefit in Patients With Refractory Gastrointestinal Stromal Tumors: A Phase 1b/2a Nonrandomized Clinical Trial.
Alcantar, O; Bollag, G; Burton, EA; Carias, H; Chan, K; Chugh, R; Ewing, T; Habets, G; Ibrahim, PN; Inokuchi, K; Lin, J; Marimuthu, A; Matusow, B; Michelson, G; Nespi, M; Patnaik, A; Rezaei, H; Sanftner, L; Severson, PL; Shellooe, R; Shields, AF; Spevak, W; Tap, WD; Tinoco, G; Trent, JC; Tsai, J; Tsang, G; Tsiatis, AC; Wagner, AJ; Wu, G; Zhang, C; Zhang, Y, 2021)		0.62
" The challenge of understanding the cardiac safety data of ponatinib and the unique dosing schedule based on individual response will be discussed."( How I treat chronic-phase chronic myelogenous leukemia.
Berman, E, 2022)		0.72
", low dosage bamlanivimab, baricitinib, imatinib, and sotrovimab) are a better choice for treating severe or non-severe COVID-19 patients."( Efficacy and safety of current medications for treating severe and non-severe COVID-19 patients: an updated network meta-analysis of randomized placebo-controlled trials.
Chen, J; Cheng, Q; Fang, Z; Jia, Q; Zhao, G, 2021)		0.62
" These data suggest that RWPs require more precise dosing to achieve CML clinical milestones and to mitigate AEs, but findings should be validated prospectively."( Response to Tyrosine Kinase Inhibitors in Real-World Patients With Chronic Myeloid Leukemia.
Ahmad, M; Bucci, T; Cass, AS; Crona, DJ; Deal, A; Foster, MC; Kemper, R; Muluneh, B; Sketch, MR; Szeto, AH; Zeidner, JF; Zhu, A, 2022)		0.72
"Although therapeutic drug monitoring (TDM) is an important tool in guiding drug dosing for other areas of medicine including infectious diseases, cardiology, psychiatry and transplant medicine, it has not gained wide acceptance in oncology."( Therapeutic drug monitoring in oncology: International Association of Therapeutic Drug Monitoring and Clinical Toxicology consensus guidelines for imatinib therapy.
Chatelut, E; Clarke, WA; Fotoohi, AK; Larson, RA; Martin, JH; Mathijssen, RHJ; Salamone, SJ, 2021)		0.62
" After 7 weeks of treatment with an imatinib dose reduction(200 mg), the dosage was increased and the patient was admitted to the hospital with edema of the face and lower limbs, and pleural and pericardial effusions(grade 2)."( [Long-Term Suppression with Short-Term Dose Reduction of Imatinib for Metastatic Lateral Lymph Nodes after Resection of a Rectal Gastrointestinal Stromal Tumor-A Case Report].
Funahashi, K; Ikeda, Y; Kagami, S; Kaneko, T; Kurihara, A; Mitsuda, A; Miura, Y; Nagashima, Y; Tochigi, N; Ushigome, M; Yoshino, S; Yoshino, Y, 2021)		0.62
" Imatinib is first-line treatment for unresectable gastrointestinal stromal tumors (GISTs) unless they harbor a PDGFRA D842V mutation; it is recommended to escalate imatinib to twice daily dosing for KIT exon 9 mutant tumors."( Gastrointestinal Stromal Tumors: What Is the Best Sequence of TKIs?
Ahr, K; Senchak, J; von Mehren, M, 2022)		0.72
" Hence, they should be highly suspicious to early detect these distinct histologic entities, handle these undesired complications and guarantee satisfactory immediate outcomes, avoiding frivolous IM dosage modifications."( Lichenoid drug eruption associated with imatinib mesylate therapy.
Alevizopoulos, N; Alexandris, D; Gakiopoulou, C; Kanellis, G; Marinos, L, 2023)		1.18
" Therefore, pharmacogenetic-based dosing of imatinib is an attractive proposition."( Role of ADME gene polymorphisms on imatinib disposition: results from a population pharmacokinetic study in chronic myeloid leukaemia.
Gokarn, A; Gota, V; Govalkar, R; Jadhav, S; Khattry, N; Krishnamurthy, MN; Kumar, S; Mehta, P; Patil, A; Punatar, S; Puri, AS; Shriyan, B, 2022)		0.72
"Our study conclusively proves that genetic polymorphisms in the CYP3A4 and ABC family of transporters do not have any role in the personalized dosing of imatinib in CML."( Role of ADME gene polymorphisms on imatinib disposition: results from a population pharmacokinetic study in chronic myeloid leukaemia.
Gokarn, A; Gota, V; Govalkar, R; Jadhav, S; Khattry, N; Krishnamurthy, MN; Kumar, S; Mehta, P; Patil, A; Punatar, S; Puri, AS; Shriyan, B, 2022)		0.72
"This patient was initially received imatinib (400 mg) orally once a day, and the dosage was adjusted to 100 mg owing to suffering from grade IV bone marrow suppression."( A rare cause of persistent leukocytosis with massive splenomegaly: Myeloid neoplasm with BCR-PDGFRA rearrangement-Case report and literature review.
Gao, L; Tian, ZG; Weng, LC; Xu, Y, 2022)		0.72
" Data interpretation carried some caveats: there was a potential for replication of patient-derived data between older and new publications; only predicted protein sequences were presented; the criteria used to record clinical response were not uniform across all publications; and imatinib dosage could vary between different clinical publications."( A literature review and database of how the primary KIT/PDGFRA variant of a gastrointestinal stromal tumour predicts for sensitivity to imatinib.
Andrew, N; Dangoor, A; Garcia-Petit, C; Wong, NACS, 2022)		0.72
"This study utilised a previously validated a Chinese cancer population and assessed the impact of imatinib virtual-TDM in Chinese and Caucasian cancer populations across a dosing range from 200-800 mg daily."( The Application of Virtual Therapeutic Drug Monitoring to Assess the Pharmacokinetics of Imatinib in a Chinese Cancer Population Group.
Badhan, RKS; Yu, H, 2023)		0.91
"1% (Caucasian) subjects possessing plasma concentration < 550 ng/mL when dosed at 400 mg daily."( The Application of Virtual Therapeutic Drug Monitoring to Assess the Pharmacokinetics of Imatinib in a Chinese Cancer Population Group.
Badhan, RKS; Yu, H, 2023)		0.91
", a hyperimmune anti-COVID-19 intravenous immunoglobulin), methylprednisolone, interferon-beta/standard-of-care (SOC), interferon-beta-1b, convalescent plasma, remdesivir, lopinavir/ritonavir, immunoglobulin gamma, high dosage sarilumab (HS), auxora, and imatinib were effective when compared with placebo or SOC group."( Comparative efficacy and safety of pharmacological interventions for severe COVID-19 patients: An updated network meta-analysis of 48 randomized controlled trials.
Chen, J; Cheng, Q; Fang, Z; Jia, Q; Zhao, G, 2022)		0.72
" These results are to some extent in line with ours, although our analyses of dose-response matrices from combinations of asciminib with imatinib, nilotinib or dasatinib, show neither synergy nor antagonism, but suggest additive antiproliferative effects on BCR-ABL-dependent KCL22 cells."( Correspondence on "Synergy and Antagonism between Allosteric and Active-Site Inhibitors of Abl Tyrosine Kinase".
Cowan Jacob, SW; Grzesiek, S; Habazettl, JM; Jahnke, W; Loo, A; Manley, PW; Paladini, J; Wiget, A, 2022)		0.72
" TKI switches (49 times) and dosing changes (165 times) due to intolerance or insufficient response were frequent."( A multicenter real-world evidence study in the Swiss treatment landscape of chronic myeloid leukemia.
Balabanov, S; Cantoni, N; Kahn, S; Kulenkampff, E; Lambert, JF; Schmidt, A; Seitz, P; Sommavilla, R; Zenhaeusern, R, 2022)		0.72
" Forty-one patients were enrolled and divided into two groups on the basis of the starting dosage: the standard dosage group (50 mg/day, 21 patients) and the reduced dosage group (37."( Sunitinib therapy for imatinib-resistant and/or intolerant gastrointestinal stromal tumors: comparison of safety and efficacy between standard and reduced dosage regimens.
Hirota, S; Ishikawa, T; Kanda, T; Matsumoto, Y; Saijo, Y; Sasaki, K, 2023)		0.91
"Three patients (14%) in the standard dosage group and another three (15%) in the reduced dosage group (P = 1."( Sunitinib therapy for imatinib-resistant and/or intolerant gastrointestinal stromal tumors: comparison of safety and efficacy between standard and reduced dosage regimens.
Hirota, S; Ishikawa, T; Kanda, T; Matsumoto, Y; Saijo, Y; Sasaki, K, 2023)		0.91
"The reduced dosage of 37."( Sunitinib therapy for imatinib-resistant and/or intolerant gastrointestinal stromal tumors: comparison of safety and efficacy between standard and reduced dosage regimens.
Hirota, S; Ishikawa, T; Kanda, T; Matsumoto, Y; Saijo, Y; Sasaki, K, 2023)		0.91
" The TKI dosing is more flexible than has been described in the registration trials, and dose adjustments can be considered both in the frontline and later-line settings (e."( Management of chronic myeloid leukemia in 2023 - common ground and common sense.
Issa, GC; Jabbour, E; Kantarjian, HM; Lipton, JH; Radich, JP; Sasaki, K; Senapati, J, 2023)		0.91
" Intermittent dosing of imatinib was suggested to delay outgrow of the imatinib-resistant clones in a preclinical study, and it could potentially reduce the adverse events."( A randomised phase 2 study of continuous or intermittent dosing schedule of imatinib re-challenge in patients with tyrosine kinase inhibitor-refractory gastrointestinal stromal tumours.
Kang, YK; Kim, HD; Ryu, MH; Yoo, C, 2023)		0.91
"The intermittent dosage did not improve the efficacy outcomes as compared to the continuous dosage, but showed slightly better safety profiles."( A randomised phase 2 study of continuous or intermittent dosing schedule of imatinib re-challenge in patients with tyrosine kinase inhibitor-refractory gastrointestinal stromal tumours.
Kang, YK; Kim, HD; Ryu, MH; Yoo, C, 2023)		0.91
" Patients receiving sunitinib demonstrated within-cycle variation in self-reported HRQoL, corresponding to the on/off dosing regimen."( Patient-reported outcomes and tolerability in patients receiving ripretinib versus sunitinib after treatment with imatinib in INTRIGUE, a phase 3, open-label study.
Attia, S; Bauer, S; Becker, C; Blay, JY; Boye, K; Chi, P; Druta, M; Gelderblom, H; George, S; Goldstein, D; Harrow, B; Heinrich, MC; Jones, RL; Kang, YK; Le Cesne, A; Razak, AA; Reichmann, W; Ruiz-Soto, R; Rutkowski, P; Sanchez, C; Serrano, C; Sherman, ML; Siontis, BL; Somaiah, N; Steeghs, N; Trent, J; von Mehren, M; Zalcberg, JR, 2023)		0.91
"Patients receiving ripretinib experienced better HRQoL than patients receiving sunitinib during the dosing period and similar HRQoL to patients who had not received sunitinib for 2 weeks for all QLQ-C30 domains except constipation."( Patient-reported outcomes and tolerability in patients receiving ripretinib versus sunitinib after treatment with imatinib in INTRIGUE, a phase 3, open-label study.
Attia, S; Bauer, S; Becker, C; Blay, JY; Boye, K; Chi, P; Druta, M; Gelderblom, H; George, S; Goldstein, D; Harrow, B; Heinrich, MC; Jones, RL; Kang, YK; Le Cesne, A; Razak, AA; Reichmann, W; Ruiz-Soto, R; Rutkowski, P; Sanchez, C; Serrano, C; Sherman, ML; Siontis, BL; Somaiah, N; Steeghs, N; Trent, J; von Mehren, M; Zalcberg, JR, 2023)		0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Roles (4)

RoleDescription
antineoplastic agentA substance that inhibits or prevents the proliferation of neoplasms.
apoptosis inducerAny substance that induces the process of apoptosis (programmed cell death) in multi-celled organisms.
tyrosine kinase inhibitorAny protein kinase inhibitor that interferes with the action of tyrosine kinase.
anticoronaviral agentAny antiviral agent which inhibits the activity of coronaviruses.
[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
methanesulfonate salt
[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 (45)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, MAJOR APURINIC/APYRIMIDINIC ENDONUCLEASEHomo sapiens (human)Potency0.63100.003245.467312,589.2998AID2517
LuciferasePhotinus pyralis (common eastern firefly)Potency12.30180.007215.758889.3584AID1224835
acetylcholinesteraseHomo sapiens (human)Potency34.67130.002541.796015,848.9004AID1347398
glp-1 receptor, partialHomo sapiens (human)Potency28.18380.01846.806014.1254AID624417
thioredoxin reductaseRattus norvegicus (Norway rat)Potency0.28180.100020.879379.4328AID588453
SMAD family member 2Homo sapiens (human)Potency1.34480.173734.304761.8120AID1346859
SMAD family member 3Homo sapiens (human)Potency1.34480.173734.304761.8120AID1346859
TDP1 proteinHomo sapiens (human)Potency21.28890.000811.382244.6684AID686978; AID686979
GLI family zinc finger 3Homo sapiens (human)Potency2.94170.000714.592883.7951AID1259369; AID1259392
AR proteinHomo sapiens (human)Potency28.35740.000221.22318,912.5098AID1259243; AID1259247; AID743035; AID743042; AID743054; AID743063
estrogen receptor 2 (ER beta)Homo sapiens (human)Potency21.13170.000657.913322,387.1992AID1259378
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency13.87550.001022.650876.6163AID1224838; AID1224839; AID1224893
progesterone receptorHomo sapiens (human)Potency26.60320.000417.946075.1148AID1346795
cytochrome P450 family 3 subfamily A polypeptide 4Homo sapiens (human)Potency17.37680.01237.983543.2770AID1645841
glucocorticoid receptor [Homo sapiens]Homo sapiens (human)Potency8.21690.000214.376460.0339AID720691; AID720692
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency4.21630.003041.611522,387.1992AID1159552
retinoid X nuclear receptor alphaHomo sapiens (human)Potency5.75580.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency18.76020.001530.607315,848.9004AID1224841; AID1224842; AID1224848; AID1224849; AID1259401; AID1259403
farnesoid X nuclear receptorHomo sapiens (human)Potency33.48890.375827.485161.6524AID743217
pregnane X nuclear receptorHomo sapiens (human)Potency7.72050.005428.02631,258.9301AID1346982; AID1346985
estrogen nuclear receptor alphaHomo sapiens (human)Potency26.35150.000229.305416,493.5996AID1259244; AID1259248; AID743069; AID743078; AID743079; AID743080; AID743091
peroxisome proliferator-activated receptor deltaHomo sapiens (human)Potency33.48890.001024.504861.6448AID743215
IDH1Homo sapiens (human)Potency20.59620.005210.865235.4813AID686970
aryl hydrocarbon receptorHomo sapiens (human)Potency17.49330.000723.06741,258.9301AID743085; AID743122
cytochrome P450, family 19, subfamily A, polypeptide 1, isoform CRA_aHomo sapiens (human)Potency26.60320.001723.839378.1014AID743083
thyroid stimulating hormone receptorHomo sapiens (human)Potency31.67040.001628.015177.1139AID1259385; AID1259395
parathyroid hormone/parathyroid hormone-related peptide receptor precursorHomo sapiens (human)Potency22.38723.548119.542744.6684AID743266
thyroid hormone receptor beta isoform 2Rattus norvegicus (Norway rat)Potency26.10240.000323.4451159.6830AID743065; AID743067
serine/threonine-protein kinase mTOR isoform 1Homo sapiens (human)Potency16.28730.00378.618923.2809AID651784
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency10.28780.000627.21521,122.0200AID743202; AID743219
DNA polymerase iota isoform a (long)Homo sapiens (human)Potency89.12510.050127.073689.1251AID588590
gemininHomo sapiens (human)Potency1.12200.004611.374133.4983AID624297
Voltage-dependent calcium channel gamma-2 subunitMus musculus (house mouse)Potency26.60320.001557.789015,848.9004AID1259244
Glutamate receptor 2Rattus norvegicus (Norway rat)Potency26.60320.001551.739315,848.9004AID1259244
Spike glycoproteinSevere acute respiratory syndrome-related coronavirusPotency21.49560.009610.525035.4813AID1479145; AID1479148
ATPase family AAA domain-containing protein 5Homo sapiens (human)Potency11.88320.011917.942071.5630AID651632
Ataxin-2Homo sapiens (human)Potency11.88320.011912.222168.7989AID651632
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Tyrosine-protein kinase ABL1Homo sapiens (human)IC50 (µMol)0.31000.00010.712810.0000AID1876062; AID266584
Mast/stem cell growth factor receptor KitHomo sapiens (human)IC50 (µMol)0.10000.00070.470810.0000AID1342286
Platelet-derived growth factor receptor alphaHomo sapiens (human)IC50 (µMol)22.00000.00010.491210.0000AID1342287; AID1342288
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Activation Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Tyrosine-protein kinase ABL1Homo sapiens (human)EC50 (µMol)0.09000.00000.03450.1400AID266585
Mast/stem cell growth factor receptor KitHomo sapiens (human)EC50 (µMol)0.94290.10000.52150.9429AID1342294
Breakpoint cluster region proteinHomo sapiens (human)EC50 (µMol)0.09000.00000.03930.1400AID266585
Platelet-derived growth factor receptor alphaHomo sapiens (human)EC50 (µMol)0.68020.09000.38510.6802AID1342295
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Other Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
DNA repair protein RAD52 homolog isoform aHomo sapiens (human)AC5018.97000.150012.066235.2100AID652116
Cytochrome P450 3A4Homo sapiens (human)Km14.40001.93005.90608.7000AID1214004
Cytochrome P450 2C8Homo sapiens (human)Km9.34000.05002.98255.7000AID1214003; AID1214004
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (282)

Processvia Protein(s)Taxonomy
response to oxidative stressTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of cytosolic calcium ion concentrationTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ubiquitin-protein transferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of phospholipase C activityTyrosine-protein kinase ABL1Homo sapiens (human)
mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
neural tube closureTyrosine-protein kinase ABL1Homo sapiens (human)
B-1 B cell homeostasisTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of protein phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
B cell proliferation involved in immune responseTyrosine-protein kinase ABL1Homo sapiens (human)
transitional one stage B cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
mismatch repairTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of DNA-templated transcriptionTyrosine-protein kinase ABL1Homo sapiens (human)
autophagyTyrosine-protein kinase ABL1Homo sapiens (human)
DNA damage responseTyrosine-protein kinase ABL1Homo sapiens (human)
integrin-mediated signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
canonical NF-kappaB signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
associative learningTyrosine-protein kinase ABL1Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageTyrosine-protein kinase ABL1Homo sapiens (human)
response to xenobiotic stimulusTyrosine-protein kinase ABL1Homo sapiens (human)
post-embryonic developmentTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of autophagyTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of endothelial cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
peptidyl-tyrosine phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
cerebellum morphogenesisTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of cell-cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
microspike assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
actin cytoskeleton organizationTyrosine-protein kinase ABL1Homo sapiens (human)
actin filament polymerizationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of endocytosisTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
neuron differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
BMP signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of BMP signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of axon extensionTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of microtubule polymerizationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of Cdc42 protein signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of type II interferon productionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of interleukin-2 productionTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of actin cytoskeleton organizationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of osteoblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
substrate adhesion-dependent cell spreadingTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to oxidative stressTyrosine-protein kinase ABL1Homo sapiens (human)
response to endoplasmic reticulum stressTyrosine-protein kinase ABL1Homo sapiens (human)
platelet-derived growth factor receptor-beta signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
protein modification processTyrosine-protein kinase ABL1Homo sapiens (human)
peptidyl-tyrosine autophosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
Fc-gamma receptor signaling pathway involved in phagocytosisTyrosine-protein kinase ABL1Homo sapiens (human)
neuropilin signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
signal transduction in response to DNA damageTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of neuron apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
endothelial cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of T cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of vasoconstrictionTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of mitotic cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IITyrosine-protein kinase ABL1Homo sapiens (human)
alpha-beta T cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
protein autophosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of fibroblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
spleen developmentTyrosine-protein kinase ABL1Homo sapiens (human)
thymus developmentTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of peptidyl-tyrosine phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
activated T cell proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
T cell receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
B cell receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
neuromuscular process controlling balanceTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of release of sequestered calcium ion into cytosolTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of oxidoreductase activityTyrosine-protein kinase ABL1Homo sapiens (human)
neuron apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ubiquitin-protein transferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
myoblast proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of stress fiber assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
establishment of localization in cellTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell cycleTyrosine-protein kinase ABL1Homo sapiens (human)
mitochondrial depolarizationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of focal adhesion assemblyTyrosine-protein kinase ABL1Homo sapiens (human)
Bergmann glial cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
cardiac muscle cell proliferationTyrosine-protein kinase ABL1Homo sapiens (human)
neuroepithelial cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to hydrogen peroxideTyrosine-protein kinase ABL1Homo sapiens (human)
ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeTyrosine-protein kinase ABL1Homo sapiens (human)
DNA conformation changeTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to lipopolysaccharideTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to transforming growth factor beta stimulusTyrosine-protein kinase ABL1Homo sapiens (human)
response to epinephrineTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of protein serine/threonine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of cell migration involved in sprouting angiogenesisTyrosine-protein kinase ABL1Homo sapiens (human)
cellular senescenceTyrosine-protein kinase ABL1Homo sapiens (human)
cell-cell adhesionTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of dendrite developmentTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of substrate adhesion-dependent cell spreadingTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of long-term synaptic potentiationTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of hematopoietic stem cell differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of extracellular matrix organizationTyrosine-protein kinase ABL1Homo sapiens (human)
podocyte apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
cellular response to dopamineTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of establishment of T cell polarityTyrosine-protein kinase ABL1Homo sapiens (human)
DN4 thymocyte differentiationTyrosine-protein kinase ABL1Homo sapiens (human)
protein localization to cytoplasmic microtubule plus-endTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of microtubule bindingTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of actin filament bindingTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of modification of synaptic structureTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of blood vessel branchingTyrosine-protein kinase ABL1Homo sapiens (human)
activation of protein kinase C activityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of double-strand break repair via homologous recombinationTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of Wnt signaling pathway, planar cell polarity pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
regulation of cell motilityTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of endothelial cell apoptotic processTyrosine-protein kinase ABL1Homo sapiens (human)
positive regulation of T cell migrationTyrosine-protein kinase ABL1Homo sapiens (human)
negative regulation of cellular senescenceTyrosine-protein kinase ABL1Homo sapiens (human)
epidermal growth factor receptor signaling pathwayTyrosine-protein kinase ABL1Homo sapiens (human)
protein phosphorylationTyrosine-protein kinase ABL1Homo sapiens (human)
lipid hydroxylationCytochrome P450 3A4Homo sapiens (human)
lipid metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid catabolic processCytochrome P450 3A4Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 3A4Homo sapiens (human)
steroid metabolic processCytochrome P450 3A4Homo sapiens (human)
cholesterol metabolic processCytochrome P450 3A4Homo sapiens (human)
androgen metabolic processCytochrome P450 3A4Homo sapiens (human)
estrogen metabolic processCytochrome P450 3A4Homo sapiens (human)
alkaloid catabolic processCytochrome P450 3A4Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 3A4Homo sapiens (human)
calcitriol biosynthetic process from calciolCytochrome P450 3A4Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D metabolic processCytochrome P450 3A4Homo sapiens (human)
vitamin D catabolic processCytochrome P450 3A4Homo sapiens (human)
retinol metabolic processCytochrome P450 3A4Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 3A4Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 3A4Homo sapiens (human)
aflatoxin metabolic processCytochrome P450 3A4Homo sapiens (human)
oxidative demethylationCytochrome P450 3A4Homo sapiens (human)
lipid hydroxylationCytochrome P450 2C8Homo sapiens (human)
organic acid metabolic processCytochrome P450 2C8Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 2C8Homo sapiens (human)
steroid metabolic processCytochrome P450 2C8Homo sapiens (human)
estrogen metabolic processCytochrome P450 2C8Homo sapiens (human)
epoxygenase P450 pathwayCytochrome P450 2C8Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 2C8Homo sapiens (human)
retinol metabolic processCytochrome P450 2C8Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 2C8Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 2C8Homo sapiens (human)
icosanoid biosynthetic processCytochrome P450 2C8Homo sapiens (human)
oxidative demethylationCytochrome P450 2C8Homo sapiens (human)
omega-hydroxylase P450 pathwayCytochrome P450 2C8Homo sapiens (human)
ovarian follicle developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
myeloid progenitor cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
lymphoid progenitor cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
immature B cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
mast cell chemotaxisMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of dendritic cell cytokine productionMast/stem cell growth factor receptor KitHomo sapiens (human)
glycosphingolipid metabolic processMast/stem cell growth factor receptor KitHomo sapiens (human)
inflammatory responseMast/stem cell growth factor receptor KitHomo sapiens (human)
signal transductionMast/stem cell growth factor receptor KitHomo sapiens (human)
spermatogenesisMast/stem cell growth factor receptor KitHomo sapiens (human)
spermatid developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
germ cell migrationMast/stem cell growth factor receptor KitHomo sapiens (human)
regulation of cell shapeMast/stem cell growth factor receptor KitHomo sapiens (human)
visual learningMast/stem cell growth factor receptor KitHomo sapiens (human)
male gonad developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of phospholipase C activityMast/stem cell growth factor receptor KitHomo sapiens (human)
cytokine-mediated signaling pathwayMast/stem cell growth factor receptor KitHomo sapiens (human)
stem cell population maintenanceMast/stem cell growth factor receptor KitHomo sapiens (human)
lamellipodium assemblyMast/stem cell growth factor receptor KitHomo sapiens (human)
actin cytoskeleton organizationMast/stem cell growth factor receptor KitHomo sapiens (human)
hemopoiesisMast/stem cell growth factor receptor KitHomo sapiens (human)
T cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
erythrocyte differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
melanocyte differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of pseudopodium assemblyMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of mast cell cytokine productionMast/stem cell growth factor receptor KitHomo sapiens (human)
somatic stem cell population maintenanceMast/stem cell growth factor receptor KitHomo sapiens (human)
embryonic hemopoiesisMast/stem cell growth factor receptor KitHomo sapiens (human)
ectopic germ cell programmed cell deathMast/stem cell growth factor receptor KitHomo sapiens (human)
intracellular signal transductionMast/stem cell growth factor receptor KitHomo sapiens (human)
hematopoietic stem cell migrationMast/stem cell growth factor receptor KitHomo sapiens (human)
megakaryocyte developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
Fc receptor signaling pathwayMast/stem cell growth factor receptor KitHomo sapiens (human)
Kit signaling pathwayMast/stem cell growth factor receptor KitHomo sapiens (human)
erythropoietin-mediated signaling pathwayMast/stem cell growth factor receptor KitHomo sapiens (human)
regulation of cell population proliferationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of tyrosine phosphorylation of STAT proteinMast/stem cell growth factor receptor KitHomo sapiens (human)
negative regulation of programmed cell deathMast/stem cell growth factor receptor KitHomo sapiens (human)
mast cell degranulationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of MAPK cascadeMast/stem cell growth factor receptor KitHomo sapiens (human)
pigmentationMast/stem cell growth factor receptor KitHomo sapiens (human)
tongue developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of Notch signaling pathwayMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of receptor signaling pathway via JAK-STATMast/stem cell growth factor receptor KitHomo sapiens (human)
response to cadmium ionMast/stem cell growth factor receptor KitHomo sapiens (human)
protein autophosphorylationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of long-term neuronal synaptic plasticityMast/stem cell growth factor receptor KitHomo sapiens (human)
digestive tract developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
stem cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
epithelial cell proliferationMast/stem cell growth factor receptor KitHomo sapiens (human)
detection of mechanical stimulus involved in sensory perception of soundMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of DNA-binding transcription factor activityMast/stem cell growth factor receptor KitHomo sapiens (human)
negative regulation of developmental processMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionMast/stem cell growth factor receptor KitHomo sapiens (human)
cell chemotaxisMast/stem cell growth factor receptor KitHomo sapiens (human)
mast cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
mast cell proliferationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of mast cell proliferationMast/stem cell growth factor receptor KitHomo sapiens (human)
melanocyte migrationMast/stem cell growth factor receptor KitHomo sapiens (human)
melanocyte adhesionMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of pyloric antrum smooth muscle contractionMast/stem cell growth factor receptor KitHomo sapiens (human)
regulation of bile acid metabolic processMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of colon smooth muscle contractionMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of small intestine smooth muscle contractionMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of vascular associated smooth muscle cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
negative regulation of reproductive processMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of cell migrationMast/stem cell growth factor receptor KitHomo sapiens (human)
positive regulation of MAP kinase activityMast/stem cell growth factor receptor KitHomo sapiens (human)
multicellular organism developmentMast/stem cell growth factor receptor KitHomo sapiens (human)
B cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
hematopoietic progenitor cell differentiationMast/stem cell growth factor receptor KitHomo sapiens (human)
negative regulation of cellular extravasationBreakpoint cluster region proteinHomo sapiens (human)
renal system processBreakpoint cluster region proteinHomo sapiens (human)
protein phosphorylationBreakpoint cluster region proteinHomo sapiens (human)
phagocytosisBreakpoint cluster region proteinHomo sapiens (human)
signal transductionBreakpoint cluster region proteinHomo sapiens (human)
small GTPase-mediated signal transductionBreakpoint cluster region proteinHomo sapiens (human)
brain developmentBreakpoint cluster region proteinHomo sapiens (human)
actin cytoskeleton organizationBreakpoint cluster region proteinHomo sapiens (human)
keratinocyte differentiationBreakpoint cluster region proteinHomo sapiens (human)
regulation of Rho protein signal transductionBreakpoint cluster region proteinHomo sapiens (human)
inner ear morphogenesisBreakpoint cluster region proteinHomo sapiens (human)
regulation of vascular permeabilityBreakpoint cluster region proteinHomo sapiens (human)
neutrophil degranulationBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of neutrophil degranulationBreakpoint cluster region proteinHomo sapiens (human)
focal adhesion assemblyBreakpoint cluster region proteinHomo sapiens (human)
homeostasis of number of cellsBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of inflammatory responseBreakpoint cluster region proteinHomo sapiens (human)
positive regulation of phagocytosisBreakpoint cluster region proteinHomo sapiens (human)
modulation of chemical synaptic transmissionBreakpoint cluster region proteinHomo sapiens (human)
neuromuscular process controlling balanceBreakpoint cluster region proteinHomo sapiens (human)
regulation of small GTPase mediated signal transductionBreakpoint cluster region proteinHomo sapiens (human)
regulation of cell cycleBreakpoint cluster region proteinHomo sapiens (human)
definitive hemopoiesisBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of respiratory burstBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of blood vessel remodelingBreakpoint cluster region proteinHomo sapiens (human)
intracellular protein transmembrane transportBreakpoint cluster region proteinHomo sapiens (human)
cellular response to lipopolysaccharideBreakpoint cluster region proteinHomo sapiens (human)
activation of GTPase activityBreakpoint cluster region proteinHomo sapiens (human)
macrophage migrationBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of macrophage migrationBreakpoint cluster region proteinHomo sapiens (human)
negative regulation of reactive oxygen species metabolic processBreakpoint cluster region proteinHomo sapiens (human)
cellular response to reactive oxygen speciesPlatelet-derived growth factor receptor alphaHomo sapiens (human)
luteinizationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
in utero embryonic developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cell activationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
hematopoietic progenitor cell differentiationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
estrogen metabolic processPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of cell population proliferationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
negative regulation of platelet activationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of phospholipase C activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
peptidyl-tyrosine phosphorylationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
signal transduction involved in regulation of gene expressionPlatelet-derived growth factor receptor alphaHomo sapiens (human)
extracellular matrix organizationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
lung developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
adrenal gland developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of cell migrationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
male genitalia developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
regulation of actin cytoskeleton organizationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
Leydig cell differentiationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet-derived growth factor receptor-alpha signaling pathwayPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of cell proliferation by VEGF-activated platelet derived growth factor receptor signaling pathwayPlatelet-derived growth factor receptor alphaHomo sapiens (human)
wound healingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
odontogenesis of dentin-containing toothPlatelet-derived growth factor receptor alphaHomo sapiens (human)
protein autophosphorylationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet-derived growth factor receptor signaling pathwayPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of fibroblast proliferationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
embryonic digestive tract morphogenesisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
embryonic cranial skeleton morphogenesisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
embryonic skeletal system morphogenesisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of calcium-mediated signalingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
white fat cell differentiationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of chemotaxisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cardiac myofibril assemblyPlatelet-derived growth factor receptor alphaHomo sapiens (human)
roof of mouth developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
face morphogenesisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cell chemotaxisPlatelet-derived growth factor receptor alphaHomo sapiens (human)
retina vasculature development in camera-type eyePlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadePlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet aggregationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cellular response to amino acid stimulusPlatelet-derived growth factor receptor alphaHomo sapiens (human)
metanephric glomerular capillary formationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
regulation of mesenchymal stem cell differentiationPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cell surface receptor protein tyrosine kinase signaling pathwayPlatelet-derived growth factor receptor alphaHomo sapiens (human)
positive regulation of kinase activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
multicellular organism developmentPlatelet-derived growth factor receptor alphaHomo sapiens (human)
lipid hydroxylationCytochrome P450 3A5Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 3A5Homo sapiens (human)
steroid metabolic processCytochrome P450 3A5Homo sapiens (human)
estrogen metabolic processCytochrome P450 3A5Homo sapiens (human)
alkaloid catabolic processCytochrome P450 3A5Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 3A5Homo sapiens (human)
retinol metabolic processCytochrome P450 3A5Homo sapiens (human)
retinoic acid metabolic processCytochrome P450 3A5Homo sapiens (human)
aflatoxin metabolic processCytochrome P450 3A5Homo sapiens (human)
oxidative demethylationCytochrome P450 3A5Homo sapiens (human)
cell population proliferationATPase family AAA domain-containing protein 5Homo sapiens (human)
positive regulation of B cell proliferationATPase family AAA domain-containing protein 5Homo sapiens (human)
nuclear DNA replicationATPase family AAA domain-containing protein 5Homo sapiens (human)
signal transduction in response to DNA damageATPase family AAA domain-containing protein 5Homo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorATPase family AAA domain-containing protein 5Homo sapiens (human)
isotype switchingATPase family AAA domain-containing protein 5Homo sapiens (human)
positive regulation of DNA replicationATPase family AAA domain-containing protein 5Homo sapiens (human)
positive regulation of isotype switching to IgG isotypesATPase family AAA domain-containing protein 5Homo sapiens (human)
DNA clamp unloadingATPase family AAA domain-containing protein 5Homo sapiens (human)
regulation of mitotic cell cycle phase transitionATPase family AAA domain-containing protein 5Homo sapiens (human)
negative regulation of intrinsic apoptotic signaling pathway in response to DNA damage by p53 class mediatorATPase family AAA domain-containing protein 5Homo sapiens (human)
positive regulation of cell cycle G2/M phase transitionATPase family AAA domain-containing protein 5Homo sapiens (human)
negative regulation of receptor internalizationAtaxin-2Homo sapiens (human)
regulation of translationAtaxin-2Homo sapiens (human)
RNA metabolic processAtaxin-2Homo sapiens (human)
P-body assemblyAtaxin-2Homo sapiens (human)
stress granule assemblyAtaxin-2Homo sapiens (human)
RNA transportAtaxin-2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (73)

Processvia Protein(s)Taxonomy
supercoiled DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
magnesium ion bindingTyrosine-protein kinase ABL1Homo sapiens (human)
four-way junction DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
bubble DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
phosphotyrosine residue bindingTyrosine-protein kinase ABL1Homo sapiens (human)
DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
transcription coactivator activityTyrosine-protein kinase ABL1Homo sapiens (human)
actin monomer bindingTyrosine-protein kinase ABL1Homo sapiens (human)
nicotinate-nucleotide adenylyltransferase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein tyrosine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
non-membrane spanning protein tyrosine kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
protein kinase C bindingTyrosine-protein kinase ABL1Homo sapiens (human)
protein bindingTyrosine-protein kinase ABL1Homo sapiens (human)
ATP bindingTyrosine-protein kinase ABL1Homo sapiens (human)
kinase activityTyrosine-protein kinase ABL1Homo sapiens (human)
SH3 domain bindingTyrosine-protein kinase ABL1Homo sapiens (human)
syntaxin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
manganese ion bindingTyrosine-protein kinase ABL1Homo sapiens (human)
neuropilin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
SH2 domain bindingTyrosine-protein kinase ABL1Homo sapiens (human)
ephrin receptor bindingTyrosine-protein kinase ABL1Homo sapiens (human)
actin filament bindingTyrosine-protein kinase ABL1Homo sapiens (human)
mitogen-activated protein kinase bindingTyrosine-protein kinase ABL1Homo sapiens (human)
proline-rich region bindingTyrosine-protein kinase ABL1Homo sapiens (human)
delta-catenin bindingTyrosine-protein kinase ABL1Homo sapiens (human)
sequence-specific double-stranded DNA bindingTyrosine-protein kinase ABL1Homo sapiens (human)
monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
steroid bindingCytochrome P450 3A4Homo sapiens (human)
iron ion bindingCytochrome P450 3A4Homo sapiens (human)
protein bindingCytochrome P450 3A4Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
oxidoreductase activityCytochrome P450 3A4Homo sapiens (human)
oxygen bindingCytochrome P450 3A4Homo sapiens (human)
enzyme bindingCytochrome P450 3A4Homo sapiens (human)
heme bindingCytochrome P450 3A4Homo sapiens (human)
vitamin D3 25-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
caffeine oxidase activityCytochrome P450 3A4Homo sapiens (human)
quinine 3-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
testosterone 6-beta-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1-alpha,25-dihydroxyvitamin D3 23-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 8,9 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 11,12 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
anandamide 14,15 epoxidase activityCytochrome P450 3A4Homo sapiens (human)
aromatase activityCytochrome P450 3A4Homo sapiens (human)
vitamin D 24-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
estrogen 2-hydroxylase activityCytochrome P450 3A4Homo sapiens (human)
1,8-cineole 2-exo-monooxygenase activityCytochrome P450 3A4Homo sapiens (human)
monooxygenase activityCytochrome P450 2C8Homo sapiens (human)
iron ion bindingCytochrome P450 2C8Homo sapiens (human)
protein bindingCytochrome P450 2C8Homo sapiens (human)
arachidonic acid epoxygenase activityCytochrome P450 2C8Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 2C8Homo sapiens (human)
caffeine oxidase activityCytochrome P450 2C8Homo sapiens (human)
aromatase activityCytochrome P450 2C8Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 2C8Homo sapiens (human)
heme bindingCytochrome P450 2C8Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygen, reduced flavin or flavoprotein as one donor, and incorporation of one atom of oxygenCytochrome P450 2C8Homo sapiens (human)
protease bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
protein tyrosine kinase activityMast/stem cell growth factor receptor KitHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activityMast/stem cell growth factor receptor KitHomo sapiens (human)
stem cell factor receptor activityMast/stem cell growth factor receptor KitHomo sapiens (human)
protein bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
ATP bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
cytokine bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
SH2 domain bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
protein homodimerization activityMast/stem cell growth factor receptor KitHomo sapiens (human)
metal ion bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
growth factor bindingMast/stem cell growth factor receptor KitHomo sapiens (human)
protein serine/threonine kinase activityBreakpoint cluster region proteinHomo sapiens (human)
protein tyrosine kinase activityBreakpoint cluster region proteinHomo sapiens (human)
guanyl-nucleotide exchange factor activityBreakpoint cluster region proteinHomo sapiens (human)
GTPase activator activityBreakpoint cluster region proteinHomo sapiens (human)
protein bindingBreakpoint cluster region proteinHomo sapiens (human)
ATP bindingBreakpoint cluster region proteinHomo sapiens (human)
protein serine kinase activityBreakpoint cluster region proteinHomo sapiens (human)
protein kinase activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
transmembrane receptor protein tyrosine kinase activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet-derived growth factor alpha-receptor activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
vascular endothelial growth factor receptor activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet-derived growth factor receptor bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
protein bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
ATP bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
vascular endothelial growth factor bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
protein homodimerization activityPlatelet-derived growth factor receptor alphaHomo sapiens (human)
protein-containing complex bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
platelet-derived growth factor bindingPlatelet-derived growth factor receptor alphaHomo sapiens (human)
monooxygenase activityCytochrome P450 3A5Homo sapiens (human)
iron ion bindingCytochrome P450 3A5Homo sapiens (human)
protein bindingCytochrome P450 3A5Homo sapiens (human)
retinoic acid 4-hydroxylase activityCytochrome P450 3A5Homo sapiens (human)
oxidoreductase activityCytochrome P450 3A5Homo sapiens (human)
oxygen bindingCytochrome P450 3A5Homo sapiens (human)
heme bindingCytochrome P450 3A5Homo sapiens (human)
aromatase activityCytochrome P450 3A5Homo sapiens (human)
estrogen 16-alpha-hydroxylase activityCytochrome P450 3A5Homo sapiens (human)
testosterone 6-beta-hydroxylase activityCytochrome P450 3A5Homo sapiens (human)
protein bindingATPase family AAA domain-containing protein 5Homo sapiens (human)
ATP bindingATPase family AAA domain-containing protein 5Homo sapiens (human)
ATP hydrolysis activityATPase family AAA domain-containing protein 5Homo sapiens (human)
DNA clamp unloader activityATPase family AAA domain-containing protein 5Homo sapiens (human)
DNA bindingATPase family AAA domain-containing protein 5Homo sapiens (human)
RNA bindingAtaxin-2Homo sapiens (human)
epidermal growth factor receptor bindingAtaxin-2Homo sapiens (human)
protein bindingAtaxin-2Homo sapiens (human)
mRNA bindingAtaxin-2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (42)

Processvia Protein(s)Taxonomy
ruffleTyrosine-protein kinase ABL1Homo sapiens (human)
nucleusTyrosine-protein kinase ABL1Homo sapiens (human)
nucleoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
nucleolusTyrosine-protein kinase ABL1Homo sapiens (human)
cytoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
mitochondrionTyrosine-protein kinase ABL1Homo sapiens (human)
cytosolTyrosine-protein kinase ABL1Homo sapiens (human)
actin cytoskeletonTyrosine-protein kinase ABL1Homo sapiens (human)
nuclear bodyTyrosine-protein kinase ABL1Homo sapiens (human)
dendriteTyrosine-protein kinase ABL1Homo sapiens (human)
growth coneTyrosine-protein kinase ABL1Homo sapiens (human)
nuclear membraneTyrosine-protein kinase ABL1Homo sapiens (human)
neuronal cell bodyTyrosine-protein kinase ABL1Homo sapiens (human)
perinuclear region of cytoplasmTyrosine-protein kinase ABL1Homo sapiens (human)
postsynapseTyrosine-protein kinase ABL1Homo sapiens (human)
protein-containing complexTyrosine-protein kinase ABL1Homo sapiens (human)
plasma membraneTyrosine-protein kinase ABL1Homo sapiens (human)
cytoplasmCytochrome P450 3A4Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 3A4Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 3A4Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2C8Homo sapiens (human)
plasma membraneCytochrome P450 2C8Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C8Homo sapiens (human)
cytoplasmCytochrome P450 2C8Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C8Homo sapiens (human)
fibrillar centerMast/stem cell growth factor receptor KitHomo sapiens (human)
acrosomal vesicleMast/stem cell growth factor receptor KitHomo sapiens (human)
extracellular spaceMast/stem cell growth factor receptor KitHomo sapiens (human)
plasma membraneMast/stem cell growth factor receptor KitHomo sapiens (human)
cell-cell junctionMast/stem cell growth factor receptor KitHomo sapiens (human)
external side of plasma membraneMast/stem cell growth factor receptor KitHomo sapiens (human)
cytoplasmic side of plasma membraneMast/stem cell growth factor receptor KitHomo sapiens (human)
plasma membraneMast/stem cell growth factor receptor KitHomo sapiens (human)
receptor complexMast/stem cell growth factor receptor KitHomo sapiens (human)
cytosolBreakpoint cluster region proteinHomo sapiens (human)
plasma membraneBreakpoint cluster region proteinHomo sapiens (human)
postsynaptic densityBreakpoint cluster region proteinHomo sapiens (human)
membraneBreakpoint cluster region proteinHomo sapiens (human)
axonBreakpoint cluster region proteinHomo sapiens (human)
dendritic spineBreakpoint cluster region proteinHomo sapiens (human)
extracellular exosomeBreakpoint cluster region proteinHomo sapiens (human)
protein-containing complexBreakpoint cluster region proteinHomo sapiens (human)
Schaffer collateral - CA1 synapseBreakpoint cluster region proteinHomo sapiens (human)
glutamatergic synapseBreakpoint cluster region proteinHomo sapiens (human)
membraneBreakpoint cluster region proteinHomo sapiens (human)
nucleusPlatelet-derived growth factor receptor alphaHomo sapiens (human)
nucleoplasmPlatelet-derived growth factor receptor alphaHomo sapiens (human)
cytoplasmPlatelet-derived growth factor receptor alphaHomo sapiens (human)
endoplasmic reticulum membranePlatelet-derived growth factor receptor alphaHomo sapiens (human)
Golgi apparatusPlatelet-derived growth factor receptor alphaHomo sapiens (human)
plasma membranePlatelet-derived growth factor receptor alphaHomo sapiens (human)
microvillusPlatelet-derived growth factor receptor alphaHomo sapiens (human)
ciliumPlatelet-derived growth factor receptor alphaHomo sapiens (human)
external side of plasma membranePlatelet-derived growth factor receptor alphaHomo sapiens (human)
membranePlatelet-derived growth factor receptor alphaHomo sapiens (human)
cell junctionPlatelet-derived growth factor receptor alphaHomo sapiens (human)
protein-containing complexPlatelet-derived growth factor receptor alphaHomo sapiens (human)
receptor complexPlatelet-derived growth factor receptor alphaHomo sapiens (human)
plasma membranePlatelet-derived growth factor receptor alphaHomo sapiens (human)
plasma membraneGlutamate receptor 2Rattus norvegicus (Norway rat)
endoplasmic reticulum membraneCytochrome P450 3A5Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 3A5Homo sapiens (human)
virion membraneSpike glycoproteinSevere acute respiratory syndrome-related coronavirus
Elg1 RFC-like complexATPase family AAA domain-containing protein 5Homo sapiens (human)
nucleusATPase family AAA domain-containing protein 5Homo sapiens (human)
cytoplasmAtaxin-2Homo sapiens (human)
Golgi apparatusAtaxin-2Homo sapiens (human)
trans-Golgi networkAtaxin-2Homo sapiens (human)
cytosolAtaxin-2Homo sapiens (human)
cytoplasmic stress granuleAtaxin-2Homo sapiens (human)
membraneAtaxin-2Homo sapiens (human)
perinuclear region of cytoplasmAtaxin-2Homo sapiens (human)
ribonucleoprotein complexAtaxin-2Homo sapiens (human)
cytoplasmic stress granuleAtaxin-2Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (221)

Assay IDTitleYearJournalArticle
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.
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
AID1347407qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Pharmaceutical Collection2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347100qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for LAN-5 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
AID1347425Rhodamine-PBP qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
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.
AID1347424RapidFire Mass Spectrometry qHTS Assay for Modulators of WT P53-Induced Phosphatase 1 (WIP1)2019The Journal of biological chemistry, 11-15, Volume: 294, Issue:46
Physiologically relevant orthogonal assays for the discovery of small-molecule modulators of WIP1 phosphatase in high-throughput screens.
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.
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.
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.
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.
AID1347086qHTS for Inhibitors of the Functional Ribonucleoprotein Complex (vRNP) of Lymphocytic Choriomeningitis Arenaviruses (LCMV): LCMV Primary Screen - GLuc reporter signal2020Antiviral research, 01, Volume: 173A cell-based, infectious-free, platform to identify inhibitors of lassa virus ribonucleoprotein (vRNP) activity.
AID1347154Primary screen GU AMC qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
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.
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.
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.
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.
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.
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.
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.
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.
AID1346986P-glycoprotein substrates identified in KB-3-1 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1346987P-glycoprotein substrates identified in KB-8-5-11 adenocarcinoma cell line, qHTS therapeutic library screen2019Molecular pharmacology, 11, Volume: 96, Issue:5
A High-Throughput Screen of a Library of Therapeutics Identifies Cytotoxic Substrates of P-glycoprotein.
AID1876064Cytotoxicity against African green monkey Vero E6 cells2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1224763Delta TM value showing the stabilisation of CLK3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID764723Induction of apoptosis in human imatinib mesylate-resistant LAMA-84 cells at 1 uM after 3 hrs using propidium iodide staining by FACS analysis2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Evaluation of novel aryloxyalkyl derivatives of imidazole and 1,2,4-triazole as heme oxygenase-1 (HO-1) inhibitors and their antitumor properties.
AID1426821Cytotoxicity against human K562 cells measured after 72 hrs by MTT assay2017Journal of medicinal chemistry, 02-09, Volume: 60, Issue:3
Total Syntheses and Biological Activities of Vinylamycin Analogues.
AID1875893Antiviral activity against SARS-CoV infected in 2 hrs pretreated African green monkey Vero E6 cells assessed as inhibition of cytopathic effect incubated for 48 hrs by celltitre-glo luminescent assay2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1224755Delta TM value showing the stabilisation of CAMK4 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224797Delta TM value showing the stabilisation of MPSK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680872Inhibition of Abl (unknown origin) at 3.3 uM relative control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1214029Activity of human recombinant CYP2A6 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID682137TP_TRANSPORTER: increase in Topotecan intracellular accumulation (Topotecan: 1 uM, Imanitib mesylate: 1 uM) in BCRP-expressing SaoS2 cells2004Cancer research, Apr-01, Volume: 64, Issue:7
Imatinib mesylate is a potent inhibitor of the ABCG2 (BCRP) transporter and reverses resistance to topotecan and SN-38 in vitro.
AID1224796Delta TM value showing the stabilisation of LOK produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680874Inhibition of Abl (unknown origin) at 10 uM relative control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1214027Cmax in chronic myeloid leukemia patient at 400 mg, qd by multiple dose study2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224748Delta TM value showing the stabilisation of AMPKA2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID588213Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in non-rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1224792Delta TM value showing the stabilisation of RIOK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680904Induction of 16 kDa CTF-141 bands in mouse N2a695 cells expressing human APP assessed as at 10 uM incubated for 5 hrs by Western blot analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213996Activity of human recombinant CYP2C8 in supersomes assessed as intrinsic clearance for enzyme-mediated N-desmethylimatinib formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1680887Stability in mouse liver microsomes assessed as parent compound remaining level at 1 uM after 1 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1680873Inhibition of Abl (unknown origin) at 1 uM relative control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1214036Activity of human recombinant CYP3A4 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 0.1 to 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1779214Cytotoxicity against Bcr-Abl expressing human KU812 cells assessed as cell growth inhibition measured after 48 hrs by MTT assay2021European journal of medicinal chemistry, Oct-05, Volume: 221Discovery of pyrrole derivatives for the treatment of glioblastoma and chronic myeloid leukemia.
AID1680888Stability in human liver microsomes assessed as parent compound remaining level at 10 uM after 0.5 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213985Activity of human recombinant CYP1A2 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224773Delta TM value showing the stabilisation of ASK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224757Delta TM value showing the stabilisation of CDK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID764731Cytotoxicity against human imatinib mesylate-resistant LAMA-84 cells assessed as reduction of cell survival at 1 uM after 20 mins by ATP-lite1step assay2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Evaluation of novel aryloxyalkyl derivatives of imidazole and 1,2,4-triazole as heme oxygenase-1 (HO-1) inhibitors and their antitumor properties.
AID1213984Activity of human recombinant CYP3A4 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1680885Stability in human liver microsomes assessed as parent compound remaining level at 10 uM after 1 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213994Activity of human recombinant CYP1A2 in supersomes assessed as intrinsic clearance for enzyme-mediated drug metabolism by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID629494Cytotoxicity against human MCF7 cells after 24 hrs by MTT assay2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1224764Delta TM value showing the stabilisation of CK1G1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214002Activity of human recombinant CYP3A5 in supersomes assessed as intrinsic clearance for enzyme-mediated metabolite formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224774Delta TM value showing the stabilisation of p38beta produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID680881TP_TRANSPORTER: efflux in MDR1-expressing LLC-PK1 cells2003The Journal of pharmacology and experimental therapeutics, Nov, Volume: 307, Issue:2
Interaction of imatinib mesilate with human P-glycoprotein.
AID1224795Delta TM value showing the stabilisation of SLK produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680892Inhibition of beta-secretase in mouse N2a cells expressed in FL-APP assessed as reduction of sAPPalpha levels at 10 uM incubated for 5 hrs by MSD-ELISA relative to control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213989Activity of human recombinant CYP2C9 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID404304Effect on human MRP2-mediated estradiol-17-beta-glucuronide transport in Sf9 cells inverted membrane vesicles relative to control2008Journal of medicinal chemistry, Jun-12, Volume: 51, Issue:11
Prediction and identification of drug interactions with the human ATP-binding cassette transporter multidrug-resistance associated protein 2 (MRP2; ABCC2).
AID1224776Delta TM value showing the stabilisation of ERK3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214033Activity of human recombinant CYP2D6 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214004Activity of human recombinant CYP3A4 in supersomes after 3 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214008Fraction unbound in human liver microsomes containing CYP2C8 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224805Delta TM value showing the stabilisation of VRK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214006Fraction unbound in human liver microsomes containing CYP1A2 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224750Delta TM value showing the stabilisation of CAMK1G produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID360938Inhibition of formation of erythroid burst-forming units in human polycythemia vera cells at 1 uM2007The Journal of biological chemistry, Feb-09, Volume: 282, Issue:6
Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth.
AID1224777Delta TM value showing the stabilisation of MST4(1) produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1743004Antiproliferative activity against human A549 cells assessed as reduction in cell viability incubated for 48 hrs by xCELLigence RTCA2020European journal of medicinal chemistry, Dec-01, Volume: 207Design, synthesis and anti-cancer activity of pyrrole-imidazole polyamides through target-downregulation of c-kit gene expression.
AID1224771Delta TM value showing the stabilisation of MEK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680886Stability in mouse liver microsomes assessed as parent compound remaining level at 10 uM after 1 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1680890Stability in mouse liver microsomes assessed as parent compound remaining level at 10 uM after 0.5 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213988Activity of human recombinant CYP2C19 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1213983Activity of human recombinant CYP2C8 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID360729Inhibition of human JAK2 V617F mutant expressed in COS7 cells2007The Journal of biological chemistry, Feb-09, Volume: 282, Issue:6
Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth.
AID1214031Activity of human recombinant CYP2C9 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214030Activity of human recombinant CYP2B6 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224769Delta TM value showing the stabilisation of GSK3B produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1876062Inhibition of c-Abl (unknown origin)2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1214009Fraction unbound in human liver microsomes containing CYP2D6 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224758Delta TM value showing the stabilisation of CDK6 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214010Fraction unbound in human liver microsomes containing CYP3A4 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1213995Activity of human recombinant CYP2B6 in supersomes assessed as intrinsic clearance for enzyme-mediated drug metabolism by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1876063Antiviral activity against MERS-CoV2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1224760Delta TM value showing the stabilisation of CHEK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1512396Inhibition of BACE1 in mouse N2a695 cells assessed as reduction in Abeta40 production at 10 uM incubated for 6 hrs by ELISA
AID629493Cytotoxicity against human K562 cells after 24 hrs by MTT assay2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1224788Delta TM value showing the stabilisation of PIM3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224803Delta TM value showing the stabilisation of PBK produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1359969Inhibition of porcine brain GSK-3alpha/beta using YRRAAVPPSPSLSRHSSPHQSpEDEEE as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1224768Delta TM value showing the stabilisation of DMPK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213999Activity of human recombinant CYP3A4 in supersomes assessed as intrinsic clearance for enzyme-mediated N-desmethylimatinib formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214025Elimination half life in chronic myeloid leukemia patient2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224749Delta TM value showing the stabilisation of CAMK1D produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224756Delta TM value showing the stabilisation of CAMKK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213992Activity of human recombinant CYP3A4 in supersomes assessed as enzyme-mediated metabolite M5 formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1680897Inhibition of beta-secretase in mouse N2a cells expressed in FL-APP assessed as increase in APP alpha-CTF levels at 10 uM incubated for 5 hrs by MSD-ELISA relative to control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224767Delta TM value showing the stabilisation of DAPK3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224782Delta TM value showing the stabilisation of PAK5 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214034Activity of human recombinant CYP2E1 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID588211Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in humans2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1214020Activity of CYP2C8 in human liver microsomes assessed as inhibition of montelukast-mediated N-desmethylimatinib formation at 0.1 uM after 5 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1779215Cytotoxicity against Imatinib mesylate sensitive wild-type human KBM5 cells assessed as cell growth inhibition measured after 48 hrs by MTT assay2021European journal of medicinal chemistry, Oct-05, Volume: 221Discovery of pyrrole derivatives for the treatment of glioblastoma and chronic myeloid leukemia.
AID1680891Stability in mouse liver microsomes assessed as parent compound remaining level at 1 uM after 0.5 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213986Activity of human recombinant CYP3A5 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 0.1 to 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224765Delta TM value showing the stabilisation of CK1G2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680901Inhibition of gamma secretase in mouse N2a cells expressing APP-C99 assessed as reduction of A-beta levels at 10 uM incubated for 5 hrs by MSD-ELISA2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID680974TP_TRANSPORTER: uptake in BCRP-expressing HEK cells2004Blood, Nov-01, Volume: 104, Issue:9
Imatinib mesylate (STI571) is a substrate for the breast cancer resistance protein (BCRP)/ABCG2 drug pump.
AID1224793Delta TM value showing the stabilisation of RSK2a produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214035Activity of human recombinant CYP2C8 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 0.1 to 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1359964Inhibition of human CDK2/CyclinA using histone H1 as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID629497Cell cycle arrest in human K562 cells assessed as accumulation at G1 phase at 10 uM after 24 hrs by propidium iodide staining-based FACS analysis (Rvb = 74.25 +/- 1.511 %)2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1359968Inhibition of porcine brain CK1delta/epsilon using RRKHAAIGSpAYSITA as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1224761Delta TM value showing the stabilisation of CLK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224780Delta TM value showing the stabilisation of OSR1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213991Activity of human recombinant CYP2D6 in supersomes assessed as enzyme-mediated metabolite M5 formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1359965Inhibition of recombinant human CDK9/CyclinT expressed in baculovirus infected Sf9 insect cells using YSPTSPSYSPTSPSYSPTSPSKKKK as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1224770Delta TM value showing the stabilisation of JAK1~B produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214023Activity of CYP3A4 in human liver microsomes assessed as inhibition of troleandomycin-mediated N-desmethylimatinib formation at 0.1 uM after 5 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214024Oral bioavailability in chronic myeloid leukemia patient2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224781Delta TM value showing the stabilisation of PAK4 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680905Inhibition of beta secretase in mouse N2a695 cells expressing human APP assessed as induction of 16 kDa CTF-141 bands at 10 uM incubated for 5 hrs by Western blot analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224778Delta TM value showing the stabilisation of NEK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224784Delta TM value showing the stabilisation of PCTK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID629496Cell cycle arrest in human K562 cells assessed as accumulation at sub-G1 phase at 10 uM after 24 hrs by propidium iodide staining-based FACS analysis (Rvb = 0.27 +/- 0.04 %)2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1224802Delta TM value showing the stabilisation of TNIK produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214011Fraction unbound in human liver microsomes containing CYP3A5 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224794Delta TM value showing the stabilisation of RSK2b produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID629498Cell cycle arrest in human K562 cells assessed as accumulation at S phase at 10 uM after 24 hrs by propidium iodide staining-based FACS analysis (Rvb = 11.23 +/- 0.8 %)2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1680909Drug level in C57BL/6J mouse brain at 50 mg/kg, ip measured after 4 hrs by LC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224789Delta TM value showing the stabilisation of PLK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID629499Cell cycle arrest in human K562 cells assessed as accumulation at G2/M phase at 10 uM after 24 hrs by propidium iodide staining-based FACS analysis (Rvb = 14.24 +/- 0.76 %)2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1214001Activity of human recombinant CYP3A5 in supersomes assessed as intrinsic clearance for enzyme-mediated N-desmethylimatinib formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID595155Growth inhibition of human GIST882 cells expressing c-Kit after 96 hrs by SRB assay2010ACS medicinal chemistry letters, Oct-14, Volume: 1, Issue:7
Targeting the c-Kit Promoter G-quadruplexes with 6-Substituted Indenoisoquinolines.
AID1224791Delta TM value showing the stabilisation of PRKACA produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224752Delta TM value showing the stabilisation of CAMK2B produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680884Stability in human liver microsomes assessed as parent compound remaining level at 1 uM after 1 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1214028Activity of human recombinant CYP3A5 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID360732Growth inhibition of human chronic myelogenous leukemia cells expressing BCR-ABL protein2007The Journal of biological chemistry, Feb-09, Volume: 282, Issue:6
Erlotinib effectively inhibits JAK2V617F activity and polycythemia vera cell growth.
AID1875917Antiviral activity against SARS-CoV2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1224786Delta TM value showing the stabilisation of PIM1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214022Activity of CYP3A4 in human liver microsomes assessed as inhibition of ketoconazole-mediated N-desmethylimatinib formation at 0.1 uM after 5 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1779216Cytotoxicity against imatinib mesylate resistant wild-type human KBM5 cells expressing T315I mutant assessed as cell growth inhibition measured after 48 hrs by MTT assay2021European journal of medicinal chemistry, Oct-05, Volume: 221Discovery of pyrrole derivatives for the treatment of glioblastoma and chronic myeloid leukemia.
AID1224790Delta TM value showing the stabilisation of PLK4 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1743002Antiproliferative activity against human MKN-45 cells assessed as reduction in cell viability incubated for 48 hrs by xCELLigence RTCA2020European journal of medicinal chemistry, Dec-01, Volume: 207Design, synthesis and anti-cancer activity of pyrrole-imidazole polyamides through target-downregulation of c-kit gene expression.
AID1680889Stability in human liver microsomes assessed as parent compound remaining level at 1 uM after 0.5 hrs by HPLC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224787Delta TM value showing the stabilisation of PIM2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213998Activity of human recombinant CYP2D6 in supersomes assessed as intrinsic clearance for enzyme-mediated drug metabolism by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1359963Inhibition of recombinant rat DYRK1A kinase domain (1 to 499 residues) expressed in bacterial expression system using KKISGRLSPIMTEQ as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1680900Inhibition of beta secretase in mouse N2a cells expressing FL APP695 assessed as reduction of A-beta levels at 10 uM incubated for 5 hrs by MSD-ELISA2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1214003Activity of human recombinant CYP2C8 in supersomes after 4 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224800Delta TM value showing the stabilisation of MST4 (2) produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1743001Antiproliferative activity against human Bel-7402 cells assessed as reduction in cell viability incubated for 48 hrs by xCELLigence RTCA2020European journal of medicinal chemistry, Dec-01, Volume: 207Design, synthesis and anti-cancer activity of pyrrole-imidazole polyamides through target-downregulation of c-kit gene expression.
AID1224753Delta TM value showing the stabilisation of CAMK2D produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224801Delta TM value showing the stabilisation of MST1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224799Delta TM value showing the stabilisation of NDR1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1680894Inhibition of BACE1 (unknown origin) at 10 uM2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1213987Activity of human recombinant CYP2D6 in supersomes assessed as enzyme-mediated N-desmethylimatinib formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224754Delta TM value showing the stabilisation of CAMK2G produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224807Delta TM value showing the stabilisation of YSK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID396071Induction of apoptosis in human K562 cells after 48 hrs2008European journal of medicinal chemistry, Nov, Volume: 43, Issue:11
Synthesis and induction of G0-G1 phase arrest with apoptosis of 3,5-dimethyl-6-phenyl-8-(trifluoromethyl)-5,6-dihydropyrazolo[3,4-f][1,2,3,5]tetrazepin-4(3H)-one.
AID764728Cell cycle arrest in human imatinib mesylate-resistant LAMA-84 cells assessed as accumulation at S and G2/M phase at 1 uM after 3 hrs by FACS analysis2013Bioorganic & medicinal chemistry, Sep-01, Volume: 21, Issue:17
Evaluation of novel aryloxyalkyl derivatives of imidazole and 1,2,4-triazole as heme oxygenase-1 (HO-1) inhibitors and their antitumor properties.
AID1224798Delta TM value showing the stabilisation of DRAK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID266584Inhibition of c-ABL2006Bioorganic & medicinal chemistry letters, Jul-15, Volume: 16, Issue:14
3-Benzimidazol-2-yl-1H-indazoles as potent c-ABL inhibitors.
AID629495Cytotoxicity against human MDA-MB-231 cells after 24 hrs by MTT assay2011European journal of medicinal chemistry, Dec, Volume: 46, Issue:12
Synthesis and apoptosis inducing ability of new anilino substituted pyrimidine sulfonamides as potential anticancer agents.
AID1224785Delta TM value showing the stabilisation of PDK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1214021Activity of CYP2C8 in human liver microsomes assessed as inhibition of GEM-G-mediated N-desmethylimatinib formation at 0.1 uM after 5 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1680893Inhibition of beta-secretase in mouse N2a cells expressed in FL-APP assessed as reduction of sAPPbeta levels at 10 uM incubated for 5 hrs by MSD-ELISA relative to control2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1680915Inhibition of beta secretase in mouse N2a695 cells assessed as reduction in A-beta 40 levels at 10 uM incubated for 5 hrs by ELISA2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224751Delta TM value showing the stabilisation of CAMK2A produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224772Delta TM value showing the stabilisation of MAP2K6 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224775Delta TM value showing the stabilisation of ERK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1743003Antiproliferative activity against human SGC7901 cells assessed as reduction in cell viability incubated for 48 hrs by xCELLigence RTCA2020European journal of medicinal chemistry, Dec-01, Volume: 207Design, synthesis and anti-cancer activity of pyrrole-imidazole polyamides through target-downregulation of c-kit gene expression.
AID1680908Drug level in C57BL/6J mouse plasma at 50 mg/kg, ip measured after 4 hrs by LC-MS/MS analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224806Delta TM value showing the stabilisation of VRK3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1224766Delta TM value showing the stabilisation of CK1G3 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1359970Cytotoxicity against human KU812 cells assessed as reduction in cell viability after 48 hrs by MTT assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID266585Antiproliferative activity against K562 cells expressing Bcr-Abl2006Bioorganic & medicinal chemistry letters, Jul-15, Volume: 16, Issue:14
3-Benzimidazol-2-yl-1H-indazoles as potent c-ABL inhibitors.
AID1214000Activity of human recombinant CYP3A4 in supersomes assessed as intrinsic clearance for enzyme-mediated metabolite formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224783Delta TM value showing the stabilisation of PAK6 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213993Activity of human recombinant CYP3A4 in supersomes assessed as enzyme-mediated metabolite M6 formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1359966Inhibition of recombinant human haspin kinase domain (470 to 798 residues) expressed in bacterial expression system using histone H3 peptide as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1680903Inhibition of beta secretase in mouse N2a695 cells expressing human APP A673T mutant assessed as induction of 16 kDa CTF-141 bands at 10 uM incubated for 5 hrs by Western blot analysis2019Journal of medicinal chemistry, 03-28, Volume: 62, Issue:6
Development of Gleevec Analogues for Reducing Production of β-Amyloid Peptides through Shifting β-Cleavage of Amyloid Precursor Proteins.
AID1224804Delta TM value showing the stabilisation of VRK1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID588212Literature-mined compound from Fourches et al multi-species drug-induced liver injury (DILI) dataset, effect in rodents2010Chemical research in toxicology, Jan, Volume: 23, Issue:1
Cheminformatics analysis of assertions mined from literature that describe drug-induced liver injury in different species.
AID1224762Delta TM value showing the stabilisation of CLK2 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213997Activity of human recombinant CYP2C8 in supersomes assessed as intrinsic clearance for enzyme-mediated metabolite formation by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214032Activity of human recombinant CYP2C19 in supersomes assessed as enzyme-mediated drug metabolism measured as parent compound remaining at 0.1 to 1 uM after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214005Activity of human recombinant CYP3A5 in supersomes after 30 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224759Delta TM value showing the stabilisation of CDKL1 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID1213990Activity of human recombinant CYP2C8 in supersomes assessed as enzyme-mediated metabolite M6 formation at 1 uM after 60 mins by LC/MS analysis2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1875892Antiviral activity against MERS-CoV infected in 1 hr pretreated African green monkey Vero E6 cells ssessed as inhibition of cytopathic effect incubated for 48 hrs by plate reader method2022Journal of medicinal chemistry, 01-27, Volume: 65, Issue:2
Recent Developments in the Use of Kinase Inhibitors for Management of Viral Infections.
AID1359967Inhibition of recombinant mouse CLK1 expressed in bacterial expression system using GRSRSRSRSRSR as substrate after 30 mins by ADP-Glo reagent based luminescence assay2018European journal of medicinal chemistry, Jun-25, Volume: 154Structure-based design of novel quinoxaline-2-carboxylic acids and analogues as Pim-1 inhibitors.
AID1214007Fraction unbound in human liver microsomes containing CYP2B6 after 60 mins2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1214026Cmin in chronic myeloid leukemia patient at 400 mg, qd by multiple dose study2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Autoinhibition of CYP3A4 leads to important role of CYP2C8 in imatinib metabolism: variability in CYP2C8 activity may alter plasma concentrations and response.
AID1224779Delta TM value showing the stabilisation of NEK6 produced by compound binding2007Proceedings of the National Academy of Sciences of the United States of America, Dec-18, Volume: 104, Issue:51
A systematic interaction map of validated kinase inhibitors with Ser/Thr kinases.
AID595156Growth inhibition of human HT-29 cells expressing c-Kit after 96 hrs by SRB assay2010ACS medicinal chemistry letters, Oct-14, Volume: 1, Issue:7
Targeting the c-Kit Promoter G-quadruplexes with 6-Substituted Indenoisoquinolines.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588499High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain A protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588497High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Botulinum neurotoxin light chain F protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Current protocols in cytometry, Oct, Volume: Chapter 13Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2006Cytometry. Part A : the journal of the International Society for Analytical Cytology, May, Volume: 69, Issue:5
Microsphere-based protease assays and screening application for lethal factor and factor Xa.
AID588501High-throughput multiplex microsphere screening for inhibitors of toxin protease, specifically Lethal Factor Protease, MLPCN compound set2010Assay and drug development technologies, Feb, Volume: 8, Issue:1
High-throughput multiplex flow cytometry screening for botulinum neurotoxin type a light chain protease inhibitors.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).2014Journal of biomolecular screening, Jul, Volume: 19, Issue:6
A High-Throughput Assay to Identify Inhibitors of the Apicoplast DNA Polymerase from Plasmodium falciparum.
AID1794808Fluorescence-based screening to identify small molecule inhibitors of Plasmodium falciparum apicoplast DNA polymerase (Pf-apPOL).
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (11,074)

TimeframeStudies, This Drug (%)All Drugs %
pre-19900 (0.00)18.7374
1990's17 (0.15)18.2507
2000's4641 (41.91)29.6817
2010's5115 (46.19)24.3611
2020's1301 (11.75)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 59.02

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

MetricThis Compound (vs All)
Research Demand Index59.02 (24.57)
Research Supply Index9.43 (2.92)
Research Growth Index6.91 (4.65)
Search Engine Demand Index101.37 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (59.02)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials960 (8.36%)5.53%
Reviews1,800 (15.68%)6.00%
Case Studies2,269 (19.77%)4.05%
Observational69 (0.60%)0.25%
Other6,379 (55.58%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (500)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
An Open Label Clinical Trial of Imatinib Mesylate(Glivec)in Patients With Moderate to Severe Nephrogenic Systemic Fibrosis [NCT00981942]Phase 310 participants (Actual)Interventional2009-09-30Completed
Randomized Phase II Trial of Gemcitabine and Imatinib Mesylate Versus Gemcitabine Alone in Patients With Previously Treated Locally Advanced or Metastatic Breast Cancer [NCT00323063]Phase 249 participants (Actual)Interventional2006-05-01Terminated(stopped due to Slow accrual)
A Phase I-II Study Evaluating the Safety and Efficacy of Imatinib Mesylate (Gleevec) Combined With Reinduction Chemotherapy Using Mitoxantrone, Etoposide and Cytarabine in Patients With Relapsed/Refractory C-kit Positive Acute Myeloid Leukemia [NCT01126814]Phase 1/Phase 235 participants (Actual)Interventional2004-07-31Completed
A Randomized Study Comparing Imatinib And Imatinib/Pegylated Interferon Alpha-2B in Newly Diagnosed Non-high Risk Chronic Myeloid Leukemia Patients in Complete Hematological Remission After Imatinib Induction Therapy [NCT01227356]Phase 2112 participants (Actual)Interventional2004-09-30Completed
A Global Imatinib and Nilotinib Pregnancy Exposure Registry A Post-Authorisation Safety Study (PASS) [NCT01289054]4 participants (Actual)Observational2011-01-31Completed
Treatment With Second Generation TYROSINE KINASE INHIBITORS (2G TKI) Post Imatinib Failure: Factors Predicting Response and Predictive Value of Response [NCT01188278]173 participants (Actual)Observational2010-07-31Completed
A Phase II Study of the Mammalian Target of Rapamycin (mTOR) Inhibitor RAD001 in Combination With Imatinib Mesylate in Patients With Previously Treated Advanced Renal Carcinoma [NCT00331409]Phase 223 participants (Actual)Interventional2006-01-31Completed
A Phase II, Open-label, Multicenter Study Evaluating the Efficacy of Imatinib Plus Hydroxyurea (HU) in Patients With Progressive Glioblastoma Multiforme (GBM) Receiving or Not Receiving Enzyme-inducing Anticonvulsant Drugs (EIACDs) [NCT00290771]Phase 2231 participants (Actual)Interventional2006-02-28Terminated(stopped due to Lack of efficacy)
An Open-label, Multicenter, Phase II Study to Evaluate the Ability of Glivec® (Imatinib, Formerly Known as STI571) to Produce a Biochemical Response in Patients With Rising PSA Following Radical Prostatectomy [NCT01316458]Phase 251 participants (Actual)Interventional2003-06-30Completed
Open, Randomized, Phase II Study of Glivec in Patients With Unresectable or Metastatic Gastrointestinal Stromal Tumors Expressing C-kit Plus 10 Year Extension Study [NCT00237185]Phase 2148 participants (Actual)Interventional2000-06-30Completed
A Phase II Trial of Neoadjuvant/Adjuvant STI-571 (Gleevec NSC #716051) for Primary and Recurrent Operable Malignant GIST Expressing the KIT Receptor Tyrosine Kinase (CD117) [NCT00028002]Phase 263 participants (Actual)Interventional2002-03-31Completed
Therapy of Early Chronic Phase Chronic Myelogenous Leukemia (CML) With Higher-Dose Gleevec (STI571) [NCT00038649]Phase 2117 participants (Actual)Interventional2001-06-30Terminated(stopped due to Sponsor discontinued providing study drug.)
Therapy of Late Chronic Phase Chronic Myelogenous Leukemia (CML) With High-Dose Gleevec (STI571) [NCT01092741]Phase 247 participants (Actual)Interventional2001-07-31Completed
A Phase II Trial of the Treatment of Polycythemia Vera With Gleevec [NCT01120821]Phase 236 participants (Actual)Interventional2002-08-31Completed
CHOICES: A Randomized Phase II Trial of Imatinib (IM) Versus Hydroxychloroquine (HCQ) and IM for Patients With Chronic Myeloid Leukemia (CML) in Major Cytogenetic Response (MCyR) With Residual Disease Detectable by Quantitative Polymerase Chain Reaction ( [NCT01227135]Phase 266 participants (Anticipated)Interventional2010-03-31Recruiting
A Phase Ib/II Study of PDR001 Plus Imatinib for Metastatic or Unresectable GIST With Prior Failure of Imatinib, Sunitinib and Regorafenib [NCT03609424]Phase 1/Phase 239 participants (Actual)Interventional2019-02-14Completed
Randomized Phase 2 Study of Intermittent vs Continuous Dosing Schedule of Imatinib in Patients With Tyrosine Kinase Inhibitor Refractory Gastrointestinal Stromal Tumors (GISTs) [NCT02712112]Phase 251 participants (Actual)Interventional2016-03-16Completed
Perioperative Imatinib Mesylate in Treating Patients With Locally Advanced Gastrointestinal Stromal Tumor [NCT01267695]Phase 220 participants (Actual)Interventional2010-05-31Completed
Newly Diagnosed Adult Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ ALL). Sequential Treatment With Ponatinib and the Bispecific Monoclonal Antibody Blinatumomab vs Chemotherapy and Imatinib [NCT04722848]Phase 3236 participants (Anticipated)Interventional2021-09-08Recruiting
Multicenter Phase I Study of Imatinib, a Platelet-derived Growth Factor Receptor Inhibitor, and LBH589, a Histone Deacetylase Inhibitor, in the Treatment of Newly Diagnosed and Recurrent Chordoma [NCT01175109]Phase 136 participants (Anticipated)Interventional2011-10-31Active, not recruiting
Effects of Tyrosine Kinase Inhibitors on Liver Enzymes and Electrolytes in Relation to Hematologic Response in Patients With Chronic Phase Chronic Meyloid Leukemia: Assiut University Hospital Insight [NCT04326933]40 participants (Anticipated)Observational2020-01-01Active, not recruiting
Phase 2 Study of Imatinib in Children With Neurofibromatosis and Airway Tumors [NCT03688568]Phase 20 participants (Actual)Interventional2018-09-01Withdrawn(stopped due to Enrollment not feasible)
Sustained Treatment-free Remission in BCR-ABL+ Chronic Myeloid Leukemia: a Prospective Study Comparing Nilotinib Versus Imatinib With Switch to Nilotinib in Absence of Optimal Response. SUSTRENIM Study - GIMEMA CLM1415 [NCT02602314]Phase 4450 participants (Actual)Interventional2016-11-11Active, not recruiting
Front-line Treatment of Philadelphia Positive (Ph Pos), BCRABL Positive, Chronic Myeloid Leukemia (CML) With Two Tyrosine Kinase Inhibitors (TKI) (Nilotinib and Imotinib) A Phase II Exploratory Multicentric Centre. [NCT00769327]Phase 2129 participants (Actual)Interventional2009-02-09Completed
A Phase I/II, Randomized, Double-Blind Intervention Trial for Evaluating the Safety and Efficacy of Imatinib in Subjects With Advance Fibrosis [NCT05224128]Phase 1/Phase 220 participants (Actual)Interventional2021-02-20Active, not recruiting
Triple Antimalarial Combination (Imatinib-DHA-PPQ) to Accelerate the Parasite Clearance and to Prevent the Selection of Resistant Parasites [NCT03697668]Phase 250 participants (Anticipated)Interventional2017-09-17Recruiting
A Phase II Study of Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin (DA-EPOCH) as Front-Line Therapy for Adults With Acute Lymphoblastic Leukemia/Lymphoma [NCT03023046]Phase 254 participants (Actual)Interventional2017-02-23Completed
Therapy of Hypereosinophilic Syndrome, Polycythemia Vera, Atypical CML or CMML With Platelet Derived Growth Factor (PDGF-R) Fusion Genes, or Mastocytosis With Imatinib Mesylate (STI571) [NCT00038675]125 participants (Actual)Interventional2001-06-30Completed
Phase II Study of Adding the Anti-PD-1 Pembrolizumab to Tyrosine Kinase Inhibitors in Patients With Chronic Myeloid Leukemia and Persistently Detectable Minimal Residual Disease [NCT03516279]Phase 240 participants (Anticipated)Interventional2019-06-26Recruiting
Multicenter Trial Estimating the Persistence of Molecular Remission in Chronic Myeloid Leukaemia in Long Term After Stopping Imatinib [NCT01343173]220 participants (Anticipated)Interventional2011-04-06Completed
LAM Pilot Study With Imatinib Mesylate [NCT03131999]Phase 1/Phase 218 participants (Actual)Interventional2018-01-23Completed
[NCT01491763]Phase 470 participants (Anticipated)Interventional2008-01-31Recruiting
A Phase 2 Study of 5 Years of Adjuvant Imatinib in Patients With Gastrointestinal Stromal Tumor With a High Risk of Recurrence Following Surgical Resection [NCT05385549]Phase 235 participants (Anticipated)Interventional2022-09-07Recruiting
Phase II Study to Evaluate the Efficacy of a Chemotherapy Combination With Imatinib (Glivec®) and 5-FU/Leucovorin in Patients With Advanced Carcinoma of the Gallbladder and Bile Duct [NCT01153750]Phase 244 participants (Actual)Interventional2007-04-30Completed
A Multi-center, Single Arm, Phase II Study of Adjuvant Imatinib (Glivec®) in Patients Following the Resection of Primary Gastrointestinal Stromal Tumor ( GIST) [NCT01172548]Phase 2132 participants (Actual)Interventional2008-08-31Completed
Role of Surgery in Patients With Focally Progressive Gastrointestinal Stromal Tumors (GISTs) After Imatinib Treatment: A Prospective, Multicenter, Randomized Trial [NCT03862768]92 participants (Anticipated)Interventional2019-07-31Not yet recruiting
Dose Individualization of Antineoplastic Drugs and Anti-Infective Drug in Children With Hematoplastic Disease [NCT03844360]Phase 41,500 participants (Anticipated)Interventional2016-01-31Recruiting
A Randomised, Double-blind, Placebo-controlled Study to Investigate the Safety and Efficacy of Intravenous Imatinib Mesylate (Impentri®) in Subjects With Acute Respiratory Distress Syndrome Induced by COVID-19 [NCT04794088]Phase 267 participants (Actual)Interventional2021-03-14Terminated(stopped due to Due to the decline of COVID-19 patients on Dutch ICUs. A sample size reestimation based on blinded study data of 66 patients was furthermore favorable, indicating sufficient power to detect a difference in primary endpoint between groups.)
A Randomized Open-label Study of 400 mg Versus 800 mg of Imatinib Mesylate in Patients With Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Using Molecular Endpoints. [NCT00124748]Phase 3476 participants (Actual)Interventional2005-06-30Terminated(stopped due to This study was prematurely discontinued because no improvement was observed in the 800mg dose compared to 400mg dose)
Imatinib in Acute Ischaemic Stroke: A Phase 3, Randomized, Double-blind, Placebo Controlled, Parallel-arm Efficacy Trial of Imatinib in Acute Ischaemic Stroke [NCT03639922]Phase 31,260 participants (Anticipated)Interventional2018-10-01Recruiting
A Prospective Phase II Clinical Trial Evaluating the Efficacy and the Safety of Tyrosine Kinase Inhibitors Withdrawal After a Previous Two-step Dose Reduction in Patients With Chronic Myeloid Leukemia in Deep Molecular Remission [NCT04147533]Phase 2150 participants (Anticipated)Interventional2020-06-16Active, not recruiting
A Phase II Trial Of Imatinib Mesylate (Gleevec) In Patients With HIV Related Kaposi's Sarcoma [NCT00090987]Phase 230 participants (Actual)Interventional2005-06-30Completed
Phase II Trial of STI571 (NSC 716051) in Patients With Recurrent Meningioma [NCT00045734]Phase 223 participants (Actual)Interventional2003-02-28Completed
Imatinib Continuation Versus Nilotinib 300 mg Twice Daily in Patients With Chronic Myeloid Leukemia (CML) in Chronic Phase and Major Molecular Re-sponse (MMR) Without Molecular Response ≥ 4.5 Log (MR4.5) Receiving Imatinib at a Dose of 400 to 800 mg Daily [NCT02174445]Phase 314 participants (Actual)Interventional2014-03-31Terminated(stopped due to very slow recruitment rate and a lot of pat. didn't fulfil BCR-ABL requirements)
A Phase II Study of Binimetinib in Combination With Imatinib in Patients With Advanced KIT-Mutant Melanoma [NCT04598009]Phase 225 participants (Anticipated)Interventional2021-03-03Recruiting
A Trial of Dovitinib in Combination With Imatinib in Patients With Metastatic or Unresectable Gastrointestinal Stromal Tumors After Failure to Imatinib and Sunitinib [NCT02268435]Phase 10 participants (Actual)Interventional2015-03-31Withdrawn(stopped due to Dovitinib Production stopped)
Phase I/II Study of Temozolomide and Gleevec (Imatinib Mesylate, Formerly Known as STI571) in Advanced Melanoma [NCT00667953]Phase 1/Phase 232 participants (Actual)Interventional2003-01-31Terminated(stopped due to Difficulty enrolling subjects)
A Phase II Study of Perifosine Plus Imatinib Mesylate for Patients With Resistant Gastrointestinal Stromal Tumor [NCT00455559]Phase 240 participants (Actual)Interventional2006-08-31Completed
Extension Study of a Study to Evaluate Efficacy and Safety of Imatinib (Glinib®) 600mg/Day Depending on Early Molecular Response in Newly Diagnosed Patients With Chronic Myeloid Leukemia in Chronic Phase [NCT02421926]0 participants (Actual)Observational2014-10-31Withdrawn
Imatinib for Multiple Sclerosis (MS) Relapses - a Phase II, Randomised Study [NCT03674099]Phase 2200 participants (Anticipated)Interventional2018-10-01Recruiting
A Phase 2, Randomized, Open Label, Pivotal Study to Evaluate the Efficacy and Safety of HQP1351 in CML CP Patients Who Are Resistant and/or Intolerant to First- and Second-Generation Tyrosine Kinase Inhibitors [NCT04126681]Phase 2144 participants (Actual)Interventional2019-10-21Active, not recruiting
A Randomized, Double-blind, Multicentre 2-arm, Parallel-group, Placebo-controlled Study to Investigate the Efficacy and Safety of Intravenous Imatinib Mesylate in Reducing the Severity of Hypoxemic Respiratory Failure in Patients With Critical COVID-19 Re [NCT04953052]Phase 20 participants (Actual)Interventional2021-10-14Withdrawn(stopped due to Number of moderate to severe ARDS patients hospitalised due to COVID19 diminishingly small. Not expected to recruit required minimum number of patients.)
A Phase II, Open-label, Study in Patients With Refractory, Metastatic Cancer Harboring KIT Mutation or Amplification to Investigate the Clinical Efficacy and Safety of Imatinib Therapy [NCT02461849]Phase 214 participants (Actual)Interventional2014-04-04Active, not recruiting
I-SPY COVID TRIAL: An Adaptive Platform Trial to Reduce Mortality and Ventilator Requirements for Critically Ill Patients [NCT04488081]Phase 21,500 participants (Anticipated)Interventional2020-07-31Recruiting
A Phase I, Multicenter, Open-label Study of Oral ABL001 in Patients With Chronic Myelogenous Leukemia (CML) or Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia (Ph+ ALL) [NCT02081378]Phase 1326 participants (Actual)Interventional2014-04-24Completed
An Open Label, Multi-center Imatinib Roll-over Protocol for Patients Who Have Completed a Previous Novartis-sponsored Imatinib Study and Are Judged by the Investigator to Benefit From Continued Imatinib Treatment [NCT01742299]Phase 4155 participants (Actual)Interventional2013-03-26Active, not recruiting
An Open-Label, Randomised, Multi-Centre, Phase II Study to Investigate the Safety and Efficacy of AT13387, Either as Monotherapy or in Combination With Imatinib, in Patients With Unresectable and/or Metastatic Malignant GIST Whose Tumour Has Progressed Fo [NCT01294202]Phase 226 participants (Actual)Interventional2011-03-31Completed
Explore the Synergy of Combination TKI Therapy - A Pilot Study to Evaluate the Effect of Imatinib on Dasatinib Pharmacokinetics in Healthy Volunteers [NCT02129166]Phase 10 participants (Actual)Interventional2014-09-30Withdrawn(stopped due to PI resigned)
Evaluation of the Therapeutic Effect of Hydroxyurea Pulse Therapy for Chronic Myeloid Leukemia Patients [NCT03515018]Phase 360 participants (Anticipated)Interventional2018-05-01Recruiting
A Phase II Study of Imatinib Dose Escalation to 800 mg/Day in Korean Patients With Metastatic or Unresectable GIST Harboring KIT Exon 9 Mutation: Imatinib Dose Escalation [NCT01541709]Phase 223 participants (Actual)Interventional2012-03-31Active, not recruiting
A Prospective, Multicenter, Randomized, Open-label, Active-controlled, 2-parallel Group, Phase III Study to Compare Efficacy and Safety of Masitinib at 7.5 mg/kg/Day to Imatinib at 400 or 600 mg in Treatment of Patients With Gastro-intestinal Stromal Tumo [NCT00812240]Phase 3335 participants (Actual)Interventional2009-01-31Terminated(stopped due to Sponsor decision based on portfolio prioritization)
Phase-III Randomized Study to Optimize TKIs Multiple Approaches - (OPTkIMA) - and Quality of Life (QoL) in Elderly Patients (≥60 Years) With Ph+ Chronic Myeloid Leukemia (CML) and MR3.0 / MR4.0 Stable Molecular Response [NCT02326311]Phase 3502 participants (Anticipated)Interventional2015-06-10Recruiting
Phase II Multicenter Clinical Trial on Imatinib Treatment for Patients With Resectable Hepatic Metastasis From Gastrointestinal Stromal Tumors (GISTs) [NCT00764595]Phase 25 participants (Actual)Interventional2008-10-31Completed
Asciminib as Initial Therapy for Patients With Chronic Myeloid Leukemia in Chronic Phase With Addition of Lower Dose Tyrosine Kinas Inhibitors for Patients With Chronic Myeloid Leukemia Who do Not Achieve a Deep Molecular Remission [NCT05143840]Phase 28 participants (Anticipated)Interventional2022-04-22Recruiting
A Phase III, Multi-center, Open-Label, Randomized Study of the Efficacy of Radotinib Versus Imatinib in Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myeloid Leukemia Chinese Patients in Chronic Phase [NCT03722420]Phase 3238 participants (Anticipated)Interventional2018-12-28Active, not recruiting
KISS Study: A Phase II Study of Dasatinib Followed by Imatinib in Newly Diagnosed, Previously Untreated Patients With Chronic Phase CML [NCT03193281]Phase 291 participants (Actual)Interventional2017-07-17Active, not recruiting
A Randomized Trial for Adults With Newly Diagnosed Acute Lymphoblastic Leukemia [NCT01085617]Phase 31,033 participants (Actual)Interventional2010-12-31Active, not recruiting
Front-line Treatment of Ph Positive (Ph+)/Bcr-Abl Positive Acute Lymphoblastic Leukemia (ALL) With Two Tyrosine Kinase Inhibitors (TKI) (Imatinib and Nilotinib). A Phase II Exploratory Multicentric Study in Elderly Patients and in Patients Unfit for Progr [NCT01025505]Phase 240 participants (Actual)Interventional2012-06-30Completed
Phase II Study for Safety and Efficacy Evaluation of Imatinib Mesylate in Children With Chronic Myeloid Leukemia (CML) Philadelphia Chromosome-positive (Ph+) [NCT01221376]Phase 220 participants (Anticipated)Interventional2011-02-28Active, not recruiting
Phase II Study to Evaluate Glivec (Imatinib Mesylate) to Induce Progression Arrest in Aggressive Fibromatosis / Desmoid Tumors Not Amenable to Surgical Resection With R0 Intent or Accompanied by Unacceptable Function Loss [NCT01137916]Phase 239 participants (Actual)Interventional2010-06-30Completed
Phase I Study Investigating the Safety and Feasibility of Combining Imatinib Mesylate (Gleevec) With Sorafenib in Patients With Androgen-Independent Chemotherapy-Failure Prostate Cancer. [NCT00424385]Phase 117 participants (Actual)Interventional2007-01-31Completed
Randomized, Multi-center, Open-label Phase III Study of the Efficacy and Safety of Flumatinib vs Imatinib as First Line Treatment in Patients With Newly Diagnosed Chronic Phase Chronic Myelogenous Leukemia. [NCT02204644]Phase 3400 participants (Actual)Interventional2014-06-30Completed
A Phase IV Study to Evaluate Efficacy and Safety of Imatinib(Glinib®) 600mg/Day Depending on Early Molecular Response in Newly Diagnosed Patients With Chronic Myeloid Leukemia in Chronic Phase [NCT02204722]Phase 455 participants (Actual)Interventional2014-10-13Terminated(stopped due to Sponsor's decision to halt the study.)
Phase I/II Trial of Imatinib Mesylate; (Gleevec; STI571) in Treatment of Recurrent Oligodendroglioma and Mixed Oligoastrocytoma [NCT00049127]Phase 1/Phase 264 participants (Actual)Interventional2003-06-30Completed
A Phase II Trial of Sequential Chemotherapy, Imatinib Mesylate (Gleevec, STI571) (NSC # 716051), and Transplantation for Adults With Newly Diagnosed Ph+ Acute Lymphoblastic Leukemia by the CALGB and SWOG [NCT00039377]Phase 258 participants (Actual)Interventional2002-04-30Completed
Impact of the Inhibitors of Tyrosine Kinase on the Male Fertility [NCT01114087]2 participants (Actual)Interventional2008-10-31Completed
A Randomized Phase II Study of Ruxolitinib (NSC-752295) in Combination With BCR-ABL Tyrosine Kinase Inhibitors in Chronic Myeloid Leukemia (CML) Patients With Molecular Evidence of Disease [NCT03654768]Phase 284 participants (Anticipated)Interventional2018-10-24Active, not recruiting
ALLTogether1 - A Treatment Study Protocol of the ALLTogether Consortium for Children and Young Adults (0-45 Years of Age) With Newly Diagnosed Acute Lymphoblastic Leukaemia (ALL) [NCT04307576]Phase 36,430 participants (Anticipated)Interventional2020-07-13Recruiting
International Phase 3 Trial in Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia (Ph+ALL) Testing Imatinib in Combination With Two Different Cytotoxic Chemotherapy Backbones [NCT03007147]Phase 3475 participants (Anticipated)Interventional2017-08-08Recruiting
An Open Label, Time-To-Event Continuous Reassessment Method, Phase I/II Study of the Mammalian Target of Rapamycin (mTOR) Inhibitor RAD001 in Combination With Imatinib (Gleevec) in Patients With Chronic Phase Chronic Myeloid Leukemia (CML) With Persistent [NCT01188889]Phase 1/Phase 20 participants (Actual)Interventional2013-09-30Withdrawn(stopped due to Unable to obtain sufficient funding.)
An Exploratory Single Center Study of High-dose Treatment of Glivec® in Patients With Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP) Using Molecular Endpoints - TOPS (Tyrosine Kinase Inhibitor Optimization and Sel [NCT01216085]Phase 210 participants (Actual)Interventional2010-08-31Completed
Imatinib Mesylate Therapy in Systemic Mastocytosis Patients Lacking KIT Mutations [NCT01297777]Phase 410 participants (Actual)Interventional2011-01-31Completed
Phase II Study for Safety and Efficacy Evaluation of Imatinib Mesylate in Children With Acute Lymphoblastic Leukemia (ALL) Philadelphia Chromosome-positive (Ph+) [NCT01222013]Phase 220 participants (Anticipated)InterventionalSuspended(stopped due to Study was suspended before recruitment, due to logistic issues.)
Exploratory Study of Drug Sensitivity Prediction Software (IRCR-DReSS) With Patient-derived Tumor Cells of Metastatic Gastric Cancer [NCT03170180]Phase 266 participants (Actual)Interventional2017-03-01Completed
A Retrospective Cohort Study [NCT03424876]60 participants (Anticipated)Observational2017-06-02Recruiting
A Randomization, Double Blind, Multicenter Phase II Clinical Trial to Evaluate the Imatinib for Prophylaxis of CMV Infection After Allogeneic Hematopoietic Stem Cell Transplantation [NCT03343600]Phase 25 participants (Actual)Interventional2017-11-09Terminated(stopped due to The trial is terminated due to the extremely low recruitment rate.)
Treatment of CML Patients With Imatinib and Hydroxyurea [NCT02480608]Phase 1/Phase 2113 participants (Actual)Interventional2004-04-30Completed
Imatinib Mesylate in Combination With Pembrolizumab in Patients With Advanced KIT-mutant Melanoma Following Progression on Standard Therapy: a Phase I/II Trial [NCT04546074]Phase 1/Phase 222 participants (Anticipated)Interventional2020-09-14Recruiting
Long-term Follow-up of a Randomized Multicenter Trial on Impact of Imatinib and Infliximab on Long-COVID in Hospitalized COVID-19 Patients [NCT05220280]Phase 4400 participants (Anticipated)Interventional2022-02-06Recruiting
A Randomized Phase II Study of Imatinib and Rituximab for Cutaneous Sclerosis After Allogeneic Hematopoietic Cell Transplantation [NCT01309997]Phase 272 participants (Actual)Interventional2011-03-31Completed
The Life After Stopping Tyrosine Kinase Inhibitors Study (The LAST Study) [NCT02269267]Phase 2173 participants (Actual)Interventional2014-12-18Completed
Randomized Phase III Trial Comparing Nilotinib 800mg to Imatinib 800 mg for the Treatment of Patients With Advanced and/or Metastatic Gastrointestinal Stromal Tumors Refractory to Imatinib 400 mg [NCT00751036]Phase 394 participants (Actual)Interventional2009-06-30Terminated
A Pilot Study of Imatinib Mesylate in Steroid Refractory Chronic Graft Versus Host Disease [NCT00760981]Phase 115 participants (Actual)Interventional2008-09-30Completed
Phase III Randomized, Intergroup, International Trial Assessing the Clinical Activity of STI-571 at Two Dose Levels in Patients With Unresectable or Metastatic Gastrointestinal Stromal Tumors (GIST) Expressing the KIT Receptor Tyrosine Kinase (CD117) [NCT00685828]Phase 3946 participants (Actual)Interventional2001-01-31Active, not recruiting
A Pilot Window of Opportunity Study of Imatinib in Combination With Cetuximab in Patients With Squamous Cell Carcinomas of the Head and Neck [NCT05816785]Early Phase 115 participants (Anticipated)Interventional2023-04-18Recruiting
Phase I/II, Open Label Study of Sequential Taxotere® (Docetaxel) and Gleevec® (Imatinib Mesylate) in Hormone Refractory Prostate Cancer [NCT00861471]Phase 1/Phase 224 participants (Actual)Interventional2005-05-31Terminated(stopped due to due to slow accrual)
A PHASE 3 RANDOMIZED, OPEN-LABEL STUDY OF BOSUTINIB VERSUS IMATINIB IN SUBJECTS WITH NEWLY DIAGNOSED CHRONIC PHASE PHILADELPHIA CHROMOSOME POSITIVE CHRONIC MYELOGENOUS LEUKEMIA [NCT00574873]Phase 3502 participants (Actual)Interventional2008-02-05Completed
A 24-week Randomized Placebo-controlled, Double-blind Multi-center Clinical Trial Evaluating the Efficacy and Safety of Oral QTI571 as an add-on Therapy in the Treatment of Severe Pulmonary Arterial Hypertension: Imatinib in Pulmonary Arterial Hypertensio [NCT00902174]Phase 3202 participants (Actual)Interventional2009-09-30Completed
[NCT00845221]Phase 444 participants (Actual)Interventional2004-07-31Completed
A Multi-centre, Open-label, Proof of Concept (PoC) Study to Evaluate the Efficacy and Tolerability of STI571 for the Treatment of Fibrosis in Patients With Systemic Sclerosis [NCT00613171]Phase 227 participants (Actual)Interventional2008-01-02Completed
Phase III Study of Imatinib Mesylate in Combination With Hydroxyurea Versus Hydroxyurea Alone as an Oral Therapy in Patients With Temozolomide Resistant Progressive Glioblastoma [NCT00154375]Phase 3240 participants (Actual)Interventional2004-10-31Completed
Phase II Study of Imatinib Mesylate in Neurofibromatosis Type I Patients Aged 2 to 21 With Plexiform Neurofibromas [NCT02177825]Phase 25 participants (Actual)Interventional2014-06-30Terminated(stopped due to Slow accrual 5 patients out of 25 expected. Primary objectives could not be met without recruiting more patients.)
A Phase Ib Clinical Study of BBI608 for Adult Patients With Advanced, Refractory Hematologic Malignancies [NCT02352558]Phase 115 participants (Actual)Interventional2015-05-31Completed
A Randomised Phase II Trial of Imatinib Alternating With Regorafenib Compared to Imatinib Alone for the First Line Treatment of Advanced Gastrointestinal Stromal Tumour (GIST) [NCT02365441]Phase 278 participants (Actual)Interventional2015-06-30Active, not recruiting
Nilotinib Versus Imatinib in Treatment of Patients With Newly Diagnosed Chronic Myeloid Leukemia [NCT03228303]Early Phase 1100 participants (Anticipated)Interventional2017-12-01Not yet recruiting
A Randomized Multicenter Phase III Trial Evaluating the Interest of Imatinib Treatment Maintenance or Interruption After 3 Years of Adjuvant Treatment in Patients With Gastrointestinal Stromal Tumours (GIST) [NCT02260505]Phase 3134 participants (Anticipated)Interventional2014-12-24Recruiting
Entacapone in Combination With Imatinib Mesylate for Treatment of Patients With Gastrointestinal Stromal Tumors(GIST) Following Failure of at Least Imatinib and Sunitinib [NCT04006769]Early Phase 15 participants (Actual)Interventional2020-10-30Completed
A Phase II Study of Dose-Adjusted Etoposide, Prednisone, Vincristine, Cyclophosphamide, and Doxorubicin Plus Asparaginase (DA-EPOCH-A) for Adults With Acute Lymphoblastic Leukemia/Lymphoma [NCT02538926]Phase 20 participants (Actual)Interventional2018-07-01Withdrawn(stopped due to Drugs unavailable)
Phase II Study of Imatinib Mesylate and Docetaxel in Pretreated Patients With Metastatic NSCLC [NCT01083589]Phase 222 participants (Actual)Interventional2005-01-31Completed
A Phase III Randomized Study Evaluating Surgery of Residual Disease in Patients With Metastatic Gastro-intestinal Stromal Tumor Responding to Imatinib Mesylate. [NCT00956072]Phase 312 participants (Actual)Interventional2009-05-31Terminated(stopped due to low accrual)
Study to Evaluate Efficacy and Safety of Glivec® in Combination With Vincristine and Dexamethasone in Patients With Lymphoid Blast Crisis CML or Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia in Relapse or Refractory [NCT00763763]Phase 255 participants (Actual)Interventional2004-12-31Completed
A Phase I/II Dose Escalation Study of Subcutaneous Campath-1H (NSC #715969, IND #10864) During Intensification Therapy in Adults With Untreated Acute Lymphoblastic Leukemia (ALL) [NCT00061945]Phase 1/Phase 2302 participants (Actual)Interventional2003-06-30Completed
A Phase I/II Trial Of STI571 In Children With Newly Diagnosed Poor Prognosis Brainstem Gliomas And Recurrent Intracranial Malignant Gliomas [NCT00021229]Phase 1/Phase 285 participants (Actual)Interventional2001-05-31Terminated(stopped due to Poor accrual)
A Phase II Study of Imatinib in Patients With Mucosal or Acral/Lentiginous Melanoma and Melanomas That Arise on Chronically Sun Damaged Skin. [NCT00424515]Phase 224 participants (Actual)Interventional2006-07-31Completed
A Phase II Evaluation of Gleevec(TM) (NCI-Supplied Agent: STI571 [Imatinib Mesylate], NSC# 716051) in the Treatment of Recurrent or Persistent Carcinosarcoma of the Uterus [NCT00075400]Phase 226 participants (Actual)Interventional2004-01-31Completed
Treatment of Acute Cervical Spinal Cord Injury With Imatinib (Glivec®) - a Safety and Feasibility Study (EudraCT no 2014-002170-36) [NCT02363361]Phase 210 participants (Anticipated)Interventional2018-04-30Not yet recruiting
IMATINIB Plus Hydroxyurea in the Treatment of Recurrent or Progressive Meningiomas: a Randomized Phase II Study [NCT00904735]Phase 276 participants (Anticipated)Interventional2009-06-30Recruiting
"A Window of Opportunity Trial With Brentuximab Vedotin and Imatinib in Patients With Relapsed or Refractory ALK+ Anaplastic Large Cell Lymphoma or Patients Ineligible for Chemotherapy" [NCT02462538]Phase 1/Phase 23 participants (Actual)Interventional2015-11-03Terminated(stopped due to Due to slow recruitment, recruitment of new patients was stopped, FU was completed for enrolled patients)
Compliance to Long Term Imatinib Therapy in Newly Diagnosed Patients With Chronic Myeloid Leukaemia. [NCT00632255]88 participants (Actual)Observational2008-01-31Completed
Adjunct Targeted Biologic Inhibition in Children With Multivessel Intraluminal Pulmonary Vein Stenosis [NCT00891527]Phase 1/Phase 250 participants (Actual)Interventional2008-10-31Completed
A Phase 3, Multicenter, Randomized, Open-Label, Trial Evaluating the Efficacy and Safety of Asciminib Used in Consolidation With Imatinib v. Imatinib to Achieve Treatment-free Remission in Chronic Phase-Chronic Myelogenous Leukemia Patients [NCT05413915]Phase 3164 participants (Anticipated)Interventional2023-06-19Recruiting
IMPACT-TB (Imatinib Mesylate Per Oral as a Clinical Therapeutic for TB): A Phase II Clinical Trial of the Safety, Pharmacokinetics and Hematologic Effects of Imatinib on Myelopoiesis in Adults When Given With and Without Isoniazid and Rifabutin [NCT03891901]Phase 224 participants (Actual)Interventional2020-10-27Completed
Efficacy of Adjuvant Imatinib in Patients With Intermediate-risk Gastrointestinal Stromal Tumor With a High-risk Genomic Grade Index. Multicenter, Prospective, Randomized Study. Etude Multicentrique, Prospective, randomisée [NCT02576080]Phase 380 participants (Anticipated)Interventional2015-10-31Not yet recruiting
A Multi-center Study of the Discontinuation of Imatinib in Adult Patients With Ph+ CML in CP Who Have a Complete Molecular Response to Imatinib [NCT01564836]50 participants (Anticipated)Interventional2010-06-30Recruiting
DFCI ALL Adult Consortium Protocol: Adult ALL Trial [NCT01005758]Phase 2180 participants (Anticipated)Interventional2009-01-31Not yet recruiting
Dose Finding and Phase II Study of STI 571 in Advanced Soft Tissue Sarcoma [NCT00006357]Phase 1/Phase 291 participants (Actual)Interventional2000-08-31Completed
A Multi-centre, Adaptive, Randomized, Open-label, Controlled Clinical Trial of the Safety and Efficacy of Investigational Therapeutics for the Treatment of COVID-19 in Hospitalized Patients (CATCO: Canadian Treatments for COVID-19), in Conjunction With th [NCT04330690]Phase 32,900 participants (Anticipated)Interventional2020-03-18Active, not recruiting
Phase II Study of Letrozole (Femara) Plus Imatinib Mesylate (Gleevec) for Postmenopausal Patients With ER and/or PR Positive Metastatic Breast Cancer [NCT00338728]Phase 259 participants (Actual)Interventional2003-10-03Completed
Imatinib Mesylate And Cyclophosphamide In Metronomic Administration: Dose Escalation Study Of Imatinib Mesylate in Patient With Rare Tumor (Phase I Study) [NCT01046487]Phase 126 participants (Actual)Interventional2009-01-31Completed
A Phase IIIB, Randomized, Active Controlled Open-Label Study Of Sunitinib (Sutent) 37.5 Mg Daily Vs Imatinib Mesylate 800 Mg Daily In The Treatment Of Patients With Gastrointestinal Stromal Tumors (GIST) Who Have Had Progressive Disease While On 400 Mg Da [NCT00372567]Phase 369 participants (Actual)Interventional2007-06-30Terminated(stopped due to See termination reason in detailed description.)
A Non-randomized, Open-label Study to Characterize the Pharmacokinetics (PK) of Glivec/Gleevec® (Imatinib Mesylate) in Pediatric (Age Range 1 to Less Than 4 Years) Patients With Chronic Myeloid Leukemia (CML) or Philadelphia Chromosome Positive Acute Lymp [NCT01066468]Phase 13 participants (Actual)Interventional2010-10-31Terminated
A Phase II Study of Imatinib and Valproic Acid in Patients With CML [NCT01011998]Phase 20 participants (Actual)Interventional2009-09-30Withdrawn(stopped due to Withdrawn due to lack of accrual per Center DSMP, with PI concurrence)
Population Pharmacokinetics of Imatinib in CML Patients in Iran [NCT02146846]170 participants (Actual)Observational2012-10-31Terminated
Phase II Trial Evaluating Gleevec (Imatinib Mesylate Formerly Known as STI571) in Patients With Anaplastic Thyroid Cancer [NCT00115739]Phase 211 participants (Actual)Interventional2004-02-29Terminated(stopped due to Study was closed early due to slow accrual)
A Phase II Open-Label Study of the Intravenous Administration of Homoharringtonine (CGX-635) Combined With the Oral Administration of Gleevec in the Treatment of Patients With Chronic Myeloid Leukemia (CML) in Chronic, Accelerated, and Blast Phase [NCT00114959]Phase 215 participants (Actual)Interventional2005-10-31Terminated(stopped due to Poor enrollment)
Phase I-II Study of Ruxolitinib (INCB18424) for Patients With Chronic Myeloid Leukemia (CML) With Minimal Residual Disease While on Therapy With Tyrosine Kinase Inhibitors [NCT01751425]Phase 18 participants (Actual)Interventional2013-07-24Terminated(stopped due to Per PI Request. 2) No additional benefit was noted with the addition of Ruxolitinib.)
A Phase I/II Study of Gleevec/Taxol in Patients With Newly Diagnosed Stage IIIC or IV or Recurrent (Any Stage) Uterine Papillary Serous Carcinoma (UPSC) [NCT00506779]Phase 1/Phase 217 participants (Actual)Interventional2003-12-29Terminated(stopped due to the study was terminated early due to poor enrollment)
PrecISE (Precision Interventions for Severe and/or Exacerbation-Prone Asthma) Network Study [NCT04129931]Phase 2600 participants (Anticipated)Interventional2019-12-19Recruiting
Phase II Study of Paclitaxel With Imatinib Mesylate (Gleevec) in Taxane-pretreated Ovarian and Other Cancers of Mullerian Origin [NCT00840450]Phase 214 participants (Actual)Interventional2007-04-30Terminated(stopped due to Due to slow accrual)
An Open Label Phase 2 Pilot Study to Determine the Safety, Efficacy and Tolerability of Gleevec (Imatinib Mesylate) in the Treatment of Nephrogenic Systemic Fibrosis [NCT00677092]Phase 212 participants (Actual)Interventional2007-12-31Completed
Therapeutic and Biological Effects of Imatinib Mesylate in Primary Hypereosinophilic Syndromes [NCT00787384]Phase 225 participants (Actual)Interventional2004-10-31Completed
A Phase II, Non-Randomized, Open-Label Multicenter Study of 5 Year Adjuvant Imatinib Mesylate (Gleevec®) in Patients at Significant Risk for Recurrence Following Complete Resection of Primary Gastrointestinal Stromal Tumor (GIST) [NCT00867113]Phase 291 participants (Actual)Interventional2009-07-22Completed
A Phase II Trial Evaluating the Safety and the Efficacy of High-Dose Imatinib in Relapsed/Refractory c-Kit Positive and BCR-Abl Negative AML Patients [NCT00707408]Phase 215 participants (Actual)Interventional2004-02-29Completed
A Pilot Study of Gleevec (Imatinib Mesylate) in Relapsed/Refractory T Cell Non-Hodgkin's Lymphoma [NCT00684411]Phase 212 participants (Actual)Interventional2008-06-30Completed
A Phase I Study to Determine the Safety of Imatinib in Combination With PTK787/ZK222584 in Patients With Refractory and/or Advanced Solid Tumors [NCT00611689]Phase 145 participants (Actual)Interventional2004-07-31Completed
A Single Stage Phase II, Multi-centre, Open Label Study of Imatinib in Combination With Pioglitazone, Etoricoxib, Dexamethasone and Low-dose Treosulfane for Anti-inflammatory and Angiostatic Treatment in Patients With Hormone-refractory Prostate Cancer [NCT00427999]Phase 267 participants (Actual)Interventional2007-02-28Completed
Phase III Randomized Trial of Autologous and Allogeneic Stem Cell Transplantation Versus Intensive Conventional Chemotherapy in Acute Lymphoblastic Leukemia in First Remission [NCT00002514]Phase 31,929 participants (Actual)Interventional1993-05-07Completed
"Phase II Proof of Concept Study of TALL-104 (MHC Non-Restricted Cytotoxic T-Cell Line) and Imatinib Mesylate (Gleevec) in Chronic Myelogenous Leukemia in Chronic Phase" [NCT00415909]Phase 23 participants (Actual)Interventional2006-12-31Terminated(stopped due to Slow Accrual)
Phase II Trial of the Addition of PEG-Asparaginase to the Hyper-CVAD Regimen in Adult Newly-Diagnosed Acute Lymphoblastic Leukemia [NCT01005914]Phase 211 participants (Actual)Interventional2009-06-30Terminated(stopped due to Increased rate of bacterial infections)
Phase I Study of Zactima (ZD6474) Plus Imatinib Mesylate and Hydroxyurea for Patients With Recurrent Malignant Glioma [NCT00613054]Phase 127 participants (Actual)Interventional2007-11-30Completed
Phase I Dose Escalation of Gleevec in Combination With RAD001 Plus Hydroxyurea for Patients With Recurrent Malignant Glioma [NCT00613132]Phase 178 participants (Actual)Interventional2005-05-31Completed
A Randomized, Phase 3 Study of Dose Escalation Versus No Dose Escalation of Imatinib In Metastatic GIST Patients With Imatinib Trough Levels Less Than 1100 Nanograms/mL [NCT01031628]Phase 35 participants (Actual)Interventional2010-01-31Terminated(stopped due to Lack of feasibility secondary to slow accrual)
Randomized, Open Label Study of Dasatinib (100mg qd) vs. High-Dose Imatinib (600mg) in Patients With Chronic Phase CML Who Have Had Suboptimal Response After 3-18 Months of Therapy With Imatinib (400mg) [NCT00854841]0 participants Expanded AccessAvailable
A Phase II Study of the Association of Glivec® (Imatinib Mesylate, Formerly Known as STI 571) Plus Gemzar® (Gemcitabine) in Patients With Unresectable, Refractory, Malignant Mesothelioma Expressing Either PDGFR-Beta or C-Kit [NCT00551252]Phase 256 participants (Anticipated)Interventional2008-01-31Not yet recruiting
Evaluation of Generic Imatinib in a Real-World Setting Among Chronic Myeloid Leukemia Patients in Egypt [NCT03454503]173 participants (Actual)Observational2018-05-13Completed
Phase II Trial of Imatinib(Gleevec®) in Selected Patients With Metastatic Melanoma [NCT00881049]Phase 21 participants (Anticipated)Interventional2008-12-31Completed
A Pilot Study of the Safety and Efficacy of Imatinib in Reducing Monocytosis or Leukocytosis in Patients With Chronic Myelomonocytic Leukemia and Atypical Chronic Myelogenous Leukemia, Respectively [NCT00079313]Phase 27 participants (Actual)Interventional2004-01-14Completed
A Single-arm, Phase II Clinical Study of Imatinib Mesylate Combined With Toripalimab in the Treatment of Stage III Unresectable and Stage IV Melanoma Harbored With CKIT Mut [NCT05274438]Phase 237 participants (Anticipated)Interventional2021-01-26Recruiting
A Phase III Multi-center, Open-label, Randomized Study of the Efficacy of Nilotinib Versus Imatinib in Adult Patients With Ph+ CML in Early CP Who Have a Suboptimal Molecular Response to Imatinib [NCT01400074]Phase 3100 participants (Anticipated)Interventional2009-01-31Recruiting
Pharmacokinetic Interaction Between Metformin and Imatinib in Healthy Volunteers. [NCT01404715]Phase 111 participants (Actual)Interventional2011-10-31Completed
Preliminary Evaluation of TKI Exposure-response Relationships in Real World Patients (RWPs) With Chronic Myelogenous Leukemia (CML) [NCT03885830]45 participants (Actual)Observational2019-06-20Completed
Pilot Study to Examine The Use of Imatinib (Gleevec) For The Treatment of Active Alveolitis in Systemic Sclerosis [NCT00512902]Phase 1/Phase 220 participants (Actual)Interventional2007-08-31Completed
A Phase II Study of Gleevec® (Imatinib Mesylate, NSC 716051 Formerly ST1571) in Children With Pulmonary Hypertension [NCT00583115]Phase 21 participants (Actual)Interventional2007-10-31Terminated(stopped due to Unable to enroll subjects)
Neoadjuvant Hormonal Ablation, Imatinib Mesylate and Docetaxel Followed by Radical Prostatectomy for High-Risk Localized Prostate Cancer [NCT00500110]Phase 239 participants (Actual)Interventional2003-06-30Completed
A Phase I Dose Escalation Study of LBH589 in Combination With Imatinib Mesylate for Patients With Chronic Myeloid Leukemia in Cytogenetic Remission With Residual Disease Detectable by Q-PCR [NCT00686218]Phase 19 participants (Actual)Interventional2008-05-31Completed
A Phase I/II Study of Gleevec® Combined With Panitumumab (Vectibix®) in Patients Prescreened for C-kit/PDGFr Activated Pathways Using a Proteomic Based Assay [NCT00867334]Phase 1/Phase 210 participants (Actual)Interventional2009-06-30Completed
A Phase I/II Study of Capecitabine/Oxaliplatin (XELOX) in Combination With Bevacizumab and Imatinib as First-line Treatment of Patients With Stage IV Colorectal Cancer [NCT00784446]Phase 1/Phase 251 participants (Actual)Interventional2008-04-30Completed
A Randomized, Open Label, Multi-center Phase III Study to Evaluate the Efficacy and Safety of Nilotinib Versus Imatinib in Adult Patients With Unresectable or Metastatic Gastrointestinal Stromal Tumors (GIST) [NCT00785785]Phase 3644 participants (Actual)Interventional2009-03-31Completed
STI571 (Imatinib) in KIT-expressing Gastrointestinal Stromal Tumors (GIST): a Prospective, Open-label, Multicenter Study on Best Clinical Use in the Advanced Disease. [NCT00940563]Phase 2135 participants (Actual)Interventional2002-03-31Completed
A Phase 1b/2a, Open-label, Multicentre Study to Assess the Safety, Tolerability, Pharmacokinetics, and Antitumor Activity of Vactosertib in Combination With Imatinib in Patients With Advanced Desmoid Tumor (Aggressive Fibromatosis) [NCT03802084]Phase 1/Phase 224 participants (Anticipated)Interventional2019-04-15Active, not recruiting
Busulfan, Cyclophosphamide, Imatinib Mesylate and Autologous Stem Cell Transplantation in Patients With Chronic Myelogenous Leukemia [NCT01003054]Phase 224 participants (Actual)Interventional2005-03-31Completed
An Open Label, Randomized Study of Nilotinib vs. Standard Imatinib (400/600 mg QD) Comparing the Kinetics of Complete Molecular Response for CML-CP Patients With Evidence of Persistent Leukemia by RQ-PCR. [NCT00760877]Phase 3207 participants (Actual)Interventional2009-06-30Completed
Efficacy and Safety of Generic Imatinib (Carcemia®) Compared to Glivec® in Real-Life Management of Chronic Phase of Chronic Myeloid Leukemia; a Multicenter, Observational Study [NCT05282108]240 participants (Anticipated)Observational2022-07-20Recruiting
Gleevec (Imatinib) Plus Multi-Agent Chemotherapy For Newly-Diagnosed Philadelphia Chromosome-Positive Acute Lymphoblastic Leukemia [NCT00618501]Phase 250 participants (Anticipated)Interventional2005-10-31Completed
A Prospective, Randomized, Multicenter, Comparative Study of the Efficacy of Imatinib Resumption Combined With Atezolizumab Versus Imatinib Resumption Alone in Patients With Unresectable Advanced Gastrointestinal Stromal Tumors (GIST) After Failure of Sta [NCT05152472]Phase 2110 participants (Anticipated)Interventional2022-01-14Recruiting
A Phase III, Multi-center, Open-label, Randomized Study of Oral Asciminib Versus Investigator Selected TKI in Patients With Newly Diagnosed Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase [NCT04971226]Phase 3405 participants (Actual)Interventional2021-10-06Active, not recruiting
An Open-Label Study to Determine the Efficacy and Safety of STI571 in Patients With Chronic Myeloid Leukemia in Blast Crisis [NCT00006475]Phase 20 participants Interventional2000-09-30Completed
A Multicenter, Phase Ib/II Trial of Selinexor as a Single Agent and in Combination With Imatinib in Patients With Metastatic and/or Unresectable Gastrointestinal Stromal Tumors (GISTs) [NCT04138381]Phase 1/Phase 230 participants (Actual)Interventional2019-08-16Active, not recruiting
Imatinib Mesylate in Patients With Various Types of Malignancies Involving Activated Tyrosine Kinase Enzymes [NCT00171912]Phase 238 participants (Actual)Interventional2004-09-30Completed
Phase II Study of Imatinib Mesylate for Philadelphia-Positive Acute Lymphocytic Leukemia [NCT00154349]Phase 28 participants (Actual)Interventional2003-10-31Completed
Phase II Study of Imatinib Mesylate in Patients With Life Threatening Malignant Rare Diseases [NCT00154388]Phase 2185 participants (Actual)Interventional2001-02-28Completed
Phase II Study of Imatinib (Glivec) Administered as a Daily Oral Treatment in Patients With Recurrent/Metastatic Adenoid Cystic Carcinoma of the Head and Neck Overexpressing KIT [NCT00180921]Phase 230 participants (Anticipated)Interventional2004-07-31Recruiting
An Open Label, 3-arm, Randomised Phase II Study to Compare the Safety and Efficacy of Ponatinib in Combination With Either Chemotherapy or Blinatumomab With Imatinib Plus Chemotherapy as Front-line Therapy for Patients Aged 55 Years and Over With Philadel [NCT04688983]Phase 2180 participants (Anticipated)Interventional2021-01-31Not yet recruiting
A Phase III Randomized Study of Imatinib, With or Without Bevacizumab (NSC-704865), in Patients With Metastatic or Unresectable Gastrointestinal Stromal Tumors [NCT00324987]Phase 312 participants (Actual)Interventional2008-04-30Terminated(stopped due to The trial failed to accrue)
A Phase I Study of Gemcitabine Plus Oxaliplatin in Combination With Imatinib Mesylate (Glivec) in Patients With Gemcitabine-refractory Advanced Adenocarcinoma of the Pancreas [NCT01048320]Phase 136 participants (Anticipated)Interventional2006-07-31Completed
Safety And Efficacy Of Tyrosine Kinase Inhibitor Cessation For Chronic Myeloid Leukemia Patients With Stable Molecular Response In A Real World Population [NCT04626024]Phase 2100 participants (Anticipated)Interventional2020-12-22Recruiting
A Phase II Study of Gleevec in Patients With Recurrent Platinum-Resistant, Taxane-Resistant Epithelial Ovarian Cancer, Primary Peritoneal Cancer, or Fallopian Tube Cancer [NCT00510653]Phase 273 participants (Actual)Interventional2002-03-31Completed
A Phase 2 Study of Imatinib Mesylate (Gleevec) as Maintenance Therapy After Induction and Consolidation Chemotherapy in Patients With Newly Diagnosed C-kit Positive Acute Myeloid Leukemia [NCT00509093]Phase 232 participants (Actual)Interventional2008-10-31Completed
A Pilot Study of Imatinib in the Treatment of Refractory Systemic Sclerosis [NCT00506831]Phase 1/Phase 29 participants (Actual)Interventional2007-07-31Completed
A Phase III Study of STI571 Versus Interferon-α (IFN-α) Combined With Cytarabine (Ara-C) in Patients With Newly Diagnosed Previously Untreated Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) [NCT00333840]Phase 31,106 participants (Actual)Interventional2000-06-30Completed
An Open-label, Randomized Study of Dasatinib vs High-dose (800-mg) Imatinib in the Treatment of Subjects With Chronic Phase Chronic Myeloid Leukemia Who Have Had a Suboptimal Response After at Least 3 Months of Therapy With 400 mg Imatinib [NCT00320190]Phase 252 participants (Actual)Interventional2006-08-31Terminated(stopped due to Terminated due to slow participant accrual)
Imatinib Mesylate, Busulfan, Fludarabine, Antithymocyte Globulin and Allogeneic Stem Cell Transplantation for Chronic Myelogenous Leukemia [NCT00499889]Phase 242 participants (Actual)Interventional2003-02-28Terminated(stopped due to Support issue.)
An Open-Label, Randomized, Multicenter Phase III Trial of Dasatinib (SPRYCEL®) vs. Standard Dose Imatinib (400 mg) in the Treatment of Subjects With Newly Diagnosed Chronic Phase Philadelphia Chromosome Positive Chronic Myeloid Leukemia [NCT00481247]Phase 3547 participants (Actual)Interventional2007-09-30Completed
A Phase III Multi-center, Open-label, Randomized Study of Imatinib Versus Nilotinib in Adult Patients With Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) [NCT00471497]Phase 3846 participants (Actual)Interventional2007-07-31Completed
A Phase II Trial of STI571 in the Treatment of Metastatic Gastric Cancer [NCT00068380]Phase 217 participants (Actual)Interventional2004-03-31Completed
Phase II Evaluation of Gleevec Combined With Camptosar Plus Paraplatin in Patients With Previously Untreated Extensive Stage SCLC [NCT00193349]Phase 260 participants Interventional2002-09-30Completed
A Phase II Study of Imatinib Mesylate (STI571;NSC#716051:IND 61135) in Patients With Inoperable AJCC Stage III or IV Melanoma Harboring Somatic Alterations of C-KIT [NCT00470470]Phase 230 participants (Actual)Interventional2007-04-30Completed
Phase II Study of Gleevec (Imatinib Mesylate) in Patients With Idiopathic Hypereosinophilic Syndrome (HES) [NCT00230334]Phase 25 participants (Actual)Interventional2003-06-12Terminated(stopped due to terminated by PI due to insufficient accrual)
Phase II Trial to Study the Tolerability and the Effectiveness of Imatinib in Patients With Chronic Myelogenous Leukemia in Chronic Phase With Age More Than 70, Diagnosis of CML is Being Performed Within 1 Year [NCT00219752]Phase 230 participants Interventional2002-05-31Completed
Phase II Study of Nilotinib Plus Pegylated Interferon Alfa-2b as First-line Therapy in Chronic Phase Chronic Myelogenous Leukaemia Aiming to Maximize Complete Molecular Response and Major Molecular Response. [NCT02001818]Phase 2100 participants (Anticipated)Interventional2014-04-30Recruiting
Preoperative Imatinib Mesylate Combined With Rectal-sparing Surgery in Patients With c-KIT Gene-mutant Rectal GIST: an Open-label, Single-arm, Phase III Trial（PIRKER） [NCT05970900]Phase 323 participants (Anticipated)Interventional2023-10-01Not yet recruiting
A Pilot Study of Genomic Sequencing Guided Individualized Therapy in Gastrointestinal Cancers [NCT02013089]50 participants (Anticipated)Interventional2013-12-31Recruiting
A National Multicenter, Noninterventional Clinical Study Evaluating the Safety and Efficacy of Avapritinib in Chinese Patients With Gastrointestinal Stromal Tumor (GIST) in the Real World [NCT05381753]200 participants (Anticipated)Observational2022-08-29Recruiting
Phase I Dose Escalation of Gleevec in Combination With PTK787/ZK 222584 (PTK/ZK) Plus Hydroxyurea [NCT00387933]Phase 137 participants (Actual)Interventional2005-07-31Completed
A Study to Determine the Efficacy and Safety of STI571 in Patients With Chronic Myeloid Leukemia in Accelerated Phase [NCT00006052]Phase 20 participants Interventional2000-06-30Completed
A Phase III Study of STI571 Versus Interferon-a (IFN-a) Combined With Cytarabine (Ara-C) in Patients With Newly Diagnosed Previously Untreated Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) [NCT00006343]Phase 30 participants Interventional2000-06-30Completed
Phase Ib Study of Imatinib to Increase RUNX1 Activity in Participants With Germline RUNX1 Deficiency [NCT06090669]Phase 178 participants (Anticipated)Interventional2024-01-03Recruiting
Low-Dose Oral Imatinib in the Treatment of Scleroderma Pulmonary Involvement: A Phase II Pilot Study [NCT00573326]Phase 230 participants (Anticipated)Interventional2009-02-28Recruiting
A Phase I Study of Imatinib Mesylate and SU011248 for Patients With Gastrointestinal Stromal Tumors [NCT00573404]Phase 16 participants (Actual)Interventional2007-07-31Terminated(stopped due to slow accrual)
An Extension to a Phase II Open-label Study to Determine the Safety and Anti-leukemic Effects of STI571 in Patients With Philadelphia Chromosome-positive Chronic Myeloid Leukemia in Myeloid Blast Crisis [NCT00171158]Phase 2260 participants (Actual)Interventional1999-07-26Completed
A Randomised, Double-blind, Placebo-controlled Study to Evaluate the Safety and Efficacy of the Six Months Treatment With the Tyrosine Kinase Inhibitor STI571 for the Treatment of Pulmonary Arterial Hypertension (PAH) [NCT00477269]Phase 2/Phase 359 participants (Actual)Interventional2006-04-30Completed
An Extension to a Phase II Study to Determine the Safety and Anti-Leukemic Effects of STI571 in Adult Patients With Philadelphia Chromosome Positive Leukemia Including Acute Lymphoblastic Leukemia, Acute Myeloid Leukemia, and Accelerated Phase Chronic Mye [NCT00171249]Phase 2293 participants (Actual)Interventional1999-08-09Completed
An Extension to QTI571A2301 to Evaluate the Long-term Safety, Tolerability and Efficacy of Oral QTI571 (Imatinib) in the Treatment of Severe Pulmonary Arterial Hypertension: IMPRES Extension [NCT01117987]Phase 3144 participants (Actual)Interventional2010-04-30Terminated(stopped due to Novartis discontinued the development of imatinib in PAH due to requirement of regulatory authorities for additional data to secure marketing approval in PAH.)
A Phase 2 Study of Imatinib Therapeutic Drug Monitoring in Gastrointestinal Stromal Tumor [NCT05493215]Phase 228 participants (Anticipated)Interventional2023-11-30Not yet recruiting
A Phase II Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Refractory or Relapsed Acute Myeloid Leukemia [NCT00594555]Phase 220 participants (Anticipated)Interventional2007-11-30Withdrawn(stopped due to Principal Investigator resigned position with the University of Cincinnati, closing study at this site will reopen study in new position)
Evaluating the Efficacy and Safety of Flumatinib Versus Imatinib for in Patients With Newly Diagnosed Chronic Myeloid Leukemia (CML)-in Chronic Phase (CP): A Multicenter, Open-label, Real World Study [NCT05367765]Phase 42,400 participants (Anticipated)Interventional2022-04-30Not yet recruiting
A Randomized Phase Lll Study of Imatinib Dose Optimization Compared With Nilotinib in Patients With Chronic Myelogenous Leukemia and Suboptimal Response to Standard-dose Imatinib [NCT00802841]Phase 3191 participants (Actual)Interventional2009-05-31Completed
A Phase II Study Combining Targeted Therapy With Immunotherapy Using Imatinib Plus Peginterferon α-2b in Gastrointestinal Stromal Tumor (GIST) Patients [NCT00585221]Phase 28 participants (Actual)Interventional2007-07-31Terminated(stopped due to PI terminated at the recommendation of DSMC & IRB)
A Double-blinded, Randomized, Placebo-Controlled Dose Escalation Study to Examine the Efficacy and Microfilaricidal Kinetics and Safety of Imatinib for the Treatment of Loa Loa (A Pilot Study) [NCT02644525]Phase 220 participants (Actual)Interventional2019-09-16Terminated(stopped due to Planned interim analysis demonstrated futility of intervention)
Effect of Calcium Supplements on Imatinib Mesylate (Gleevec®) Pharmacokinetics in Healthy Volunteers (CSTI571BUS 280) (UPCI 08-072) [NCT00732784]Phase 111 participants (Actual)Interventional2008-11-30Completed
Effect of Imatinib on Suppression of Malaria Parasites in Patients With Uncomplicated Plasmodium Falciparum Malaria [NCT02614404]Phase 115 participants (Actual)Interventional2015-11-30Completed
Phase 2 Study to Assess the Safety and Efficiency of Pioglitazone in Combination With Imatinib Mesylate to Treat Chronic Phase Chronic Myelogenous Leukemia Patients [NCT02687425]Phase 220 participants (Anticipated)Interventional2016-02-29Not yet recruiting
A 28 Week, Treatment Randomized, Double -Blind, Placebo-controlled Study of the Effects of cKit Inhibition by Imatinib in Patients With Severe Refractory Asthma (KIA) [NCT01097694]Phase 2176 participants (Actual)Interventional2010-11-30Completed
Targeted Therapy With Imatinib for Treatment of Poor Prognosis Mesenchymal-type Resectable Colon Cancer: a Proof-of-concept Study in the Preoperative Window Period. [NCT02685046]Phase 25 participants (Actual)Interventional2016-04-30Terminated(stopped due to Low accrual rate)
A Multi-arm Dose-finding Phase Ib Multicenter Study of Imatinib in Combination With the Oral Phosphatidyl-inositol 3-kinase (PI3-K) Inhibitor BKM120 in Patients With Gastrointestinal Stromal Tumor (GIST) Who Failed Prior Therapy With Imatinib and Sunitini [NCT01468688]Phase 160 participants (Actual)Interventional2012-04-20Completed
A Phase 1/2 Trial of Pembrolizumab in Combination With Imatinib in Patients With Locally Advanced or Metastatic Melanoma With c-KIT Mutation or Amplification [NCT02812693]Phase 1/Phase 20 participants (Actual)Interventional2016-11-04Withdrawn(stopped due to poor accrual)
An Open-Label, Multicenter, Expanded Access Study of Oral AMN 107 in Adult Patients With Imatinib (Glivec®/Gleevec®_ - Resistant or Intolerant Chronic Myeloid Leukemia in Blast Crisis, Accelerated Phase or Chronic Phase [NCT00538109]8 participants (Actual)Interventional2007-10-31Completed
Retrospective, Non-interventional Study to Evaluate Chronic Myeloid Leukemia Treatment Landscape and Real-life Treatment Outcomes in Hungary: Analysis of National Health Insurance Fund Database [NCT05286528]1,484 participants (Actual)Observational2020-11-18Completed
A Study to Determine the Safety and Efficacy of STI571 in Patients With Chronic Myeloid Leukemia Who Are Hematologically or Cytogenetically Resistant or Refractory to Interferon-Alpha, or Intolerant of, Interferon-Alpha [NCT00006053]Phase 20 participants Interventional2000-06-30Completed
Ph I/II Study of PTK 787 (Vatalanib) and Gleevec (Imatinib) in Patients With Refractory Acute Myelogenous Leukemia (AML), Agnogenic Myeloid Metaplasia (AMM), and Chronic Myelogenous Leukemia- Blastic Phase (CML-BP) [NCT00088231]Phase 1/Phase 29 participants (Actual)Interventional2004-07-31Completed
A Phase I Trial of Imatinib, Bevacizumab, & Metronomic Cyclophosphamide as Antiangiogenic Therapy in Refractory Metastatic Solid Tumors [NCT00390156]Phase 135 participants (Actual)Interventional2006-08-31Completed
A Phase IIA Study to Determine the Safety and Efficacy of A NCI-Supplied Agent: G3139 (NSC 683428, IND 58842) and Imatinib Mesylate in Patients With Refractory or Relapsed Gastrointestinal Stromal Tumor [NCT00091078]Phase 296 participants (Actual)Interventional2005-09-30Terminated
A Study to Determine the Safety and Efficacy of Imatinib Mesylate in Patients With Idiopathic Hypereosinophilic Syndrome [NCT00171860]Phase 224 participants (Actual)Interventional2002-09-30Terminated
Study Comparing Standard Dose and High-dose Imatinib Mesylate in Patients With Chronic Phase Ph+ CML [NCT00171899]Phase 480 participants (Actual)Interventional2005-04-30Completed
Open-label Trial of Imatinib Mesylate in Patients With Unresectable Recurrent Glioblastoma Multiforme Expressing PDGFR (Platelet Derived Growth Factor Receptors) [NCT00171938]Phase 230 participants (Actual)Interventional2004-04-30Terminated
A Randomized, Open Label, Two-Treatment, Multiple Dose, Steady State, Two-period, Cross-over, Multi-Centre Comparative Bioequivalence Study of Imatinib Mesylate Tablet 400 mg of Amneal Pharmaceuticals, USA With GLEEVEC® (Imatinib Mesylate) Tablets 400 mg [NCT02103322]Phase 2/Phase 348 participants (Actual)Interventional2014-02-28Completed
An Open-Label, Randomized, Multicenter Phase II Trial Comparing the Depletion of Malignant Stem Cells With Dasatinib vs. Imatinib in Patients With Newly Diagnosed Chronic Phase Chronic Myeloid [NCT00852566]Phase 246 participants (Actual)Interventional2009-03-31Completed
Phase II Explorative Study of Intermittent Imatinib (IM) Treatment (INTERIM) in Elderly Patients With Ph+ Chronic Myeloid Leukemia (CML) Who Achieved a Stable Complete Cytogenetic Response (CCgR) With Standard IM Therapy [NCT00858806]Phase 278 participants (Actual)Interventional2008-04-30Completed
Imatinib Mesylate (Glivec) as Maintenance Therapy After Cytogenetic Response With Nilotinib (AMN107, Tasigna) First Line in Newly Diagnosed Chronic Myelogenous Leukemia [NCT01316250]25 participants (Anticipated)Interventional2010-08-31Recruiting
Prospective Non-randomized Stratified Study of REduction And DIscontinuation Treatment of TKI (Imatinib, Nilotinib, Dasatinib and Bosutinib) in Adults With Ph+ Chronic Myeloid Leukemia With Stable Deep Molecular Response [NCT04578847]Phase 2100 participants (Anticipated)Interventional2020-01-15Active, not recruiting
Open Label, Pilot Phase II Study of Glivec in Children and Adolescents With Life Threatening Diseases Known to Be Associated With One or More Glivec-Sensitive Tyrosine Kinases [NCT00180830]Phase 236 participants Interventional2003-12-31Terminated
Phase II Trial of Gleevec (Imatinib Mesylate) and Taxotere (Docetaxel) as a Combined Regimen for Advanced Gastric Adenocarcinoma [NCT00209079]Phase 25 participants (Actual)Interventional2004-09-30Terminated(stopped due to Terminated 4/17/07. Drug sponsor withdrew.)
Phase II Study of Imatinib Mesylate in Chordoma [NCT00150072]Phase 255 participants (Actual)Interventional2004-10-31Completed
Phase I/II Study of Xeloda and Gleevec in Patients With Advanced Solid Tumors [NCT00183833]Phase 140 participants (Actual)Interventional2002-12-31Completed
Protein-Tyrosine Kinase Inhibitor (STI571) for Treatment of Patients With Ph+ Chronic Myeloid Leukemia Who Are Resistant to or Intolerant of *-Interferon. A Phase II Study [NCT00511303]Phase 2200 participants Interventional2000-08-31Completed
Protein-Tyrosine Kinase Inhibitor (STI571) for Treatment of Patients With Ph+ Chronic Myeloid Leukemia in Accelerated and Blastic Phase. A Phase II Study [NCT00514969]Phase 20 participants Interventional2000-08-31Completed
Phase II Trial to Study the Tolerability and the Effectiveness of Imatinib in Patients With Chronic Myelogenous Leukemia in Chronic Phase in Relapse After Allogeneic Stem Cell Transplantation [NCT00219726]Phase 230 participants (Anticipated)Interventional2002-05-31Completed
Phase I/II Trial to Study the Dose, Tolerability and the Effectiveness of Imatinib in Combination With Daunorubicine and Cytarabine for Patients With Chronic Myelogenous Leukemia in Myeloid Acute Phase [NCT00219765]Phase 1/Phase 230 participants Interventional2001-05-31Terminated
Phase II Study of Gleevec and Taxotere in Recurrent Non-Small Cell Lung Cancer [NCT00222144]Phase 223 participants (Actual)Interventional2004-09-30Completed
An Open Label, Multi-center Asciminib Roll-over Study to Assess Long-term Safety in Patients Who Have Completed a Novartis Sponsored Asciminib Study and Are Judged by the Investigator to Benefit From Continued Treatment [NCT04877522]Phase 4347 participants (Anticipated)Interventional2022-08-30Recruiting
Phase IIA Study of the Safety and Tolerability of the Use of Imatinib Mesylate (Gleevec) in the Treatment of Systemic Sclerosis [NCT00555581]Phase 230 participants (Actual)Interventional2007-08-31Completed
A Phase 2, Multi-center, Open-label, Randomized Study of Oral Asciminib Added to Imatinib Versus Continued Imatinib Versus Switch to Nilotinib in Patients With CML-CP Who Have Been Previously Treated With Imatinib and Have Not Achieved Deep Molecular Resp [NCT03578367]Phase 2104 participants (Anticipated)Interventional2018-11-22Recruiting
A Phase III Randomized, Open- Label Multi-center Study of Nilotinib Versus Imatinib in Adult Patients With Ph+ Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) Who Have a Suboptimal Cytogenetic Response (CyR) on Imatinib [NCT00519090]Phase 36 participants (Actual)Interventional2007-10-31Terminated(stopped due to This study was terminated due to limited enrollment.)
Phase ll Study of Imatinib Mesylate for the Neoadjuvant Treatment of Patients With Gastrointestinal Stromal Tumors (GIST) [NCT01483014]Phase 230 participants (Actual)Interventional2008-06-30Completed
A Phase II Multicentric Trial to Assess Efficacy and Toxicity of Imatinib in Adult Patients With Metastatic Ocular Melanoma [NCT00421317]Phase 213 participants (Actual)Interventional2005-12-31Terminated(stopped due to Study stopped at the end of the first step)
Effect of Antacids (Mg-Al-based) on Imatinib Mesylate (Gleevec®) Pharmacokinetics in Healthy Volunteers (CSTI571BUS257) [NCT00446316]Phase 112 participants (Actual)Interventional2007-04-30Completed
A Phase I Study of Imatinib Mesylate in Combination With Temozolomide in Patients With Malignant Glioma [NCT00354068]Phase 165 participants (Actual)Interventional2004-07-31Completed
An Exploratory Study of the Effects of Imatinib on Allergic Inflammation Following Out of Allergy Season Repeated Nasal Allergen Challenge in Subjects With Seasonal Allergic Rhinitis Sensitive to Timothy Grass Pollen - an Exploratory Study of c-Kit Inhibi [NCT00426179]Phase 1/Phase 230 participants (Anticipated)Interventional2006-12-31Completed
An Open-label Multicenter Phase II Study of Imatinib Mesylate Treatment of Patients With Malignant Peripheral Nerve Sheath Tumors [NCT00427583]Phase 2/Phase 311 participants (Actual)Interventional2006-05-31Terminated(stopped due to stopped due to slow recruitment and no effect)
A Non-randomized, Open-label Study to Investigate the Effects of Imatinib Mesylate on the Pharmacokinetics of Acetaminophen/Paracetamol in Patients With Newly Diagnosed, Previously Untreated Chronic Myeloid Leukemia in Chronic Phase (CML-CP) [NCT00428909]Phase 112 participants (Actual)Interventional2006-11-30Completed
An Extension to a Phase I Multicenter, Dose Escalation Study of Nilotinib in Combination With Imatinib on a Continuous Daily Dosing Schedule in Adult Patients With Imatinib-Resistant Gastrointestinal Stromal Tumors (GIST) [NCT00441155]Phase 114 participants (Actual)Interventional2006-11-30Completed
A Phase I Study of Capecitabine, Cisplatin and Imatinib in Patients With Unresectable or Metastatic Gastric Cancer. [NCT00601510]Phase 138 participants (Actual)Interventional2007-11-30Completed
Efficacy and Safety of Nilotinib in Patients With a Chronic Disease of the Graft Against the Host (Graft Versus Host, GVH) Did Not Respond to Imatinib Mesylate. [NCT02891395]Phase 265 participants (Actual)Interventional2012-12-24Completed
Evaluation of the Persistence of the Complete Molecular Remission After Stopping Imatinib Chronic Myeloid Leukemia (STIM) [NCT00478985]100 participants (Actual)Interventional2007-06-30Completed
Pilot Study of Imatinib Discontinuation in Patients With Chronic Myeloid Leukemia With Deep Molecular Response - Evaluation of Pioglitazone in Treatment-free Remission (EDI-PIO) [NCT02852486]Phase 231 participants (Actual)Interventional2016-06-22Active, not recruiting
A Phase Ib/II Study of MEK162 in Combination With Imatinib Mesylate in Patients With Untreated Advanced Gastrointestinal Stromal Tumor (GIST) [NCT01991379]Phase 1/Phase 275 participants (Actual)Interventional2013-11-30Active, not recruiting
Multicenter, Single-arm, Two Stage Phase II Trial of RAD001 (Everolimus) With Imatinib in Imatinib-resistant Patients With Progressive GIST [NCT00510354]Phase 428 participants (Actual)Interventional2006-10-31Completed
"CML/021 A Phase II Exploratory Study of IMATINIB High Dose (800mg/gg) in the Treatment of Newly Diagnosed Intermediate Risk Chronic Myeloid Leukemia in Chronic Phase" [NCT00510926]Phase 280 participants Interventional2004-01-31Completed
An Exploratory Phase II Study of the Combination of a Tyrosine Kinase Inhibitor (STI571) and a Pegylated Human Recombinant Interferon alfa2b (PEGINTRON) in the Treatment of Chronic Myeloid Leukemia in Chronic Phase [NCT00511121]Phase 25 participants Interventional2001-04-30Terminated
A Phase 1b/2 Study of Imatinib in Combination With Everolimus in Synovial Sarcoma [NCT01281865]Phase 1/Phase 214 participants (Actual)Interventional2011-01-31Completed
A Multicentre, Open-label Phase II Trial Evaluating the Safety and Efficacy of Ponatinib Induction Followed by Imatinib Maintenance in Adult Patients With Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) ≤ 65 Years [NCT04070443]Phase 2170 participants (Anticipated)Interventional2019-11-13Active, not recruiting
Follow-up of the Persistence of the Complete Molecular Remission After Stopping Imatinib Chronic Myeloid Leukemia [NCT02896829]97 participants (Actual)Observational2013-04-03Completed
Randomized, Multicentre, Phase II Study Evaluating the Interest of Imatinib Treatment Maintenance or Interruption After at Least 10 Years of Treatment in Patients With Locally Advanced/Metastatic Gastrointestinal Stromal Tumors (GISTs) [NCT05009927]Phase 250 participants (Anticipated)Interventional2022-01-03Recruiting
A Prospective Randomized Phase II Study Evaluating the Monitoring of Imatinib Mesylate (Glivec®) Plasmatic Through Level in Patients Newly Diagnosed With Chronic Phase Chronic Myelogenous Leukaemia (CP-CML). [NCT02896842]Phase 2139 participants (Actual)Interventional2010-09-30Completed
Positioning Imatinib for Pulmonary Arterial Hypertension [NCT04416750]Phase 217 participants (Actual)Interventional2021-01-20Active, not recruiting
Flumatinib Versus Imatinib Combined With Multiagent Chemotherapy for Newly Diagnosed Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia: A Prospective, Open-label，Randomized，Multi-center Clinical Trial [NCT05071482]Phase 4238 participants (Anticipated)Interventional2021-09-16Recruiting
Multicentric Phase II Study to Evaluate Feasibility and Efficacy of Association of Imatinib Mesylate and Zoledronic Acid in Patients With Chronic Myeloid Leukaemia in Cytogenetic Response Without Molecular Response After One Year of Imatinib Mesylate Mono [NCT00210119]Phase 219 participants (Actual)Interventional2006-07-12Terminated
A Phase II Study of Intermittent Gleevec® (Imatinib Mesylate) and Weekly Paclitaxel in Patients Aged 70 or Older With Advanced Non-small Cell Lung Cancer [NCT01011075]Phase 234 participants (Actual)Interventional2009-08-31Completed
A Phase I Study of STI571 in Ph+ Leukemia [NCT00004932]Phase 131 participants (Actual)Interventional2002-01-31Completed
[NCT01271166]Phase 110 participants (Actual)Interventional2007-10-31Terminated
A Phase I-II, Open-label Study of RAD001 in Combination With Glivec®/Gleevec™ (Imatinib) in Patients With Glivec/Gleevec-refractory/Resistant Gastrointestinal Stromal Tumors. [NCT01275222]Phase 1/Phase 2117 participants (Actual)Interventional2002-11-13Completed
Tyrosine Kinase Inhibitors of BCR/ABL: Pharmacokinetic and Pharmacogenetic Study in Patients Affected by Chronic Myeloid Leukemia. Evaluation of Efficacy and Tolerability [NCT01860456]412 participants (Anticipated)Observational2013-05-31Recruiting
Phase II Clinical Study of Imatinib Mesylate in Patients With Malignant Gastrointestinal Stromal Tumors (Extension Study) [NCT00237172]Phase 272 participants (Actual)Interventional2002-09-30Completed
Phase I Study Of The Combination Of 17-AAG And Imatinib Mesylate (Gleevec) In Patients With Blastic Phase, Accelerated Phase Of Chronic Mesylate Leukemia (CML) Or Patients With Chronic Phase CML Who Have Not Achieved A Cytogenetic Response With Imatinib M [NCT00066326]Phase 10 participants Interventional2003-06-30Completed
Phase II Trial of Imatinib Mesylate Maintenance Therapy in Patients With C-Kit (+) Extensive-Stage Small Cell Lung Cancer [NCT00248482]Phase 26 participants (Actual)Interventional2002-02-28Completed
A Phase II Study of Gleevec and Arsenic Trioxide in Patients With CML Who Fail to Achieve a Complete Response to Initial Gleevec Treatment [NCT00250042]Phase 26 participants (Actual)Interventional2004-04-30Completed
A Phase II Trial of STI-571/Imatinib (Gleevec®) (NSC-716051) in Neuroendocrine Carcinoma of the Skin (Merkel Cell Carcinoma) [NCT00068783]Phase 240 participants (Actual)Interventional2003-10-31Completed
A Phase I Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Refractory or Relapsed Leukemias [NCT00258271]Phase 118 participants (Anticipated)Interventional2005-03-31Completed
A Phase I Study of CCI-779 in Combination With Imatinib Mesylate in Chronic Myelogenous Leukemia [NCT00101088]Phase 121 participants (Actual)Interventional2005-04-30Terminated
A Multi-Center Phase II Study of Nonmyeloablative Conditioning With TBI and Fludarabine for HLA-Matched Related Hematopoietic Cell Transplantation for Treatment of Chronic Myeloid Leukemia in Chronic and Accelerated Phase [NCT00110058]Phase 240 participants (Anticipated)Interventional2005-02-28Completed
A Phase II Study on Preoperative Administration of Gleevec in Patients With Initially Non-Resectable Gastrointestinal Stromal Tumor [NCT00290485]Phase 250 participants Interventional2005-08-31Recruiting
Open-Label Trial of Neoadjuvant Imatinib Mesylate (Glivec) in Patients With Locally Advanced Malignant Gastrointestinal Stromal Tumors (GIST) Expressing c-Kit or Platelet-Derived Growth Factor Receptor-alpha [NCT00112632]Phase 240 participants (Anticipated)Interventional2005-02-28Completed
Phase 2 Study of Imatinib-Combined Chemotherapy for Newly Diagnosed BCR-ABL-Positive Acute Lymphoblastic Leukemia [NCT00130195]Phase 2100 participants (Actual)Interventional2002-09-30Completed
Vaccination for CML Patients With Persistent Disease on Imatinib Mesylate [NCT00301093]Phase 13 participants (Actual)Interventional2005-09-30Completed
Randomized Double-Blind Phase II Trial of Docetaxel and Imatinib Versus Docetaxel and Placebo in Metastatic Androgen-Independent Prostate Cancer (AIPC) With Bone Metastases [NCT00080678]Phase 2116 participants (Actual)Interventional2003-05-31Completed
[NCT00081926]Phase 4112 participants Interventional2003-10-31Completed
A Phase I, Two Arm, Open-label, Randomized, Study to Investigate the Effect of Food on the Bioavailability of a Single 800 mg Imatinib Dose in Modified Release Formulations (MR3 and MR4) and Compare the Bioavailability Between MR3, MR4 and Imatinib 400 mg [NCT00420043]Phase 132 participants (Actual)Interventional2006-09-30Completed
A Phase II Trial of Gemzar (Gemcitabine) and Gleevec (Imatinib Mesylate) in Patients With Metastatic Renal Cell Carcinoma [NCT00323791]Phase 2100 participants (Anticipated)Interventional2006-04-30Terminated(stopped due to slow accrual)
A Phase I-II, Study of RAD001 in Combination With Imatinib (Glivec®/Gleevec™) in Patients With Chronic Myelogenous Leukemia (CML) in Chronic Phase Who Are Not In Complete Cytogenetic Response to Imatinib-Alone at Study Entry [NCT00093639]Phase 1/Phase 20 participants Interventional2004-08-31Completed
Phase II Study of Glivec (Imatinib) in Locally Advanced and/or Metastatic Soft Tissue Sarcomas Expressing the t(17;22)(q22;q13) Translocation Resulting in a COL1A1/PDGF-beta Fusion Protein i.e. DermatoFibroSarcoma Protuberans (DFSP) and Giant Cell Fibrobl [NCT00085475]Phase 217 participants (Actual)Interventional2004-04-30Completed
Multicenter, Phase III Study Comparing Imatinib (STI571, Glivec®) Standard Dose (400 Mg/Day) With Imatinib High Dose Induction (800 Mg/Day) Followed by Standard Dose Maintenance (400 Mg/Day) in Pretreated CML Patients in Chronic Phase [NCT00327262]Phase 3240 participants Interventional2004-01-31Recruiting
Glivec (Imatinib Mesylate) in the Treatment of Polycythemia Vera [NCT00430066]Phase 29 participants (Actual)Interventional2007-02-28Completed
A Double-Blind, Placebo-Controlled, Randomized Study of the Efficacy (Gleevec Imatinib Mesylate) in Patients With Idiopathic Pulmonary Fibrosis [NCT00131274]Phase 2/Phase 3120 participants Interventional2003-04-30Completed
Determination of the In-Tumor-Concentration of Imatinib Mesylate in Malignant Glioma After Oral Administration [NCT00401024]Phase 13 participants (Actual)Interventional2006-10-12Completed
A Randomized Multi-Center Open Label Study of BMS-354825 vs Imatinib Mesylate (Gleevec®) 800 mg/d in Subjects With Chronic Phase Philadelphia Chromosome-Positive Chronic Myeloid Leukemia Who Have Disease That is Resistant to Iamtinib at a Dose of 400-600 [NCT00112775]Phase 20 participants Interventional2005-03-31Active, not recruiting
A Phase I/II Study to Evaluate the Efficacy and Toxicity of Imatinib Mesylate in Combination With Dacarbazine and Capecitabine in Medullary Thyroid Carcinoma [NCT00354523]Phase 1/Phase 221 participants (Actual)Interventional2004-12-31Terminated(stopped due to Study closed following Phase I portion, insufficient activity to continue to Phase II.)
A Phase II Study of Everolimus in Combination With Imatinib in Metastatic Melanoma [NCT00402662]Phase 23 participants (Actual)Interventional2006-02-28Terminated(stopped due to unexpected level of toxicity)
A Prospective, Randomized, Phase II Study of Preoperative Plus Postoperative Imatinib Mesylate (Gleevec, Formerly STI-571) in Patients With Primary, Recurrent, or Metastatic Resectable, Kit-Expressing, Gastrointestinal Stromal Tumor (GIST) [NCT00500188]Phase 228 participants (Actual)Interventional2003-07-31Completed
A Phase II Study Evaluating the Efficacy and Tolerance of Combination Therapy of Imatinib Mesylate (IM) +-2A Interféron for Chronic Phase CML Patients Resistant or Refractory to IM Used as Single Therapy for at Least One Year [NCT00146913]Phase 230 participants Interventional2004-03-31Active, not recruiting
A Phase I Multicenter, Dose Escalation Study of AMN107 in Combination With Imatinib on a Continuous Daily Dosing Schedule in Adult Patients With Imatinib-resistant Gastrointestinal Stromal Tumors (GIST) [NCT00135005]Phase 159 participants (Actual)Interventional2005-08-31Completed
A Phase II Study of Gleevec (Imatinib Mesylate) In Patients With BCR-Negative Myeloproliferative Disorders Including Patients With Idiopathic Myelofibrosis With Myeloid Dysplasia or Chronic Myelomonocytic Leukemia [NCT00136409]Phase 234 participants (Actual)Interventional2002-05-31Completed
Evaluation of Imatinib (GLIVEC) After Induction Therapy in Patients Aged More Than 55 Years With Philadelphia Positive Acute Lymphoblastic Leukaemia (Ph+ ALL) : a Non Randomised, Controlled, Open, Multicentric, International Phase II Clinical Study (CSTI [NCT00149136]Phase 230 participants Interventional2002-08-31Active, not recruiting
Efficacy of Tyrosine Kinase Inhibition in Reducing Eosinophilia in Patients With Myeloid and/or Steroid-Refractory Hypereosinophilic Syndrome [NCT00044304]Phase 260 participants (Anticipated)Interventional2002-09-26Recruiting
A Phase I Trial of Ipilimumab (Immunotherapy) and Imatinib Mesylate (c-Kit Inhibitor) in Patients With Advanced Malignancies [NCT01738139]Phase 168 participants (Actual)Interventional2013-02-19Active, not recruiting
Pilot Study of Gleevec/Imatinib Mesylate (STI-571, NSC 716051) in Neurofibromatosis (NF1) Patient With Plexiform Neurofibromas [NCT01140360]Phase 1/Phase 221 participants (Actual)Interventional2012-02-29Completed
A Therapeutic Trial of Bortezomib (Velcade), Vorinostat (SAHA) and Dexamethasone for Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) [NCT01312818]Phase 22 participants (Actual)Interventional2011-06-30Terminated(stopped due to Slow accrual)
A Phase I-II Trial of Gleevec (Imatinib Mesylate) in Combination With Chlorambucil in Previously Treated Chronic Lymphocytic Leukemia (CLL) Patients [NCT00558961]Phase 1/Phase 213 participants (Actual)Interventional2005-10-31Terminated(stopped due to Unsatisfactory enrollment)
Post-Marketing Clinical Study of Postoperative Adjuvant Therapy With Imatinib Mesylate in Patients With Gastrointestinal Stromal Tumors (GIST) [NCT00171977]Phase 464 participants (Actual)Interventional2004-07-31Completed
A Randomized, Open-label, Multi-center Study to Evaluate the Efficacy of Nilotinib Versus Best Supportive Care With or Without a Tyrosine Kinase Inhibitor (Investigator's Choice) in Adult Patients With Gastrointestinal Stromal Tumors Resistant to Both Ima [NCT00471328]Phase 3248 participants (Actual)Interventional2007-03-31Completed
Effect of a Proton Pump Inhibitor (Omeprazole, Prilosec®) on Imatinib Mesylate (Gleevec®) Pharmacokinetics in Healthy Volunteers (CSTI571BUS258) [NCT00446004]Phase 115 participants (Actual)Interventional2007-04-30Completed
Phase II Randomized Double Blind Clinical Trial of'Imatinib Mesylate STI571 (Glivec®) Versus Placebo in Patients With Severe Cutaneous Scleroderma or Systemic Sclerosis With Severe Cutaneous Involvement. [NCT00479934]Phase 228 participants (Actual)Interventional2007-12-31Completed
A Phase III Study Comparing Imatinib Standard Dose (400 mg/Day) Versus Imatinib High Dose (800 mg/Day) in the Treatment of Newly Diagnosed High Risk Chronic Myeloid Leukemia in Chronic Phase [NCT00514488]Phase 30 participants Interventional2004-06-30Completed
A Pivotal Registrational Phase 3 Study of Olverembatinib Combined With Chemotherapy Versus Imatinib Combined With Chemotherapy in Patients With Newly Diagnosed Philadelphia Chromosome-positive Acute Lymphoblastic Leukemia (Ph+ALL) [NCT06051409]Phase 3350 participants (Anticipated)Interventional2023-09-02Recruiting
A Proof of Concept Trial of Gleevec (Imatinib) in Active Diffuse Scleroderma [NCT01545427]Phase 210 participants (Actual)Interventional2008-04-30Terminated(stopped due to Frequent adverse events occurred early in treatment with poor tolerability.)
Intermediate and High Risk Localized, Completely Resected, Gastrointestinal Stromal Tumors (GIST) Expressing KIT Receptor: A Controlled Randomized Trial on Adjuvant Imatinib Mesylate (Glivec) Versus No Further Therapy After Complete Surgery [NCT00103168]Phase 3908 participants (Actual)Interventional2004-12-31Completed
Short (12 Months) Versus Long (36 Months) Duration of Adjuvant Treatment With the Tyrosine Kinase Inhibitor Imatinib Mesylate of Operable GIST With a High Risk of Recurrence [NCT00116935]Phase 3400 participants (Actual)Interventional2004-02-29Completed
Open-label Trial of Glivec® (Imatinib Mesylate) in Patients With Primary or Recurrent Dermatofibrosarcoma Protuberans [NCT00122473]Phase 1/Phase 230 participants Interventional2004-01-31Completed
Phase III Randomized, Intergroup Trial Assessing the Clinical Activity Of STI-571 at Two Dose Levels in Patients With Unresectable or Metastatic Gastrointestinal Stromal Tumors (GIST) Expressing the Kit Receptor Tyrosine Kinase (CD117) [NCT00009906]Phase 3748 participants (Actual)Interventional2000-12-31Terminated
A Phase II Study of Adjuvant STI571 (Gleevec TM) Therapy in Patients Following Completely Resected High-risk Primary GastroIntestinal Stromal Tumor (GIST) [NCT00025246]Phase 289 participants (Actual)Interventional2001-09-30Completed
Phase II Trial of Gleevec (Imatinib Mesylate, STI-571) in Metastatic Melanoma [NCT00027586]Phase 222 participants (Actual)Interventional2001-09-30Completed
Positive Ph Acute Lymphoblastic Leucemia With Intensive Induction Chemotherapy and Glivec, Before and After the Hematopoetic Progenitor Transplant [NCT00388895]Phase 235 participants Interventional2002-06-30Completed
A Phase II Study of Gleevec in Ph+ Chronic Phase Chronic Myelogenous Leukemia [NCT00030394]Phase 264 participants (Actual)Interventional2002-09-30Completed
A Phase II Study of Gleevec (Imatinib Mesylate, NSC 716051 Formerly STI571) in Children With Refractory or Relapsed Solid Tumors [NCT00030667]Phase 2100 participants (Actual)Interventional2002-05-31Completed
Phase II Trial of Gleevec (Formerly Known as STI571) in Patients With Soft Tissue and Bone Sarcomas: A Multi-Disciplinary Trial of the North American Sarcoma Study Group of the Connective Tissue Oncology Society [NCT00031915]Phase 20 participants Interventional2002-06-30Completed
A Phase II Trial Of STI571 For The Treatment Of Platinum And Taxane Refractory Stage III And IV Epithelial Ovarian Cancer And Primary Peritoneal Cancer [NCT00036751]Phase 240 participants (Actual)Interventional2002-04-30Completed
Phase I Trial of Fixed Dose STI571 (Imatinib Mesylate) With Escalating Doses of Docetaxel in Patients With Metastatic Androgen-Independent Prostate Cancer [NCT00038194]Phase 128 participants (Actual)Interventional2001-10-31Completed
A Phase I/II Trial of STI571 and High-Dose Cytarabine in Myeloid Blast Crisis of Chronic Myeloid Leukemia [NCT00015834]Phase 1/Phase 246 participants (Actual)Interventional2001-05-31Completed
Open Label Phase II Study On STI571 (Glivec) Administered As A Daily Oral Treatment In Gliomas [NCT00039364]Phase 2112 participants (Actual)Interventional2002-03-31Completed
Phase I Study of Zarnestra (R115777.USA30) and Gleevec (Imatinib Mesylate) in Chronic Phase Chronic Myelogenous Leukemia (CML) [NCT00040105]Phase 126 participants (Actual)Interventional2002-10-31Completed
A Phase II Evaluation Of Gleevec (Imatinib Mesylate) (IND #61135, NSC #716051) In The Treatment Of Persistent Or Recurrent Epithelial Ovarian Or Primary Peritoneal Carcinoma [NCT00041041]Phase 260 participants (Actual)Interventional2002-06-30Completed
A Phase III Randomized Double-Blind Study of Adjuvant STI571 (Gleevec™) Versus Placebo in Patients Following the Resection of Primary Gastrointestinal Stromal Tumor (GIST) [NCT00041197]Phase 3732 participants (Actual)Interventional2002-06-30Completed
A Phase II Study Of Imatinib Mesylate (Gleevec, Formerly Known As STI571; IND 61,135, NSC #716051) In Patients With Refractory Seminoma [NCT00042952]Phase 232 participants (Actual)Interventional2002-06-30Terminated(stopped due to Administratively complete.)
A Phase I Study of Imatinib (Gleevec) in Combination With Irinotecan and Cisplatin in Extensive Stage Small Cell Lung Cancer [NCT00045604]Phase 10 participants Interventional2002-07-31Completed
A PHASE II STUDY OF G3139 (GENASENSE™, NSC # 683428 IND # 58842) + IMATINIB MESYLATE (GLEEVEC®, STI571) IN PATIENTS WITH IMATINIB-RESISTANT CHRONIC MYELOID LEUKEMIA [NCT00049192]Phase 243 participants (Anticipated)Interventional2002-11-30Completed
A Phase I/II Study To Determine The Safety, Tolerability, And Anti-Leukemic Effects of Trisenox (Arsenic Trioxide) In Combination With Gleevec (STI571) In Patients With Resistant Chronic Myelogenous Leukemia In Chronic Phase [NCT00053248]Phase 1/Phase 216 participants (Actual)Interventional2002-10-31Completed
Phase II Exploratory Study Of AG-858 Plus Gleevec™ In Patients With Chronic Myelogenous Leukemia (CML) In Chronic Phase Who Are Cytogenetically Positive After Treatment With Gleevec™ [NCT00058747]Phase 240 participants Interventional2003-03-31Terminated(stopped due to Business decision of the sponsor)
Phase I Study Of Flavopiridol In Combination With Imatinib Mesylate (STI571, Gleevec) In Bcr/Abl+ Hematological Malignancies [NCT00064285]Phase 122 participants (Actual)Interventional2003-06-30Completed
A Phase I Study Of Weekly Taxotere (Docetaxel) And Gleevec (STI571, Imatinib Mesylate, CGP 57148B) In Locally Advanced Or Metastatic Breast Cancer [NCT00080665]Phase 112 participants (Actual)Interventional2003-12-31Completed
A Phase I/II Study to Determine Safety and Efficacy of Arsenic Trioxide (Trisneox™) in Combination With Imatinib (STI571, Gleevec™) in Patients With Chronic Myelogenous Leukemia in Accelerated or Blastic Phase Disease or Ph+ Acute Lymphoblastic Leukemia [NCT00081133]Phase 1/Phase 20 participants Interventional2003-12-31Completed
Phase I/II Trial of STI571 (NSC 716051) in Patients With Recurrent Malignant Gliomas [NCT00010049]Phase 1/Phase 2105 participants (Actual)Interventional2001-02-27Completed
A Phase I/II Trial of STI-571 and Chemotherapy in Lymphoid Blast Crisis of Chronic Myeloid Leukemia and Philadelphia Chromosome-Positive Acute Lymphoid Leukemia [NCT00015860]Phase 1/Phase 20 participants Interventional2001-05-31Completed
A Children's Oncology Group Pilot Study for the Treatment of Very High Risk Acute Lymphoblastic Leukemia in Children and Adolescents (Imatinib (STI571, GLEEVEC) NSC#716051) [NCT00022737]Phase 3220 participants (Actual)Interventional2002-10-31Completed
A Phase I Pharmacokinetic Study of STI571 in Patients With Advanced Malignancies and Varying Degrees of Renal Dysfunction for the CTEP-Sponsored Organ Dysfunction Working Group [NCT00026169]Phase 169 participants (Anticipated)Interventional2001-09-30Completed
Open Label Pilot Phase II Study of STI571 in the Treatment of Patients With Idiopathic Hypereosinophilic Syndrome (HES) and Eosinophilic Leukemias [NCT00276926]Phase 20 participants Interventional2003-03-31Recruiting
Phase II Study Of Gleevec (Imatinib Mesylate Formerly Known As(STI571) (NSC #716051) In Patients With Colorectal Cancer Stage IV [NCT00041340]Phase 237 participants (Actual)Interventional2002-05-31Completed
Phase II Clinical Trial With Proteomic Profiling Of Imatinib Mesylate (Gleevec; STI571), A PDGFR And C-Kit Inhibitor, In Patients With Refractory Or Relapsed Epithelial Ovarian Cancer, Fallopian Tube And Primary Peritoneal Cancer [NCT00039585]Phase 20 participants Interventional2002-05-31Completed
Intensive Induction Therapy for Children With Acute Lymphoblastic Leukemia (ALL) Who Experience a Bone Marrow Relapse [NCT00049569]126 participants (Anticipated)Interventional2003-01-31Completed
A Phase I Study Of STI 571 (Gleevec) In Combination With Cisplatin/Irinotecan In Patients With Extensive Stage Small Cell Lung Cancer [NCT00052494]Phase 19 participants (Actual)Interventional2003-04-30Completed
A Phase I Pharmacokinetic Study of STI571 in Patients With Advanced Malignancies and Varying Levels of Liver Dysfunction [NCT00025415]Phase 160 participants (Actual)Interventional2001-08-31Completed
A Dose-ranging Phase I/II Study of STI571 in Combination With Cytarabin in Patients With First Chronic Phase Chronic Myeloid Leukemia [NCT00028847]Phase 1/Phase 260 participants (Anticipated)Interventional2001-04-30Active, not recruiting
Phase II Trial of Gleevec (STI571) in Therapy of Ewing's Family of Tumors and Desmoplastic Small Round Cell Tumors [NCT00062205]Phase 240 participants (Anticipated)Interventional2002-06-30Completed
A Phase II Study Of Gleevec (Imatinib Mesylate Formerly Known as STI-571) In Patients With Myelofibrosis [NCT00039416]Phase 218 participants (Actual)Interventional2002-04-30Completed
Imatinib Mesylate (Gleevec®, STI571) in Combination With Docetaxel (Taxotere) for the Treatment of Advanced, Platinum-Refractory Ovarian Cancer and Primary Peritoneal Carcinomatosis: Hoosier Oncology Group GYN03-62 [NCT00216112]Phase 223 participants (Actual)Interventional2003-12-31Completed
A Phase III Prospective Randomized Comparison of Imatinib at a Dose of 400mg in Combination With Peg-Interferon-alpha2a (Peg-IFNa2a) or Cytarabine (Ara-C)Versus Imatinib at a Dose of 600mg Versus Imatinib a Dose of 400mg for Previously Untreated Chronic M [NCT00219739]Phase 3789 participants (Actual)Interventional2003-09-30Completed
Phase I Trial of Cisplatin, Pemetrexed, and Imatinib Mesylate in Unresectable or Metastatic Malignant Mesothelioma [NCT00402766]Phase 119 participants (Actual)Interventional2006-08-31Completed
Phase II Trial of STI571 in Metastatic Breast Cancer [NCT00045188]Phase 235 participants (Actual)Interventional2002-08-31Completed
A Phase I Study of the Inhibition of Platelet Derived Growth Factor Using Imatinib Mesylate Combined With Intravitreal Ranibizumab in the Treatment of Choroidal Neovascularization Secondary to Age-Related Macular Degeneration [NCT00403156]Phase 10 participants (Actual)Interventional2006-11-30Withdrawn(stopped due to Lack of recruitment)
A Phase II Open Label Study to Determine Safety and Efficacy of Interferon-alpha in Combination With Imantinib Mesylate (Gleevec) in Patients With Chronic Phase Chronic Myelogenous Leukemia Who Have Not Achieved a Complete Cytogenetic Response to Gleevec [NCT00045422]Phase 20 participants Interventional2002-04-30Completed
Randomized Trial of Therapy of Early Phase Chronic Myelogenous Leukemia With High-Dose Imatinib Mesylate (Gleevec) Alone or in Combination With Peg-Alpha Interferon (PEG-Intron) and Sargramostim (GM-CSF) [NCT00050531]Phase 394 participants (Actual)Interventional2003-04-30Completed
3-Month, Multi-Center, Randomized, Double-Blind, Placebo-Controlled Study to Evaluate Efficacy, Safety & Tolerability of Imatinib 400 mg Daily in Combination With Methotrexate (MTX)Compared to MTX Alone in the Treatment of Rheumatoid Arthritis (RA). [NCT00154336]Phase 250 participants (Actual)Interventional2004-07-31Completed
Phase II Trial of Gleevec (Imatinib Mesylate, STI571) Maintenance Therapy After Induction Irinotecan and Cisplatin in Patients With C-Kit Positive, Extensive-Stage Small Cell Lung Cancer [NCT00156286]Phase 220 participants Interventional2002-03-31Completed
The Possible Role of Glivec in Patients With Tumor Cells Positive for C-kit or Platelet Derived Growth Factor Receptor (PDGFR); a Multi Center Study. [NCT00159016]Phase 2100 participants Interventional2002-08-31Withdrawn(stopped due to the PI is no longer work at Hadassah)
Phase II Trial of STI571 in Patients With Relapsed Small Cell Lung Cancer [NCT00052949]Phase 291 participants (Anticipated)Interventional2003-05-31Completed
Phase II Study of Imatinib Mesylate (Gleevec, STI-571) (NSC#716051) and Decitabine (5-AZA-2'-Deoxycitidine) (NSC#127716), in Chronic Myelogenous Leukemia in Accelerated and Blastic Phases [NCT00054431]Phase 280 participants (Actual)Interventional2003-01-31Completed
A Phase 2 Study Of Imatinib Mesylate In Adenoid Cystic, Lymphoepithelioma-Like And Myoepithelial Salivary Gland Carcinomas [NCT00045669]Phase 216 participants (Actual)Interventional2002-07-31Completed
Treatment Optimization Trial in Chronic Myeloid Leukemia (CML) - Randomized Controlled Comparison of Imatinib vs. Imatinib/Interferon-alpha vs. Imatinib/Low-Dose AraC vs. Interferon-alpha Standard Therapy and Determination of the Role of Allografting in N [NCT00055874]Phase 31,551 participants (Actual)Interventional2002-06-30Completed
Phase I Study of Lonafarnib (SCH66336) and Gleevec (Imatinib Mesylate) in Chronic Myelogenous Leukemia (CML) [NCT00047502]Phase 123 participants (Actual)Interventional2002-11-01Completed
Phase I of Trastuzumab and Imatinib Mesylate (Gleevec®, Formerly Known as STI-571) in Patients With Recurrent or Metastatic Her-2/Neu Expressing Cancer [NCT00084513]Phase 118 participants (Anticipated)Interventional2004-08-31Completed
A Phase II Study of Imatinib (NSC-716051) in Patients With Locally Advanced or Metastatic Dermatofibrosarcoma Protuberans [NCT00084630]Phase 240 participants (Actual)Interventional2004-05-31Completed
Crossover From Docetaxel and Placebo to Docetaxel and Imatinib in Patients With Androgen-Independent Prostate Cancer With Bone Metastases: Extension Trial to ID03-0008 [NCT00084825]Phase 223 participants (Actual)Interventional2003-05-31Completed
A Randomized, Multicenter Open Label Phase II Study to Determine the Safety and Efficacy of Induction Therapy With Imatinib in Comparison With Standard Induction Chemotherapy in Elderly (> 55 Years) Patients With Ph Positive Acute Lymphoblastic Leukemia ( [NCT00199186]Phase 20 participants Interventional2002-03-31Recruiting
Therapy of Early Chronic Phase Chronic Myelogenous Leukemia (CML) With Gleevec (STI571) [NCT00048672]Phase 250 participants (Actual)Interventional2001-03-31Completed
A Phase II Study of Imatinib Mesylate Plus Hydroxyurea in the Treatment of Patients With Recurrent/Progressive Meningioma [NCT00354913]Phase 221 participants (Actual)Interventional2005-05-31Completed
Phase II Study of Imatinib Mesylate and Docetaxel in Patients With Metastatic or Recurrent Head and Neck Squamous Cell Cancer [NCT00485485]Phase 27 participants (Actual)Interventional2007-01-31Completed
Open-label Trial of Imatinib in Patients With Desmoid Tumor and Chondrosarcoma [NCT00928525]Phase 235 participants (Actual)Interventional2007-05-31Completed
Protocol Number: HJKC3-0003. Treatment Free Remission After Combination Therapy With Asciminib (ABL001) Plus Imatinib in Chronic Phase Chronic Myeloid Leukemia (CP-CML) Patients Who Relapsed After a Prior Attempt at TKI Discontinuation [NCT04838041]Phase 251 participants (Anticipated)Interventional2021-11-11Recruiting
Prospective, Phase II, Randomized, Open-label, Parallel Group Study to Evaluate the Efficacy of Baricitinib, Imatinib or Supportive Treatment in Patients With SARS Cov2 Pneumonia [NCT04346147]Phase 2168 participants (Actual)Interventional2020-05-07Active, not recruiting
Phase II Trial Of Imatinib Mesylate (Gleevec®) (NSC-716051) In Combination With Capecitabine (Xeloda®) (NSC-712807) In Metastatic Breast Cancer [NCT00087152]Phase 227 participants (Actual)Interventional2004-06-30Completed
An Open-Label Randomized Phase III Study of Dasatinib vs. High-Dose (600 mg) Imatinib Mesylate in the Treatment of Subjects With Chronic Phase Philadelphia Chromosome-Positive Chronic Myeloid Leukemia Who Are Imatinib Failures or Who Have Had a Suboptimal [NCT00362466]Phase 33 participants (Actual)Interventional2007-04-30Terminated(stopped due to Insufficient Enrollment)
Bioequivalence Study of Mesylate Imatinib Capsule in Chronic Myeloid Leukemia Body [NCT01795716]Phase 121 participants (Actual)Interventional2012-09-30Completed
Phase III Trial Evaluating the Effectiveness of a Dose Adjustment of IM on the Molecular Response in Patients With LMC in Chronic Phase Treated With IM 400 mg / Day for at Least Two Years, Complete Cytogenetic Response for at Least One Year [NCT01827930]Phase 368 participants (Actual)Interventional2009-07-31Terminated(stopped due to Difficulties of enrolment of Patient)
Phase II Trial of Docetaxel Plus Imatinib Mesylate in Metastatic Breast Cancer [NCT00193180]Phase 237 participants (Actual)Interventional2005-05-31Completed
Efficacy, Safety and Long-term Prognosis of Imatinib in Patients Newly Diagnosed With Chronic Myelogenous Leukemia (Chronic Phase) [NCT00237120]Phase 3100 participants Interventional2002-11-30Completed
An Extension to a Phase II Study to Determine the Efficacy and Safety of STI571 in Patients With Chronic Myeloid Leukemia Who Are Refractory to or Intolerant of Interferon-Alpha [NCT00171223]Phase 2532 participants (Actual)Interventional1999-12-06Completed
Exploring the Molecular Mechanism of Secondary Resistance to Imatinib in Gastrointestinal Stromal Tumors Based on KIT Mutation [NCT05895942]190 participants (Anticipated)Observational [Patient Registry]2021-09-10Recruiting
A Multicenter Pilot Study Evaluating the Safety and Efficacy of Imatinib as Post-Transplant Therapy for High- Risk Philadelphia Chromosome-Positive Leukemias [NCT00244829]Phase 1/Phase 20 participants Interventional2004-01-31Completed
A Phase I Dose Escalation Study of Imatinib Mesylate (Gleevec/STI571) Plus Capecitabine (Xeloda) in Advanced Solid Tumor Malignancies [NCT00253565]Phase 125 participants (Actual)Interventional2003-08-31Completed
An Open-label Trial of Glivec in Patients With Unresectable or Metastatic Malignant Gastrointestinal Stromal Tumors Expressing C-kit. [NCT00293124]Phase 3125 participants (Actual)Interventional2004-03-31Completed
Open-label Trial of Imatinib Mesylate in Patients With Refractory Desmoplastic Small Round Cell Tumors (DSRCT) Expressing PDGF-R [NCT00417807]Phase 1/Phase 29 participants (Actual)Interventional2005-08-31Completed
A Phase I Trial of Imatinib Mesylate (Gleevec, Formerly Known as STI571) in Combination With Daunorubicin and Cytarabine for C-kit Positive Relapsed AML [NCT00268229]Phase 121 participants (Actual)Interventional2003-07-31Completed
[NCT00297570]Phase 390 participants (Anticipated)Interventional2006-02-28Recruiting
Phase I/II Study of Gleevec (Imatinib Mesylate, Formerly Known as STI571) and Gemcitabine for Advanced Pancreas Cancer [NCT00281996]Phase 119 participants (Actual)Interventional2005-03-31Terminated(stopped due to Closed to accrual to allow enrollment on another more promising trial.)
Multicentric Phase I/II Study Evaluating the Efficacy and Toxicity of Imatinib in Adult Patients With Aggressive Fibromatosis That Cannot be Treated by Surgery or Curative Radiotherapy [NCT00287846]Phase 1/Phase 240 participants (Actual)Interventional2004-09-30Completed
Young Adult With Acute Lymphoblastic Leukemia (ALL) : a Multicentric Protocol. GRAALL 2005 : T ALL or B ALL Non Ph GRAALL 2005 R : B ALL Non Ph CD20+ GRAAPH 2005 : ALL Ph [NCT00327678]Phase 31,080 participants (Actual)Interventional2006-05-31Completed
Phase II Trial of Gleevec and Low-Dose Ara-C for Elderly Patients With C-Kit Positive Acute Myeloid Leukemia and High-Risk Myelodysplastic Syndromes [NCT00451997]Phase 210 participants (Actual)Interventional2004-03-31Completed
Pilot Study of Imatinib (Gleevec) as Treatment for Advanced Thymic Carcinoma [NCT00314873]Phase 111 participants (Actual)Interventional2006-04-30Completed
Phase II Study of Flumatinib Versus Imatinib in Adult Patients With Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) [NCT01503502]Phase 2150 participants (Actual)Interventional2011-08-31Active, not recruiting
An Open-label, Randomized, Single Dose, Crossover Phase I Clinical Trial to Compare Pharmacokinetic Property of SYO-1126 and Glivec Film Coated Tab., 4T (400mg) in Healthy Male Volunteers [NCT01504984]Phase 130 participants (Actual)Interventional2012-03-31Completed
A Phase 3 Multinational, Multi-center, Open-Label, Randomized Study of the Efficacy of Radotinib Versus Imatinib in Newly Diagnosed Ph+ CML Patients in Early Chronic Phase [NCT01511289]Phase 3242 participants (Actual)Interventional2011-08-31Completed
Imatinib for the Treatment of SARS-COV-2 Induced Pneumonia: A Pilot Study [NCT04422678]Phase 330 participants (Anticipated)Interventional2020-06-30Not yet recruiting
A Randomized, Open-label, Single Dose, 2-Treatment, 2-Period, 2-Way Crossover Study to Assess Safety and Pharmacokinetics of Megavec 400 mg (Imatinib Mesylate) Under Fasted Conditions in Healthy Male Subjects [NCT01653314]Phase 140 participants (Actual)Interventional2012-01-31Completed
A Multicentre, Randomized Trial in Adults With de Novo Philadelphia-Chromosome Positive Acute Lymphoblastic Leukemia to Assess the Efficacy of Ponatinib Versus Imatinib in Combination With Low-intensity Chemotherapy, to Compare End of Therapy With Indicat [NCT06061094]Phase 2220 participants (Anticipated)Interventional2023-07-14Recruiting
Treatment Protocol for Newky Diagnosed Adult Ph-Chromosome Positive (BCR::ABL1) Acute Lymphoblastic Leukemia (LALPh2022) [NCT06175702]150 participants (Anticipated)Observational2023-12-25Not yet recruiting
A Randomized, Open-label, Single-dose, Crossover Clinical Trial to Compare the Pharmacokinetics of Imatinib Mesylate Tablet 400 mg (1 Tablet) and Glivec Film-coated Tablet 100 mg (4 Tablets) After Oral Administration in Healthy Male Subjects (Phase I) [NCT01751919]Phase 137 participants (Actual)Interventional2012-05-31Completed
A Phase II Randomized Study of Imatinib Versus High Dose Interferon as Adjuvant Therapy in KIT-mutated Patients With Resected Melanoma [NCT01782508]Phase 240 participants (Anticipated)Interventional2012-08-31Recruiting
A Trial of De-escalation and Stopping Treatment in Chronic Myeloid Leukaemia Patients With Excellent Responses to Tyrosine Kinase Inhibitor Therapy [NCT01804985]Phase 2168 participants (Anticipated)Interventional2013-12-31Active, not recruiting
Low-dose Nilotinib and Imatinib Combination in Chronic Myeloid Leukemia Patients, With Failure, Suboptimal Response or Treatment Intolerance. [NCT01819389]Phase 310 participants (Actual)Interventional2012-10-31Completed
A Prospective, Double Blind, Randomized, Placebo-Controlled Phase III Trial of Imatinib Re-Challenge in Patients With Gastrointestinal Stromal Tumor Who Had Benefit From Prior Imatinib But Progression From Both Imatinib and Sunitinib [NCT01151852]Phase 381 participants (Actual)Interventional2010-06-30Completed
A Phase Ib/II Study of BGJ398 in Combination With Imatinib Mesylate in Patients With Untreated Advanced Gastrointestinal Stromal Tumor (GIST) [NCT02257541]Phase 1/Phase 216 participants (Actual)Interventional2014-10-02Completed
STI 571 (GLIVEC) in the Treatment of Philadelphia-chromosome Positive and/or BCR/ABL Rearranged Adult Acute Lymphoblastic Leukemia. GIMEMA LAL 0201. [NCT00376467]Phase 2105 participants (Actual)Interventional2001-12-31Completed
A Phase 1/2 Study of SNDX-275 in Combination With Imatinib for Relapsed/Refractory Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia [NCT01383447]Phase 1/Phase 22 participants (Actual)Interventional2010-10-31Terminated(stopped due to This study was halted prematurely by the NCI for low accrual.)
Three Versus Five Years of Adjuvant Imatinib as Treatment of Patients With Operable GIST With a High Risk for Recurrence: A Randomised Phase III Study [NCT02413736]Phase 3255 participants (Actual)Interventional2015-05-31Active, not recruiting
The Long-term Efficacy of Imatinib With Hepatic Resection or Other Local Treatment for Gastrointestinal Stromal Tumours Liver Metastases：a Retrospective Cohort Study [NCT06038552]238 participants (Actual)Observational2002-01-01Completed
A Phase III, Prospective Randomised Comparison of Imatinib (STI571, Glivec/Gleevec) 400mg Daily Versus Dasatinib 100mg in Patients With Newly-diagnosed Chronic Phase Chronic Myeloid Leukaemia [NCT01460693]Phase 3814 participants (Actual)Interventional2008-08-31Completed
Open Label Phase II Randomized Trial of Tasigna (Nilotinib) 400 mg Twice Daily Alone or in Combination With Gleevec (Imatinib Mesylate) 400 mg Daily for Patients With Advanced GIST That Have Progressed on High Dose Imatinib [NCT01089595]Phase 25 participants (Actual)Interventional2009-02-28Terminated(stopped due to Novartis is ending their research program for Nilotinib in GIST.)
Open-label, Randomized, Single-dose, 2-way Crossover Study to Evaluate the Pharmacokinetics(Cmax, Auc) of CJ Imatinib Mesylate Tablet 200mg x 1 Compared With Gleevec Film-coated Tablet 100mg x 2 in Healthy Male Volunteers [NCT01926548]Phase 128 participants (Actual)Interventional2012-02-29Completed
A Phase II Pilot Study to Determine the Safety and Preliminary Efficacy of Imatinib Mesylate (Gleevec) in Patients With Myelofibrosis With Myeloid Metaplasia [NCT00245128]Phase 210 participants (Actual)Interventional2005-08-31Terminated(stopped due to Per PI, results from another similar study were published prior to study analysis. Negative study results were published therefore analysis was not completed)
A Phase II Study To Determine The Anti-Leukemic Effects Of STI571 In Combination With Ara-C In Patients With Chronic Myelogenous Leukemia In Chronic Phase [NCT00022490]Phase 224 participants (Actual)Interventional2001-06-30Terminated
A Randomized Multi-Center Open Label Study of BMS-354825 vs. Imatinib Mesylate (Gleevec) 800 mg/d in Subjects With Chronic Phase Philadelphia Chromosome-Positive Chronic Myeloid Leukemia Who Have Disease That is Resistant to Imatinib at a Dose at 400 - 60 [NCT00103844]Phase 2150 participants (Actual)Interventional2005-02-28Completed
Potential of Immunotherapy to Convert a Complete Cytogenetic Remission in Chronic Myelogenous Leukemia to a Molecular Complete Remission: Randomized Phase II Study of Proteinase 3 PR1 Peptide Mixed With Montanide ISA-51 VG Adjuvant and Administered With G [NCT00415857]Phase 25 participants (Actual)Interventional2006-12-31Terminated(stopped due to Vaccine sponsor ceased operations.)
An Open-label, Phase II Study to Explore the Safety and Efficacy of Imatinib With Chemotherapy in Pediatric Patients With Ph+ / BCR-ABL+ Acute Lymphoblastic Leukemia (Ph+ALL) [NCT00287105]Phase 249 participants (Actual)Interventional2005-12-31Completed
Hyper-CVAD With Liposomal Vincristine (Hyper-CMAD) in Acute Lymphoblastic Leukemia [NCT01319981]Phase 231 participants (Actual)Interventional2013-03-05Completed
Open-label, Multicenter Phase II Study of Combination Therapy of Imatinib Mesylate and Mycophenolate Mofetil in Children With Steroid-Refractory Sclerotic/Fibrotic Type Chronic Graft-versus-host Disease [NCT01898377]Phase 29 participants (Actual)Interventional2013-08-31Terminated(stopped due to New treatment option introduced for patients with the study indication)
Randomized Double-Blind Placebo-Controlled Trial on the Safety and Efficacy of Imatinib for Hospitalized Adults With COVID-19 [NCT04394416]Phase 3204 participants (Anticipated)Interventional2020-06-02Active, not recruiting
A Phase I/II Dose-Finding Study to Determine the Safety, Tolerability, and Anti-Leukemic Effects of STI571 (NSC 716051) in Combination With Interferon-alpha in Patients With Chronic Myelogenous Leukemia in Chronic Phase [NCT00015847]Phase 225 participants (Actual)Interventional2001-04-30Terminated
A Pilot Phase II Trial of a Synthetic Tumor-Specific Breakpoint Peptide Vaccine in Patients With Chronic Myeloid Leukemia (CML) and Minimal Residual Disease [NCT00267085]Phase 211 participants (Actual)Interventional2005-12-31Completed
A Phase I Dose Escalation Trial to Determine if Imatinib Treatment Restores Sodium Iodide Symporter Function and Sensitivity to Radioiodine Treatment in Metastatic Thyroid Cancer Patients [NCT03469011]Phase 118 participants (Anticipated)Interventional2018-09-18Recruiting
Study of a Short Course of Neoadjuvant Gleevec (Imatinib Mesylate) in Dermatofibrosarcoma Protuberans [NCT00243191]Phase 218 participants (Actual)Interventional2006-05-31Completed
A Phase II Study of Imatinib and Docetaxel in Metastatic Hormone Refractory Prostate Cancer [NCT00251225]Phase 249 participants (Actual)Interventional2005-08-31Completed
A Phase III Randomized Open-label Multi-center Study of Ruxolitinib vs. Best Available Therapy in Patients With Corticosteroid-refractory Chronic Graft vs Host Disease After Allogeneic Stem Cell Transplantation (REACH3) [NCT03112603]Phase 3330 participants (Actual)Interventional2017-06-29Completed
IMatinib for PAin in Chronic Treatment of Sickle Cell Anemia (IMPACT SCA): A Pilot Study of Imatinib in Patients With Sickle Cell Anemia and Recurrent Vaso-occlusive Pain [NCT03997903]Phase 1/Phase 220 participants (Anticipated)Interventional2020-02-26Recruiting
A Therapeutic Trial of Decitabine and Vorinostat in Combination With Chemotherapy (Vincristine, Prednisone, Doxorubicin and PEG-Asparaginase) for Relapsed/Refractory Acute Lymphoblastic Leukemia (ALL) or Lymphoblastic Lymphoma (LL) [NCT00882206]Phase 215 participants (Actual)Interventional2009-04-30Terminated(stopped due to Slow accrual)
A Pilot Study of Treatment of Adults With Sickle Cell Disease Associated Pulmonary Hypertension Based on Hemodynamic Stratification: Safety and Tolerability Study of Imatinib and Carvedilol [NCT01568645]Phase 10 participants (Actual)Interventional2012-03-02Withdrawn
Validation of Digital-PCR Analysis Through Programmed Imatinib Interruption in PCR Negative CML Patients (ISAV) [NCT01578213]Phase 4112 participants (Actual)Interventional2011-11-09Completed
Continuation of Drug Supply in Chinese Patients After CAMN107DBR01study Termination [NCT01613053]0 participants Expanded AccessNo longer available
Dasatinib in Chronic Myelogenous Leukemia or Philadelphia Chromosome Positive Acute Lymphoblastic Leukemic Subjects Who Are Experiencing Clinical Benefit on Current START or CA180-039 Protocols: Long Term Safety and Efficacy Analysis [NCT00982488]Phase 2238 participants (Actual)Interventional2007-10-31Completed
Allogeneic Nonmyeloablative Hematopoietic Stem Cell Transplant for Patients With BCR-ABL Tyrosine Kinase Inhibitor Responsive Ph+ Acute Leukemia ? A Multi-center Trial [NCT00036738]Phase 228 participants (Actual)Interventional2001-07-13Completed
Phase II Study of Hyper-CVAD Plus Imatinib Mesylate (Gleevec, STI571) for Philadelphia-Positive Acute Lymphocytic Leukemia [NCT00038610]Phase 254 participants (Actual)Interventional2001-03-31Completed
A Phase I Dose Escalation Study of the Combination of Dasatinib (BMS-354825) and Imatinib in Subjects With Chronic Myeloid Leukemia in Chronic Phase [NCT00324077]Phase 10 participants (Actual)Interventional2006-08-31Withdrawn(stopped due to Insufficient Enrollment)
A Phase II Study Evaluating a Maintenance Strategy of Gleevce® (Imatinib Mesylate) and Bevacizumab in Patients With Advanced, Non-squamous, Non-small Cell Lung Cancer, Following Completion of First-line Chemotherapy With Bevacizumab [NCT00425646]Phase 250 participants (Anticipated)Interventional2006-11-30Completed
Apatinib Mesylate Versus Standard Second-line TKI in the Treatment of Advanced Gastrointestinal Stromal Tumors: a Randomized, Open, Controlled, Single-center Clinical Study [NCT05751733]258 participants (Anticipated)Interventional2023-02-01Recruiting
A Phase I - II Open Label Study of the Maximum Tolerated Dose, Safety and Efficacy of Docetaxel and Cisplatin Plus STI571 in Advanced Non-Small Cell Lung Cancer [NCT02127372]Phase 1/Phase 243 participants (Actual)Interventional2004-11-30Terminated(stopped due to The study was closed due to poor accrual)
An Open-label Multi-center Study of Imatinib and Nilotinib in CAMN107ECN02 On-treatment Patients With Philadelphia Chromosome Positive Chronic Myelogenous Leukemia in Chronic Phase After the End of CAMN107ECN02 Core Study [NCT02272777]Phase 3225 participants (Actual)Interventional2014-07-17Completed
Phase II Study of Imatinib Mesylate and Gemcitabine for First-line Treatment of Metastatic Pancreatic Cancer [NCT00161213]Phase 244 participants (Actual)Interventional2005-09-30Completed
A Phase I, Open-label, Randomized, Crossover Study to Investigate the Effect of Food on the Bioavailability of a Single 800 mg Imatinib Dose in a Modified Release Formulation (MR2) and Compare the Bioavailability Between MR2 and Imatinib 400 mg Twice Dail [NCT00422825]Phase 116 participants (Actual)Interventional2006-06-30Completed
Use of Imatinib to Convert Triple Negative Breast Cancer Into ER-positive Breast Cancer [NCT05722795]40 participants (Anticipated)Interventional2023-02-06Not yet recruiting
Use and Tolerability of Imatinib Mesylate (Gleevec®) in Patients With Philadelphia-Positive Chronic Myeloid or Acute Leukemia During the First 100 Days Following Bone Marrow or Stem Cell Transplantation [NCT00386373]10 participants (Actual)Interventional2003-08-31Completed
A Prospective Multicentric Randomized Study of Glivec® in Patients With Advanced Gastrointestinal Stromal Tumors Expressing C-kit Comparing Treatment Interruption After 5 Years vs Treatment Maintenance [NCT00367861]Phase 3564 participants (Actual)Interventional2002-05-31Completed
Open-label Trial of Imatinib in Combination With Vinorelbine for Patients With Advanced Breast Carcinoma: ICON [NCT00372476]Phase 433 participants (Actual)Interventional2006-06-30Completed
A Phase II Study to Determine the Efficacy and Safety of Induction-Maintenance Protocol for Patients With Chronic-Phase Chronic Myelogenous Leukaemia [NCT03241199]Phase 215 participants (Anticipated)Interventional2017-08-01Recruiting
First-Line Dasatinib or Nilotinib Followed by Response Guided Switch to Imatinib in Newly Diagnosed Chronic Phase Chronic Myeloid Leukemia [NCT02709083]Phase 27 participants (Actual)Interventional2016-10-31Terminated(stopped due to Original principal investigator left institution)
Open-labeled, Multicenter, Phase I/II Study of Imatinib Combined With ESHAP as Salvage Therapy in Relapsed/Refractory Non-Hodgkin's Lymphoma [NCT02431403]Phase 1/Phase 294 participants (Anticipated)Interventional2015-02-28Recruiting
A Phase II Study of Imatinib Mesylate in Children and Adults With Sclerotic Skin Changes of Chronic Graft-Versus-Host Disease [NCT00702689]Phase 220 participants (Actual)Interventional2008-12-15Completed
The MATRIX Clinical Studies of Precision Cancer Therapy for Rare Cancers [NCT06119789]Phase 296 participants (Anticipated)Interventional2023-11-30Not yet recruiting
Phase II Study of Gleevec/Imatinib Mesylate (STI-571, NCS 716051) in Neurofibromatosis (NF1) Patients With Plexiform Neurofibromas [NCT01673009]Phase 236 participants (Actual)Interventional2006-05-31Completed
An Open Label, Randomized (2:1) Phase IIb Study of Dasatinib Versus Imatinib in Patients With Chronic Phase Chronic Myeloid Leukemia Who Have Not Achieved an Optimal Response to 3 Months of Therapy With 400 mg Imatinib [NCT01593254]Phase 2262 participants (Actual)Interventional2012-09-12Completed
Phase II Study of Imatinib Mesylate Plus Hydroxyurea in the Treatment of Patients With Recurrent / Progressive Grade II Low-Grade Glioma [NCT00615927]Phase 264 participants (Actual)Interventional2006-02-28Completed
A Non-Randomized, Multiple Dose, Three Treatment Period, Open-Label, Single Sequence, Single Group Study to Evaluate the Pharmacokinetic Effect of Two Doses of QTI571 (Imatinib) on the Co-administered Drugs Sildenafil and Bosentan in Pulmonary Arterial Hy [NCT01392469]Phase 321 participants (Actual)Interventional2011-04-20Completed
Phase II Study of Imatinib Mesylate as Adjuvant Treatment in High-relapse Risk Localized Gastrointestinal Stromal Tumors With C-kit Mutation [NCT00278876]Phase 247 participants (Actual)Interventional2005-04-30Completed
A Phase II Study of CLAG Regimen in Combination With Imatinib Mesylate (Gleevec) in Relapsed or Refractory Acute Myeloid Leukemia [NCT00955916]Phase 238 participants (Actual)Interventional2009-08-31Completed
Frontline Asciminib Combination in Chronic Phase CML [NCT03906292]Phase 2125 participants (Actual)Interventional2019-08-19Active, not recruiting
A Phase I/II Study Of Imatinib Mesylate And Bevacizumab In Patients With Advanced Melanoma And Other Advanced Cancers [NCT00074308]Phase 1/Phase 240 participants (Actual)Interventional2003-10-31Completed
A Phase I/II Trial of Bevacizumab (Avastin), Erlotinib (Tarceva), and Imatinib (Gleevec) in the Treatment of Patients With Advanced Renal Cell Carcinoma [NCT00193258]Phase 1/Phase 294 participants (Actual)Interventional2004-06-30Completed
Phase II Study of Imatinib Mesylate and Gemcitabine for Recurrent/Metastatic Non-small Cell Lung Cancer (NSCLC) [NCT00323362]Phase 217 participants (Actual)Interventional2006-04-30Terminated(stopped due to Toxicity)
A Phase II Study of Intermittent Gleevec® (Imatinib Mesylate) and Weekly Paclitaxel in Patients Aged 70 or Older With Advanced Non-Small Cell Lung Cancer [NCT00408460]Phase 234 participants (Actual)Interventional2006-02-28Completed
Phase II Study of Adult Acute Lymphoblastic Leukaemia (ALL): Imatinib in Combination With Chemotherapy in Ph+ Patients, and Post-remissional Treatment Intensification in High-risk Ph- Patients, With Minimal Residual Disease Monitoring. [NCT00458848]Phase 2470 participants (Actual)Interventional2004-10-31Completed
An Open-label Extension Study to CQTI571A2102 to Evaluate the Long-term Safety, Tolerability and Efficacy of QTI571 (Imatinib) in the Treatment of Severe Pulmonary Arterial Hypertension [NCT01392495]Phase 317 participants (Actual)Interventional2011-06-30Terminated(stopped due to Novartis discontinued the development of imatinib in PAH due to requirement of regulatory authorities for additional data to secure marketing approval in PAH.)
A Dose Calibration and Dose Equivalence Pharmacokinetic Study in Healthy Volunteers Comparing IkT-001Pro to Imatinib Mesylate 400mg [NCT05623774]Phase 164 participants (Anticipated)Interventional2022-12-16Recruiting
Open Label, Randomized, Single-dose, Crossover Study to Evaluate the Pharmacokinetic Characteristics of Luckyvec 400mg Tablet, in Healthy Subjects [NCT01270984]Phase 130 participants (Actual)Interventional2010-11-30Completed
ENESTChina: A Phase III Multi-center, Open-label, Randomized Study of Nilotinib Versus Imatinib in Chinese Adult Patients With Newly Diagnosed Philadelphia Chromosome Positive (Ph+) Chronic Myelogenous Leukemia in Chronic Phase (CML-CP) [NCT01275196]Phase 3267 participants (Actual)Interventional2011-04-30Completed
A Phase II Trial of Gleevec and Gemzar in Patients With Epithelial Ovarian Cancer Who Have Failed at Least Two Prior Therapies [NCT00928642]Phase 28 participants (Actual)Interventional2009-06-30Completed
Observational Study in Adult Patients With Imatinib-resistant or Intolerant Chronic Myeloid Leukemia (CML) Treated With Nilotinib: Follow-up of the Italian Patients. GIMEMA Study CML0609 [NCT01475110]19 participants (Actual)Observational2012-09-13Completed
Imatinib Discontinuation in Patients With Chronic Myeloid Leukemia Chronic Phase With Sustained MR4log [NCT03239886]30 participants (Actual)Interventional2016-12-15Active, not recruiting
Platform Study of Genotyping Guided Precision Medicine for Rare Tumors in China [NCT04423185]Phase 2770 participants (Anticipated)Interventional2020-08-15Not yet recruiting
Discontinuation of Imatinib in Patients With Oligo-metastatic Gastrointestinal Stromal Tumor That Has Become Radiologically Undetectable With Treatment [NCT02924714]31 participants (Anticipated)Interventional2017-01-31Suspended(stopped due to Slow accrual)
Phase I Study of Imatinib, Gemcitabine and Capecitabine in Patients With Solid Tumors [NCT00483366]Phase 113 participants (Actual)Interventional2006-08-15Completed
Safety and Efficacy of Imatinib for Preserving Beta-Cell Function in New-Onset Type 1 Diabetes Mellitus [NCT01781975]Phase 267 participants (Actual)Interventional2014-01-31Completed
A Phase 3, Randomized, Open-label, Multicenter Study Comparing Ponatinib Versus Imatinib, Administered in Combination With Reduced-Intensity Chemotherapy, in Patients With Newly Diagnosed Philadelphia Chromosome Positive Acute Lymphoblastic Leukemia (Ph+ [NCT03589326]Phase 3245 participants (Actual)Interventional2018-10-04Active, not recruiting
A Phase II Study of the Combination of Gemcitabine and Imatinib Mesylate in Pemetrexed-pretreated Patients With Malignant Pleural Mesothelioma [NCT02303899]Phase 222 participants (Actual)Interventional2014-11-30Completed
Efficacy and Safety of Imatinib Mesylate as First-line Treatment for the Patients With Chronic Phase of Chronic Myeloid Leukemia [NCT02317159]Phase 490 participants (Anticipated)Interventional2015-02-28Not yet recruiting
Prospective Multicenter Cohort Study to Compare Pathologic Type, NIH and WHO Criteria, and Mechanism of GIST Malignant Transformation [NCT03381053]3,000 participants (Anticipated)Observational2017-07-01Recruiting
A Phase IIb Study of Molecular Responses to Imatinib, at Standard or Increased Doses, or Dasatinib (BMS-354825) (NSC-732517) for Previously Untreated Patients With Chronic Myelogenous Leukemia (CML) in Chronic Phase [NCT00070499]Phase 2406 participants (Actual)Interventional2004-08-15Active, not recruiting
A MULTICENTER PHASE 3 RANDOMIZED, OPEN-LABEL STUDY OF BOSUTINIB VERSUS IMATINIB IN ADULT PATIENTS WITH NEWLY DIAGNOSED CHRONIC PHASE CHRONIC MYELOGENOUS LEUKEMIA [NCT02130557]Phase 3536 participants (Actual)Interventional2014-07-15Completed
A Phase 1 Study of TAS-116 (Pimitespib) in Combination With Imatinib in Patients With Advanced Gastrointestinal Stromal Tumor [NCT05245968]Phase 178 participants (Anticipated)Interventional2021-12-01Recruiting
A Multicenter Phase I/II Study of the Prophylactic Inhibition of BCR-ABL Tyrosine Kinase by Tasigna ® (Nilotinib) After Hematopoietic Cell Transplantation for Philadelphia Chromosome-Positive Leukemias. [NCT00702403]Phase 1/Phase 240 participants (Actual)Interventional2008-08-14Completed
A Randomized, Placebo-controlled, Double-blind Study to Investigate the Effects of the Tyrosine Kinase Inhibitor Imatinib on Pulmonary Vascular Dysfunction in a Human Experimental Model of Acute Lung Injury [NCT03328117]Phase 147 participants (Actual)Interventional2017-11-13Completed
Prospective Multicenter Clinical Study of Neoadjuvant Imatinib Mesylate for Gastrointestinal Stromal Tumors [NCT04933669]Phase 2122 participants (Anticipated)Interventional2021-09-07Recruiting
A Phase II Trial of Imatinib for Patients With Aggressive Desmoid Tumor (Aggressive Fibromatosis) [NCT02495519]Phase 221 participants (Actual)Interventional2014-04-30Completed
Observational Study of Cemivil® (Imatinib) in Chronic Myeloid Leukemia Patients in Jordan [NCT02977312]91 participants (Actual)Observational2012-08-31Completed
A Phase 3 Randomized,Open-Label Study of Ponatinib Versus Imatinib in Adult Patients With Newly Diagnosed Chronic Myeloid Leukemia in Chronic Phase [NCT01650805]Phase 3307 participants (Actual)Interventional2012-06-30Terminated(stopped due to Study terminated based on evaluation of safety data.)
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00015847 (3) [back to overview]Treatment-related Toxicity (i.e., Grade 3 or 4 Nonhematologic Toxicity) as Measured by NCI CTCAE v3.0 (Phase I)
NCT00015847 (3) [back to overview]Major Cytogenetic Response After 6 and 12 Months of Treatment.
NCT00015847 (3) [back to overview]Complete Cytogenetic Response at 6 and 12 Months (Phase II)
NCT00021229 (9) [back to overview]Peak Concentration (Cmax)
NCT00021229 (9) [back to overview]Pre-treatment Basic Fibroblast Growth Factor Values From Plasma
NCT00021229 (9) [back to overview]Pre-treatment Basic Fibroblast Growth Factor Values From Urine
NCT00021229 (9) [back to overview]Pre-treatment Vascular Endothelial Growth Factor From Urine
NCT00021229 (9) [back to overview]Pre-treatment Vascular Endothelial Growth Factor Values From Plasma
NCT00021229 (9) [back to overview]Change From Baseline in Volume FLAIR at Two Weeks After Completion of Radiation
NCT00021229 (9) [back to overview]Median Overall Survival
NCT00021229 (9) [back to overview]Number of Participants in Phase I Stratum I With Dose Limiting Toxicities (DLT) Observed During First 8 Weeks (Courses 1 and 2) of Imatinib Therapy
NCT00021229 (9) [back to overview]Number of Participants in Phase I Stratum II With Dose Limiting Toxicities (DLT) Observed During First 8 Weeks (Courses 1 and 2) of Imatinib Therapy
NCT00022490 (1) [back to overview]The Rate of Major Cytogenetic Response at 6 Months
NCT00028002 (4) [back to overview]Percentage of Patients With Major Toxicity (Toxicity Grade ≥ 3)
NCT00028002 (4) [back to overview]FDG-PET as Biological Marker of Metabolic Response(MR) During Imatinib Mesylate (IM) Treatment, in Patients With GIST Who Are naı¨ve to Tyrosine Kinase Inhibitor Therapy
NCT00028002 (4) [back to overview]Rate of Disease Progression at 2 Years
NCT00028002 (4) [back to overview]Rates of Objective Response (Complete, Partial, and Stable)
NCT00036738 (5) [back to overview]Transplant-related Mortality
NCT00036738 (5) [back to overview]Relapse Free Survival
NCT00036738 (5) [back to overview]Overall Survival
NCT00036738 (5) [back to overview]Leukemia-free Survival
NCT00036738 (5) [back to overview]Transplant-related Mortality
NCT00038610 (3) [back to overview]Response To Induction Therapy With Hyper-CVAD Plus Imatinib Mesylate
NCT00038610 (3) [back to overview]Disease-Free Survival Rate at 2-year and 5-year.
NCT00038610 (3) [back to overview]Overall Survival Rate at 2-year and 5-year.
NCT00038649 (2) [back to overview]Participant Complete Hematologic Remission (CHR) Classified
NCT00038649 (2) [back to overview]Number of Participants With Molecular Response of Complete or Partial Hematologic Remission
NCT00038675 (3) [back to overview]Duration of Response
NCT00038675 (3) [back to overview]Number of Participants With a Complete Response (CR)
NCT00038675 (3) [back to overview]Overall Survival
NCT00039377 (5) [back to overview]5 Year Disease-free Survival for Autologous & Allogeneic Transplant Groups
NCT00039377 (5) [back to overview]5 Year Overall Survival for Autologous & Allogeneic Transplant Groups
NCT00039377 (5) [back to overview]Disease Free Survival
NCT00039377 (5) [back to overview]Overall Survival
NCT00039377 (5) [back to overview]Number of Participants Who Achieved a BCR-ABL Response at 12 Months
NCT00045734 (6) [back to overview]Concentration (Steady State) of Imatinib During Cycle One (Pharmacokinetics)
NCT00045734 (6) [back to overview]Tumor Response as Assessed by MRI Using Macdonald Criteria
NCT00045734 (6) [back to overview]Toxicity as Assessed by the Cancer Therapy Evaluation Program Common Toxicity Criteria (CTC) Version 2.0
NCT00045734 (6) [back to overview]Progression-free Survival According to Response Evaluation Using Macdonald Criteria
NCT00045734 (6) [back to overview]Determine Survival for Patients Treated With Imatinib Mesylate
NCT00045734 (6) [back to overview]6 Months - Progression-free Survival According to Response Evaluation Using Macdonald Criteria
NCT00049127 (4) [back to overview]Percentage of Patients Progression-free
NCT00049127 (4) [back to overview]Confirmed Response (i.e., an Objective Status of Complete Response (CR), Partial Response (PR), or Regression (REGR) on 2 Successive Evaluations at Least 4 Weeks Apart After the Start of Study Treatment).
NCT00049127 (4) [back to overview]6-month Progression-free Survival (PFS), Defined as a Patient Being Alive and Progression-free 183 Days After the Date of Registration.
NCT00049127 (4) [back to overview]Overall Time to Death
NCT00061945 (6) [back to overview]Maximum Tolerated Dose (MTD) of Alemtuzumab (Phase I)
NCT00061945 (6) [back to overview]Minimal Residual Disease (MRD) During Treatment With Alemtuzumab (Phase II)
NCT00061945 (6) [back to overview]Disease-free Survival, for Only Complete Response Patients
NCT00061945 (6) [back to overview]Overall Survival
NCT00061945 (6) [back to overview]Number of Participants Who Proceed to Course V Within 2-6 Weeks of the Last Dose of Alemtuzumab (Phase II)
NCT00061945 (6) [back to overview]Number of Participants Achieving Complete Remission
NCT00068380 (5) [back to overview]Toxicity Summary
NCT00068380 (5) [back to overview]Time to Treatment Failure
NCT00068380 (5) [back to overview]Response Rate
NCT00068380 (5) [back to overview]Overall Survival
NCT00068380 (5) [back to overview]Progression-free Survival
NCT00070499 (5) [back to overview]Toxicity
NCT00070499 (5) [back to overview]Two Year Relapse-free Survival
NCT00070499 (5) [back to overview]Hematologic Response
NCT00070499 (5) [back to overview]2-year Overall Survival (OS)
NCT00070499 (5) [back to overview]Molecular Response Rate at 12 Months
NCT00074308 (3) [back to overview]MTD, Defined as One Dose Level Below the Dose That Induced DLT in at Least One Third of Patients at a Dose Level, Graded According to NCI CTCAE Version 3.0 (Phase I)
NCT00074308 (3) [back to overview]Response Rate at 8 Weeks, Evaluated Using RECIST (Phase II)
NCT00074308 (3) [back to overview]Progression-free Survival at 16 Weeks (Phase II)
NCT00075400 (5) [back to overview]Tumor Response
NCT00075400 (5) [back to overview]Progression-free Survival (PFS) > 6 Months
NCT00075400 (5) [back to overview]Overall Survival
NCT00075400 (5) [back to overview]Duration of Progression Free Survival
NCT00075400 (5) [back to overview]Incidence of Adverse Effects as Assessed by CTCAE v 3.0
NCT00087152 (3) [back to overview]Number of Patients With Grade 3 Through 5 Adverse Events That Are Related to Study Drug
NCT00087152 (3) [back to overview]Confirmed Response Rate (Complete and Partial)
NCT00087152 (3) [back to overview]Progression-free Survival at 6 Months
NCT00090987 (1) [back to overview]Proportion of Patients Who Achieve a Clinical Response
NCT00103844 (13) [back to overview]Cytogenetic Response After Crossover
NCT00103844 (13) [back to overview]Adverse Events (AEs), Serious Adverse Events (SAEs), Deaths and Hematologic Toxicities Prior to Crossover
NCT00103844 (13) [back to overview]Time to MCyR Prior to Crossover
NCT00103844 (13) [back to overview]Time to CHR Prior to Crossover
NCT00103844 (13) [back to overview]Number of Participants With Major Cytogenetic Response (MCyR) at Week 12
NCT00103844 (13) [back to overview]Major Molecular Response (MMR)
NCT00103844 (13) [back to overview]Duration of MCyR at 24 Months
NCT00103844 (13) [back to overview]Complete Hematologic Response (CHR) at Any Time Prior to Crossover
NCT00103844 (13) [back to overview]CHR After Crossover
NCT00103844 (13) [back to overview]Blood Sample Collection for Pharmacokinetic (PK) Analysis of Dasatinib
NCT00103844 (13) [back to overview]MCyR at Any Time Prior to Crossover
NCT00103844 (13) [back to overview]Duration of MCyR at 12 Months and 18 Months
NCT00103844 (13) [back to overview]Duration of Complete Hematologic Response (CHR)
NCT00114959 (1) [back to overview]Number of Participants With Adverse Experiences (AEs)
NCT00115739 (4) [back to overview]6 Month Progression Free Survival Rate
NCT00115739 (4) [back to overview]6 Month Survival Rate
NCT00115739 (4) [back to overview]Overall Response (Complete and Partial Response) Rate at 8 Weeks
NCT00115739 (4) [back to overview]Rate of Grade 3, Grade 4 and Grade 5 Toxicities Experienced by Patients With Anaplastic Thyroid Cancer Who Are Treated With Gleevec
NCT00124748 (17) [back to overview]Estimated Rate of Overall Survival (OS) in Two Treatment Arms
NCT00124748 (17) [back to overview]Imatinib Pharmacokinetic Trough Plasma Concentration (Cmin) at Month 12
NCT00124748 (17) [back to overview]Mean Actual Dose Intensity Per Day
NCT00124748 (17) [back to overview]Percentage of Participants With Major Molecular Response (MMR) Rates at 12 Months
NCT00124748 (17) [back to overview]Time to First Complete Cytogenetic Response
NCT00124748 (17) [back to overview]Time to First Complete Hematological Response (CHR)]
NCT00124748 (17) [back to overview]Time to First Major Molecular Response
NCT00124748 (17) [back to overview]Estimated Rate of Progression Free Survival (PFS) in Two Treatment Arms
NCT00124748 (17) [back to overview]Estimated Rate of Progression to Accelerated Phase (AC)/Blast Crisis (BC) in Two Treatment Arms
NCT00124748 (17) [back to overview]Estimated Rates of Progression Free Survival (PFS) on Treatment by Major Molecular Response (MMR)
NCT00124748 (17) [back to overview]Kaplan-Meier Estimates of Duration of First Complete Cytogenetic Response (CCyR)
NCT00124748 (17) [back to overview]Kaplan-Meier Estimates of Duration of First Major Molecular Response Until Confirmed Loss
NCT00124748 (17) [back to overview]Percentage of Participants With Complete Cytogenetic Response (CCyR) Rate at 12, 24, 36, 42 Months
NCT00124748 (17) [back to overview]Estimated Rate of Event Free Survival (EFS) in Two Treatment Arms
NCT00124748 (17) [back to overview]Percentage of Patients With Undetectable Levels of Bcr-Abl (A Fusion Gene of the Breakpoint Cluster Region [Bcr] Gene and Abelson Proto-oncogene [Abl] Genes) Transcripts
NCT00124748 (17) [back to overview]Percentage of Participants With Major Molecular Response (MMR) Rates at 24, 36, and 42 Months
NCT00124748 (17) [back to overview]Percentage of Participants With Complete Hematological Response (CHR) Rates at 12, 24, 36, and 42 Months
NCT00154375 (2) [back to overview]Percentage of Participants With Progression Free Survival (PFS) During the Study Duration
NCT00154375 (2) [back to overview]Number of Participants With Death, Other Serious or Clinically Significant Adverse Events (AEs) or Related Discontinuations
NCT00161213 (4) [back to overview]Progression-free Survival
NCT00161213 (4) [back to overview]Overall Survival
NCT00161213 (4) [back to overview]1-year Survival Rate
NCT00161213 (4) [back to overview]Response Rate
NCT00171158 (2) [back to overview]Overall Survival (by Month)
NCT00171158 (2) [back to overview]Overall Survival
NCT00171223 (7) [back to overview]Percentage of Participants With Cytogenetic Response (Complete Cytogenetic Response and Major Cytogenetic Response) to STI571
NCT00171223 (7) [back to overview]Number of Participants With Common Toxicity Criteria Grade 3 or 4 Cancer-related Symptoms
NCT00171223 (7) [back to overview]Time to Complete Hematologic Response to STI571
NCT00171223 (7) [back to overview]Percentage of Participants With Complete Hematologic Response to STI571
NCT00171223 (7) [back to overview]Duration of Complete Hematologic Response to STI571
NCT00171223 (7) [back to overview]Percentage of Participants Alive Over Time Based on Kaplan-Meier Estimates
NCT00171223 (7) [back to overview]Number of Participants With Grade 3 or 4 Eastern Cooperative Oncology Group (ECOG) Performance Status
NCT00171249 (7) [back to overview]Percentage of Participants With Cytogenetic Response in Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00171249 (7) [back to overview]Time to Response in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00171249 (7) [back to overview]Overall Survival by Dose in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00171249 (7) [back to overview]Overall Survival by Disease
NCT00171249 (7) [back to overview]Duration of Response in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00171249 (7) [back to overview]Time to Progression to Blast Crisis in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00171249 (7) [back to overview]Percentage of Participants With Hematologic Response in Accelerated Phase Chronic Myeloid/Myelogenous Leukemia
NCT00193180 (3) [back to overview]Overall Response Rate (ORR)
NCT00193180 (3) [back to overview]Overall Survival (OS)
NCT00193180 (3) [back to overview]Progression Free Survival (PFS)
NCT00193258 (3) [back to overview]Progression Free Survival (PFS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Worsening of Their Disease
NCT00193258 (3) [back to overview]Overall Survival (OS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Death
NCT00193258 (3) [back to overview]Objective Response Rate (ORR), the Percentage of Patients Who Experience an Objective Benefit From Treatment
NCT00210119 (2) [back to overview]Percentage of Participants With a Reduction of BCR-ABL Transcript Level > 4.5 Log From the Start of From Initiation of Treatment
NCT00210119 (2) [back to overview]Percentage of Participants With Molecular Response
NCT00237185 (12) [back to overview]Best Tumor Response (Core)
NCT00237185 (12) [back to overview]Best Tumor Response (Core + Extension)
NCT00237185 (12) [back to overview]Time to Onset of Response (Core + Extension)
NCT00237185 (12) [back to overview]Time to Onset of Response (Core)
NCT00237185 (12) [back to overview]Time to Treatment Failure (Core + Extension)
NCT00237185 (12) [back to overview]Time to Treatment Failure (Core)
NCT00237185 (12) [back to overview]Time to Progression (Core + Extension)
NCT00237185 (12) [back to overview]Progression Free Survival (PFS) (Core + Extension)
NCT00237185 (12) [back to overview]Overall Survival (Core)
NCT00237185 (12) [back to overview]Overall Survival (Core + Extension)
NCT00237185 (12) [back to overview]Duration of Response (Core)
NCT00237185 (12) [back to overview]Duration of Response (Core + Extension)
NCT00243191 (1) [back to overview]To Collect Matched Tumor Tissue of Trial Participants With Dermatofibrosarcoma Protuberans Before and After Treatment With Imatinib for Future Use in cDNA Microarray and Tissue Array Studies.
NCT00251225 (3) [back to overview]Overall Time To Progression (TTP)
NCT00251225 (3) [back to overview]Overall Survival (OS)
NCT00251225 (3) [back to overview]Prostate-Specific Antigen (PSA) Response Rate
NCT00267085 (1) [back to overview]Response: One Log Decrease in BCR-ABL
NCT00278876 (3) [back to overview]2-year Relapse Free Survival Rate
NCT00278876 (3) [back to overview]2-year Overall Survival Rate
NCT00278876 (3) [back to overview]Toxicity Profile
NCT00290771 (6) [back to overview]Percentage of Patients Who Had Clinical Benefit
NCT00290771 (6) [back to overview]Percentage of Patients With an Objective Overall Response (OOR)
NCT00290771 (6) [back to overview]Percentage of Patients Surviving at Months 6, 12, and 24
NCT00290771 (6) [back to overview]Duration of Objective Overall Response (OOR)
NCT00290771 (6) [back to overview]Percentage of Patients With Progression-free Survival at Months 6 and 12
NCT00290771 (6) [back to overview]Number of Patients With at Least 1 Adverse Event
NCT00320190 (2) [back to overview]Percentage of Participants With On-study AEs of Special Interest
NCT00320190 (2) [back to overview]Percentage of Participants With Death as Outcome, Adverse Events (AEs), Treatment-related AEs, Serious Adverse Events (SAEs), Treatment-related SAEs, and AEs Leading to Discontinuation
NCT00323063 (2) [back to overview]Time to Progression
NCT00323063 (2) [back to overview]Response Rate (Complete and Partial Response)
NCT00323362 (3) [back to overview]Time to Progression
NCT00323362 (3) [back to overview]Percentage of Patients Who Meet Critieria for Response
NCT00323362 (3) [back to overview]1-year Survival
NCT00324987 (3) [back to overview]Overall Survival
NCT00324987 (3) [back to overview]Progression Free Survival
NCT00324987 (3) [back to overview]Number of Patients With Grade 3 Through Grade 5 Adverse Events That Are Related to Study Drug
NCT00331409 (5) [back to overview]Median Time to Progression
NCT00331409 (5) [back to overview]Number of Participants With Adverse Events
NCT00331409 (5) [back to overview]Number of Subjects That Demonstrated a Reduction in Tumor Measurements.
NCT00331409 (5) [back to overview]Overall Number of Participants Who Achieve a Response Rate (Complete Response, Partial Response, and Stable Disease) at 3 Months
NCT00331409 (5) [back to overview]Progression-free Survival at 3 Months
NCT00333840 (10) [back to overview]Number of Participants With Serious Adverse Events as a Measure of Safety (Second-line Treatment)
NCT00333840 (10) [back to overview]Kaplan Meier Estimates of Event Free Survival (All Randomized Participants)
NCT00333840 (10) [back to overview]Kaplan-Meier Estimates of Overall Survival (All Randomized Participants)
NCT00333840 (10) [back to overview]Kaplan Meier Estimates of Time to Progression to Accelerated Phase (AP) or Blast Crisis (BC) (All Randomized Participants)
NCT00333840 (10) [back to overview]Percentage of Participants With Major Molecular Response (Second-line Treatment)
NCT00333840 (10) [back to overview]Percentage of Participants With Major Molecular Response (First-line Treatment)
NCT00333840 (10) [back to overview]Percentage of Participants With Event Free Survival Events (All Randomized Participants)
NCT00333840 (10) [back to overview]Percentage of Participants With Best Cytogenetic Response (Second-line Treatment)
NCT00333840 (10) [back to overview]Percentage of Participants With Best Cytogenetic Response (First-line Treatment)
NCT00333840 (10) [back to overview]Number of Participants With Serious Adverse Events as a Measure of Safety (First-line Treatment)
NCT00338728 (2) [back to overview]Overall Survival of Participants
NCT00338728 (2) [back to overview]Objective Response Rate (ORR)
NCT00354913 (4) [back to overview]Median Progression-free Survival (PFS)
NCT00354913 (4) [back to overview]Median Overall Survival (OS)
NCT00354913 (4) [back to overview]Objective Response Rate
NCT00354913 (4) [back to overview]Progression-free Survival at 6 Months
NCT00362466 (1) [back to overview]Adverse Events (AEs), Serious Adverse Events (SAEs), Deaths, and Discontinuations Due to AEs
NCT00372567 (14) [back to overview]Number of Participants With Pain Progression
NCT00372567 (14) [back to overview]Number of Participants With Pain Relief Response
NCT00372567 (14) [back to overview]Number of Participants With Objective Response of Complete Response or Partial Response
NCT00372567 (14) [back to overview]Duration of Response (DR)
NCT00372567 (14) [back to overview]Euro Quality of Life (EQ-5D) - Health State Profile Utility Score - Imatinib Treatment Arm
NCT00372567 (14) [back to overview]Euro Quality of Life (EQ-5D)- Visual Analog Scale (VAS) - Sunitinib Treatment Arm
NCT00372567 (14) [back to overview]Euro Quality of Life (EQ-5D)- Visual Analog Scale (VAS) - Imatinib Treatment Arm
NCT00372567 (14) [back to overview]Euro Quality of Life (EQ-5D) - Health State Profile Utility Score- Sunitinib Treatment Arm
NCT00372567 (14) [back to overview]Time to Tumor Response (TTR)
NCT00372567 (14) [back to overview]Time to Treatment Failure (TTF)
NCT00372567 (14) [back to overview]Time to Pain Relief Response (TTPR)
NCT00372567 (14) [back to overview]Time to Pain Progression (TTPP)
NCT00372567 (14) [back to overview]Progression-Free Survival (PFS)
NCT00372567 (14) [back to overview]Overall Survival (OS)
NCT00408460 (3) [back to overview]Overall Response Rate (Complete and Partial Responses) as Assessed by RECIST Criteria
NCT00408460 (3) [back to overview]Overall Survival
NCT00408460 (3) [back to overview]Time to Tumor Progression
NCT00415857 (2) [back to overview]Number of Participants With Immunologic Response
NCT00415857 (2) [back to overview]Molecular Response Rate
NCT00415909 (1) [back to overview]Response Rate (Major and Complete Cytogenetic Response)
NCT00424385 (3) [back to overview]Overall Clinical Benefit
NCT00424385 (3) [back to overview]Number of Patients Experiencing Dose Limiting Toxicities (DLT's)
NCT00424385 (3) [back to overview]Time to Disease Progression (TTP)
NCT00424515 (3) [back to overview]Overall Survival
NCT00424515 (3) [back to overview]Best Overall Response
NCT00424515 (3) [back to overview]Time to Progression
NCT00427999 (5) [back to overview]Time to Progression-free Survival
NCT00427999 (5) [back to overview]Overall Survival Rate
NCT00427999 (5) [back to overview]Quality of Life Assessed With EORTC-30
NCT00427999 (5) [back to overview]PSA Response Rate
NCT00427999 (5) [back to overview]Time to PSA Response
NCT00458848 (3) [back to overview]Percentage of Participants Reaching Overall Survival
NCT00458848 (3) [back to overview]Number of Patients Reaching Complete Hematological Response After Induction Therapy
NCT00458848 (3) [back to overview]Percentage of Participants Reaching Disease Free Survival
NCT00470470 (2) [back to overview]Objective Response Rate
NCT00470470 (2) [back to overview]Time to Progression
NCT00471328 (9) [back to overview]Number of Responders With Confirmed Best Overall Response of Complete Response (CR) or Partial Response (PR) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set
NCT00471328 (9) [back to overview]Progression-free Survival (PFS) From Central Radiology Review Based on Primary Analysis (Data Cut-off: June, 2008)
NCT00471328 (9) [back to overview]Progression-free Survival (PFS) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set
NCT00471328 (9) [back to overview]Overall Survival for Treatment Crossover Analysis Set
NCT00471328 (9) [back to overview]Overall Survival During Core and Extension Phases of the Study
NCT00471328 (9) [back to overview]Overall Survival Based on Primary Analysis (Data Cut-off:June, 2008)
NCT00471328 (9) [back to overview]Overall Clinical Benefit (Complete Response [CR]/Partial Response [PR] or Stable Disease [SD]) From Central Radiology Review Based on Primary Analysis (Data Cut-off: June, 2008)
NCT00471328 (9) [back to overview]Overall Clinical Benefit (Complete Response [CR]/Partial Response [PR] or Stable Disease [SD]) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set
NCT00471328 (9) [back to overview]Number of Responders With Confirmed Best Overall Response of Complete Response (CR) or Partial Response (PR) From Central Radiology Review During Primary Analysis (Data Cut-off: June, 2008)
NCT00471497 (31) [back to overview]Rate of a ≥ 4 Log Reduction in BCR-ABL Transcripts in Nilotinib Treatment Arms With Imatinib
NCT00471497 (31) [back to overview]Rate of Complete Cytogenetic Response (CCyR) on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)
NCT00471497 (31) [back to overview]Rate of Major Molecular Response (MMR) on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)
NCT00471497 (31) [back to overview]Rate of Hematologic Response on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)
NCT00471497 (31) [back to overview]Actual Dose-intensity
NCT00471497 (31) [back to overview]Duration of CCyR
NCT00471497 (31) [back to overview]All Collected Deaths
NCT00471497 (31) [back to overview]Duration of Both a ≥ 4 and ≥ 4.5 Log Reduction in BCR-ABL Transcripts
NCT00471497 (31) [back to overview]Percentage of Participants With MMR at 12 Months Between All 3 Arms by Sokal Risk Group With Imputation
NCT00471497 (31) [back to overview]Pharmacokinetics: Cmin
NCT00471497 (31) [back to overview]Rate of a ≥ 4.5 Log Reduction in BCR-ABL Transcripts in Nilotinib Treatment Arms With Imatinib
NCT00471497 (31) [back to overview]Time to Both a ≥ 4 and ≥ 4.5 Log Reduction in BCR-ABL Transcripts
NCT00471497 (31) [back to overview]Rate of Complete Cytogenetic Response (CCyR) in Nilotinib Treatment Arms With Imatinib at 12 Months and Beyond 12 Months
NCT00471497 (31) [back to overview]Rate of Hematologic Response
NCT00471497 (31) [back to overview]Rate of MMR at 6 Months and Beyond in All 3 Treatment Arms
NCT00471497 (31) [back to overview]Time to Progression to AP/BC
NCT00471497 (31) [back to overview]Rates of Durable MMR at 24 Months Between All 3 Arms
NCT00471497 (31) [back to overview]Rate of Major Molecular Response (MMR) at 12 Months Between Two Nilotinib Arms
NCT00471497 (31) [back to overview]Time to First MMR
NCT00471497 (31) [back to overview]Time to Complete Cytogenic Response (CCyR)
NCT00471497 (31) [back to overview]Progression-free Survival (PFS)
NCT00471497 (31) [back to overview]Rate of a ≥ 4 Log Reduction in BCR-ABL Transcripts on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)
NCT00471497 (31) [back to overview]Rate of ≥ 4.5 Log Reduction in BCR-ABL Transcripts on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)
NCT00471497 (31) [back to overview]Presence of Newly Observed BCR-ABL Mutations in Patients Post-baseline and Correlate With Response to Treatment With Imatinib and Nilotinib (Extension)
NCT00471497 (31) [back to overview]Pharmacokinetics: Tmax
NCT00471497 (31) [back to overview]Pharmacokinetics: Cmax
NCT00471497 (31) [back to overview]Pharmacokinetics: AUC0-last
NCT00471497 (31) [back to overview]Overall Survival (OS)
NCT00471497 (31) [back to overview]Major Molecular Response Rate (MMR) at 12 Months Between All 3 Arms - With Imputation
NCT00471497 (31) [back to overview]Event-free Survival (EFS)
NCT00471497 (31) [back to overview]Duration of MMR
NCT00477269 (24) [back to overview]Number of Patients With Adverse Events (AEs), Serious Adverse Events (SAEs) and Death During the Core
NCT00477269 (24) [back to overview]Number of Patients With Adverse Events (AEs), Serious Adverse Events (SAEs) and Death During the Extension
NCT00477269 (24) [back to overview]Blood Gas Measurement - PvO2 at Baseline and Study Completion
NCT00477269 (24) [back to overview]Blood Gas Measurement - pH at Baseline and Study Completion
NCT00477269 (24) [back to overview]Blood Gas Measurement - PaO2 at Baseline and Study Completion
NCT00477269 (24) [back to overview]Blood Gas Measurement - PaCO2 at Baseline and Study Completion
NCT00477269 (24) [back to overview]Blood Gas Measurement - Arterial Saturation at Baseline and Study Completion
NCT00477269 (24) [back to overview]Mean Pulmonary Artery Pressure (PAP) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Change From Baseline of Six Minute Walk Test - Number of Stops at Different Time Periods
NCT00477269 (24) [back to overview]Borg Score-Systolic Blood Pressure During the Six Minutes Walk Test at Different Time Periods
NCT00477269 (24) [back to overview]Borg Score-Oxygen Saturation(SaO2) During the Six Minutes Walk Test at Different Time Periods
NCT00477269 (24) [back to overview]Borg Score-Heart Rate (HR) During the Six Minutes Walk Test at Different Time Periods
NCT00477269 (24) [back to overview]Mean Cardiac Output (CO) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Mean Heart Rate (HR) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Blood Gas Measurement - Venous Saturation at Baseline and Study Completion
NCT00477269 (24) [back to overview]Mean Pulmonary Artery Wedge Pressure (PAWP) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Number of Patients With Pulmonary Hypertension (PAH) Assessd by World Health Organization (WHO) Classification on Physical Activity
NCT00477269 (24) [back to overview]Mean Pulmonary Vascular Resistance (PVR) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Borg Score-Diastolic Blood Pressure During the Six Minutes Walk Test at Different Time Periods
NCT00477269 (24) [back to overview]Change From Baseline of Six Minute Walk Test - Total Duration of Stops at Different Time Periods
NCT00477269 (24) [back to overview]Change From Baseline of Six Minute Walk Test - Total Distance Walked at Different Time Periods
NCT00477269 (24) [back to overview]Mean Systemic Vascular Resistance (SVR) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Mean Systolic Arterial Pressure (SAP) at Baseline and Study Completion
NCT00477269 (24) [back to overview]Borg Score During the Six Minutes Walk Test at Different Time Periods
NCT00481247 (9) [back to overview]Percentage of Participants Remaining in Confirmed Complete Cytogenetic Response (cCCyR)
NCT00481247 (9) [back to overview]Number of Participants With Grade 3/4 Abnormalities in On-study Laboratory Test Results
NCT00481247 (9) [back to overview]Number of Participants With Adverse Events (AEs), Drug-related AEs, Drug-related Serious Adverse Events (SAEs), Drug-related AEs Leading to Discontinuation, and All Deaths
NCT00481247 (9) [back to overview]Time to Confirmed Complete Cytogenic Response (cCCyR) Overall
NCT00481247 (9) [back to overview]Percentage of Participants With Progression-free Survival (PFS)
NCT00481247 (9) [back to overview]Percentage of Participants With Overall Survival (OS)
NCT00481247 (9) [back to overview]Percentage of Participants With Major Molecular Response (MMR) at Any Time
NCT00481247 (9) [back to overview]Number of Participants With Best Confirmed Complete Cytogenetic Response (cCCyR) Within 12 Months
NCT00481247 (9) [back to overview]Time to Major Molecular Response (MMR) Overall
NCT00485485 (1) [back to overview]Participant Response Rate
NCT00499889 (3) [back to overview]Participants' With mCR Response to Post Transplant Imatinib Mesylate Therapy
NCT00499889 (3) [back to overview]Participants' With mCR Response to Post Transplant DLI
NCT00499889 (3) [back to overview]Number of Participants in Complete Molecular Remission at 1 Year
NCT00500110 (1) [back to overview]Number of Participants Achieving Pathological Complete Response
NCT00506779 (2) [back to overview]Number of Participants With Complete Response
NCT00506779 (2) [back to overview]Number of Participants Who Experienced Dose Limiting Toxicities (DLTs)
NCT00506831 (5) [back to overview]Cell Types That Contribute to the Gene Expression Changes Associated With Imatinib Therapy
NCT00506831 (5) [back to overview]Percent Change in Modified Rodnan Skin Score at 6 Months Compared to Baseline
NCT00506831 (5) [back to overview]Change in Scleroderma Health Assessment Questionnaire at 6 Months Compared to Baseline
NCT00506831 (5) [back to overview]Change in Pulmonary Function Tests at 6 Months Compared to Baseline
NCT00506831 (5) [back to overview]Change in Dermal Thickness and Collagen Separation on Cutaneous Histopathology at 6 Months Compared to Baseline
NCT00509093 (5) [back to overview]Median Progression-free Survival (PFS) for Patients Less Than 60 Years of Age
NCT00509093 (5) [back to overview]Toxicity as Measured by NCI CTC v. 3.0
NCT00509093 (5) [back to overview]Percent of Participants Less Than 60 Years of Age With PFS at 8 and 13 Months Post-treatment
NCT00509093 (5) [back to overview]Percent of Participants 60 Years of Age or Older With PFS at 8 and 13 Months Post-treatment
NCT00509093 (5) [back to overview]Progression-free Survival for Patients 60 Years of Age and Older
NCT00510653 (1) [back to overview]Overall Response Rate (ORR)
NCT00512902 (5) [back to overview]Change in Modified Rodnan Skin Score (MRSS)
NCT00512902 (5) [back to overview]Change in FVC (Forced Vital Capacity)
NCT00512902 (5) [back to overview]Treatment-related Adverse Events
NCT00512902 (5) [back to overview]Change in DLco
NCT00512902 (5) [back to overview]Change in TLC (Total Lung Capacity)
NCT00555581 (6) [back to overview]Improvement in Indices of Pulmonary Function Measured by Change DLCO hb Adj % Predicted
NCT00555581 (6) [back to overview]Improvement in Indices of Pulmonary Function Measured by Change in FVC % Predicted
NCT00555581 (6) [back to overview]Improvement in the Modified Rodnan Skin Score
NCT00555581 (6) [back to overview]Scleroderma Health Assessment Questionnaire Disability Index
NCT00555581 (6) [back to overview]Change From Baseline at Month 12 in Short Form-36 (SF-36) Questionnaire:Mental Component Summary
NCT00555581 (6) [back to overview]Change From Baseline at Month 12 in Short Form-36 (SF-36) Questionnaire: Physical Component Summary
NCT00574873 (6) [back to overview]Cumulative Incidence of On-Treatment Transformation to Accelerated Phase (AP) or Blast Phase (BP) at 192 Weeks
NCT00574873 (6) [back to overview]Kaplan-Meier Estimate of Probability of Retaining Complete Hematologic Response (CHR) at 192 Weeks
NCT00574873 (6) [back to overview]Percentage of Participants With Major Molecular Response (MMR) at Year 1
NCT00574873 (6) [back to overview]Percentage of Participants With Complete Cytogenetic Response (CCyR) at Year 1
NCT00574873 (6) [back to overview]Kaplan-Meier Estimate of Probability of Retaining Derived MMR at 144 Weeks
NCT00574873 (6) [back to overview]Kaplan-Meier Estimate of Probability of Retaining CCyR at 192 Weeks
NCT00613171 (3) [back to overview]Number of Participants With Non-response, Partial Response, Complete Response, and Remission Assessed by MRSS Values
NCT00613171 (3) [back to overview]Change From Baseline in Modified Rodnan Skin Score (MRSS) at Each Time Point of Analysis
NCT00613171 (3) [back to overview]Number of Participants With Adverse Events (AE's) and Serious Adverse Events (SAE's)
NCT00615927 (5) [back to overview]12-month Progression Free Survival (PFS)
NCT00615927 (5) [back to overview]Median Overall Survival (OS)
NCT00615927 (5) [back to overview]Median Progression-free Survival
NCT00615927 (5) [back to overview]Objective Response Rate
NCT00615927 (5) [back to overview]Safety and Tolerability of Gleevec + Hydroxyurea in Patients With Low-grade Gliomas
NCT00667953 (2) [back to overview]Safety - Grade 3 or 4 Adverse Events
NCT00667953 (2) [back to overview]Response
NCT00677092 (1) [back to overview]Percentage Change From Baseline in the Modified Rodnan Skin Score (mRSS) to Assess Skin Tethering
NCT00684411 (3) [back to overview]Progression-Free Survival
NCT00684411 (3) [back to overview]Overall Survival
NCT00684411 (3) [back to overview]Overall Response Rate
NCT00702403 (5) [back to overview]The Proportion of Patients at 1 Year With Treatment Efficacy Success
NCT00702403 (5) [back to overview]Survival
NCT00702403 (5) [back to overview]Number of Participants With Treatment Safety Failure
NCT00702403 (5) [back to overview]Patients Alive With Out Relapse
NCT00702403 (5) [back to overview]Relapse
NCT00702689 (8) [back to overview]Percent Change in Absolute Range of Motion (ROM) From Baseline to 6 Months
NCT00702689 (8) [back to overview]Primary Range of Motion (ROM) Response
NCT00702689 (8) [back to overview]Total Chronic Graft Versus Host Disease (cGVHD) Provider Global Rating Score at Baseline and 6 Months
NCT00702689 (8) [back to overview]Total Skin Score at Baseline and 6 Months
NCT00702689 (8) [back to overview]Average Percentage Change in Range of Motion (ROM) Deficit
NCT00702689 (8) [back to overview]Number of Participants With Adverse Events
NCT00702689 (8) [back to overview]Change in Immunosuppression
NCT00702689 (8) [back to overview]Lung Function Score at Baseline and 6 Months
NCT00751036 (4) [back to overview]Disease Control Rate (DCR)
NCT00751036 (4) [back to overview]Time to Treatment Failure
NCT00751036 (4) [back to overview]Progression-free Survival (PFS)
NCT00751036 (4) [back to overview]Overall Survival (OS)
NCT00760877 (6) [back to overview]Rate of Confirmed Best Cumulative CMR
NCT00760877 (6) [back to overview]Rate of Confirmed Best Cumulative Complete Molecular Response (CMR)
NCT00760877 (6) [back to overview]Event-free Survival
NCT00760877 (6) [back to overview]Overall Survival
NCT00760877 (6) [back to overview]Progression Free Survival (PFS)
NCT00760877 (6) [back to overview]Number of Cross-over Participants With CMR
NCT00785785 (1) [back to overview]Time to Progression Free Survival (PFS)
NCT00802841 (8) [back to overview]Duration of CCyR
NCT00802841 (8) [back to overview]Overall Survival (OS)
NCT00802841 (8) [back to overview]Time to CCyR
NCT00802841 (8) [back to overview]Percentage of Participants With CCyr
NCT00802841 (8) [back to overview]Percentage of Participants With Major Molecular Response (MMR)
NCT00802841 (8) [back to overview]Percentage of Participants With Complete Cytogenetic Response (CCyR)
NCT00802841 (8) [back to overview]Event-Free Survival (EFS)
NCT00802841 (8) [back to overview]Progression-Free Survival (PFS)
NCT00840450 (3) [back to overview]Progression-free-tolerance
NCT00840450 (3) [back to overview]the Best Overall Clinical Response
NCT00840450 (3) [back to overview]Progression-free-survival at 12 Months
NCT00861471 (5) [back to overview]Time to PSA Progression
NCT00861471 (5) [back to overview]Percentage of Participants With Prostate Specific Antigen (PSA) Response
NCT00861471 (5) [back to overview]Percentage of Participants With Measurable Disease Response
NCT00861471 (5) [back to overview]Median Overall Survival Time
NCT00861471 (5) [back to overview]Percentage of Participants With Greater or Equal to 80% PSA Reduction From Baseline Without Clinical or Radiologic Evidence of Progression
NCT00867113 (4) [back to overview]Recurrence-free Survival up to 60 Months
NCT00867113 (4) [back to overview]Overall Survival (OS) at 60 Months
NCT00867113 (4) [back to overview]Kaplan-Meier Estimates for Recurrence-free Survival up to 60 Months
NCT00867113 (4) [back to overview]Kaplan-Meier Estimates for Overall Survival (OS) up to 60 Months
NCT00867334 (2) [back to overview]Number of Patients With Adverse Events
NCT00867334 (2) [back to overview]Number of Participants With Stabilization or Reduction in Tumor Size
NCT00882206 (4) [back to overview]Level of Methylation
NCT00882206 (4) [back to overview]Level of Methylation
NCT00882206 (4) [back to overview]Level of Methylation
NCT00882206 (4) [back to overview]Response to Treatment
NCT00891527 (3) [back to overview]Number of Patients With Survival at 48 Weeks
NCT00891527 (3) [back to overview]Number of Patients With Disease Progression at 48 Weeks
NCT00891527 (3) [back to overview]Number of Patients With Disease Stabilization at 48 Weeks
NCT00902174 (16) [back to overview]Clinical Worsening Comparing Imatinib Versus Placebo for Adjudicated Cases
NCT00902174 (16) [back to overview]Plasma Concentration of QTI571 200 mg and Its Metabolite (GCP74588) Pre-dose and Between 0 Hour to 3 Hour Post-dose Per Participant
NCT00902174 (16) [back to overview]Change From Baseline in Systolic Arterial Blood Pressure
NCT00902174 (16) [back to overview]Change From Baseline in Systemic Vascular Resistance
NCT00902174 (16) [back to overview]Change From Baseline in Right Atrial Pressure
NCT00902174 (16) [back to overview]Change From Baseline in Pulmonary Vascular Resistance
NCT00902174 (16) [back to overview]Change From Baseline in Pulmonary Resistance Index
NCT00902174 (16) [back to overview]Covariance of End of Study CAMPHOR Score
NCT00902174 (16) [back to overview]Change From Baseline in Mean Pulmonary Capillary Wedge Pressure
NCT00902174 (16) [back to overview]Change From Baseline in Mean Pulmonary Arterial Pressure
NCT00902174 (16) [back to overview]Change From Baseline in Heart Rate
NCT00902174 (16) [back to overview]Change From Baseline in Diastolic Arterial Blood Pressure
NCT00902174 (16) [back to overview]Change From Baseline in Cardiac Output
NCT00902174 (16) [back to overview]Change in Borg Dyspnea Score During 6-minute Walk Test
NCT00902174 (16) [back to overview]Difference in Six-minute Walk Distance Test (6MWD) Between Imatinib and Placebo at 24 Weeks
NCT00902174 (16) [back to overview]Plasma Concentration of QTI571 400 mg and Its Metabolite (GCP74588) Pre-dose and Between 0 Hour to 3 Hour Post-dose Per Participant
NCT00928642 (5) [back to overview]Tumor Response Rates Using Modified SWOG Criteria to the Combination of Gleevec and Gemzar in Patients With Relapsed Ovarian Cancer Who Have Failed at Least One Prior Chemotherapy Treatment.
NCT00928642 (5) [back to overview]To Estimate the Clinical Response Rate(Partial and Complete Response as Defined Under the SWOG Criterial)
NCT00928642 (5) [back to overview]To Determine the Distribution of the Overall Survival
NCT00928642 (5) [back to overview]The Cystostatic, Anti-tumor Activity of the Combination of Gleevec and Gemzar Via Progression-free Survival for at Least Six Months in Patients With Recurrent or Persistent Epithelial Ovarian or Primary Peritoneal Carcinoma.
NCT00928642 (5) [back to overview]To Determine the Safety and Tolerability Via Frequency and Severity of Adverse Effect of Combination Gleevec and Gemzar in This Cohort of Patients as Assessed Byt Common Toxicity Criteria
NCT00955916 (3) [back to overview]Overall Response Rate (ORR)
NCT00955916 (3) [back to overview]Median Overall Survival (OS)
NCT00955916 (3) [back to overview]Median Progression Free Survival (PFS)
NCT00982488 (1) [back to overview]Number of Participants Who Died and Had Serious Adverse Events (SAEs), Related SAEs, Adverse Events (AEs) Leading to Discontinuation, Related AEs Leading to Discontinuation, Related AEs, and Related AEs of Special Interest
NCT01011075 (4) [back to overview]Toxicities
NCT01011075 (4) [back to overview]Progression Free Survival
NCT01011075 (4) [back to overview]Overall Survival
NCT01011075 (4) [back to overview]Response Rate
NCT01089595 (2) [back to overview]Progression Free Survival
NCT01089595 (2) [back to overview]Best Overall Response Using Response Evaluation Criteria in Solid Tumors, Choi Criteria, and Positron Emission Tomography Imaging
NCT01097694 (25) [back to overview]Airway Wall Area
NCT01097694 (25) [back to overview]Airway Wall Thickness
NCT01097694 (25) [back to overview]Asthma Quality of Life Questionnaire (AQLQ)
NCT01097694 (25) [back to overview]Asthma Symptom Utility Index (ASUI)
NCT01097694 (25) [back to overview]BAL Eosinophil %
NCT01097694 (25) [back to overview]Endobronchial Biopsy Smooth Muscle Tryptase-positive Mast Cells
NCT01097694 (25) [back to overview]Endobronchial Biopsy Total Tryptase-positive Mast Cells
NCT01097694 (25) [back to overview]Evening Peak Flow
NCT01097694 (25) [back to overview]FEV1 in Liters
NCT01097694 (25) [back to overview]Bronchoalveolar Lavage (BAL) PGD2
NCT01097694 (25) [back to overview]Urinary Leukotriene E4
NCT01097694 (25) [back to overview]Serum Total Tryptase
NCT01097694 (25) [back to overview]Number of Asthma Exacerbations
NCT01097694 (25) [back to overview]Morning Peak Flow Measurement
NCT01097694 (25) [back to overview]Fractional Exhaled Nitric Oxide (FeNO)
NCT01097694 (25) [back to overview]Asthma Control Questionnaire (ACQ)
NCT01097694 (25) [back to overview]Bronchoalveolar Lavage (BAL) Fluid Tryptase Level
NCT01097694 (25) [back to overview]Blood Eosinophils
NCT01097694 (25) [back to overview]Bronchoalveolar Lavage Histamine
NCT01097694 (25) [back to overview]Change in Maximum Post-Bronchodilator (BD) Forced Expiratory Volume in One Second (FEV1) %
NCT01097694 (25) [back to overview]Change in Mean Methacholine Responsiveness as Assessed by the Provocation Concentration Causing a 20% Fall in Forced Expiratory Volume in One Second (FEV1) (PC20) at Month 3 and 6 Versus Baseline
NCT01097694 (25) [back to overview]FEV1%
NCT01097694 (25) [back to overview]BAL Neutrophil %
NCT01097694 (25) [back to overview]Bronchoalveolar Lavage Cysteinyl Leukotrienes
NCT01097694 (25) [back to overview]Urinary Prostaglandin D2
NCT01117987 (3) [back to overview]Number of Participants With Adverse Events, Serious Adverse Events and Deaths
NCT01117987 (3) [back to overview]Percentage of Participants With Incidence of Clinical Worsening Events
NCT01117987 (3) [back to overview]Change From Core Study Baseline in Six-Minute Walk Distance (6MWD)
NCT01151852 (6) [back to overview]Progression Free Survival
NCT01151852 (6) [back to overview]Progression-free Survival
NCT01151852 (6) [back to overview]Response Rate
NCT01151852 (6) [back to overview]Safety and Tolerability of Imatinib
NCT01151852 (6) [back to overview]Overall Survival(OS) and Time to Progression(TTP)
NCT01151852 (6) [back to overview]Disease Control Rate
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Progression-free Survival (PFS) on Treatment
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Time to First CCYR
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Time to First MMR
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Time to Progression to Accelerated Phase/Blast Crisis (AP/BC) on Treatment
NCT01275196 (17) [back to overview]Summary Statistics of Trough Imatinib and Major Metabolite CGP74588 of Imatinib and Nilotinib PK Concentration by Time Point
NCT01275196 (17) [back to overview]Modified ELN2009 Criteria
NCT01275196 (17) [back to overview]MMR Rate at Each Time Point
NCT01275196 (17) [back to overview]Best MMR by Each Timepoint
NCT01275196 (17) [back to overview]Durable MMR Rate at 24 Months
NCT01275196 (17) [back to overview]Best Complete Hematologic Response (CHR)
NCT01275196 (17) [back to overview]Best Complete Cytogenic Response (CCyR) Rate by Each Time Point
NCT01275196 (17) [back to overview]Major Molecular Response (MMR) at 12 Months - With Imputation.
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Duration of First CCyR Among Patients Who Achieved CCyR
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Duration of First MMR Among Patients Who Achieved MMR
NCT01275196 (17) [back to overview]Actual Dose Intensity
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Event-free Survival (EFS) on Treatment
NCT01275196 (17) [back to overview]Kaplan-Meier Estimates of Overall Survival (OS) on Treatment
NCT01275222 (8) [back to overview]Number of Participants With Adverse Events (AEs): Phase I & II
NCT01275222 (8) [back to overview]Best Overall Response (BOR) as Assessed by Overall Response (Complete Response (CR) & Partial Response (PR)) - Phase I & II
NCT01275222 (8) [back to overview]Trough Concentrations for RAD001 and for Imatinib - Phase II
NCT01275222 (8) [back to overview]4-Month Progression-free Survival (PFS) Rate - Phase II
NCT01275222 (8) [back to overview]Trough Concentrations for RAD001 and for Imatinib - Phase II
NCT01275222 (8) [back to overview]All Collected Deaths
NCT01275222 (8) [back to overview]Progression-free Survival (PFS) - Phase II
NCT01275222 (8) [back to overview]Overall Survival (OS) - Phase I & II
NCT01281865 (1) [back to overview]Response Rate (CR + PR) Assessed by RECIST 1.1 (Phase II)
NCT01309997 (7) [back to overview]Percentage of CD27+ B Cells in Responders (SCR) and Non-responders
NCT01309997 (7) [back to overview]Significant Clinical Response
NCT01309997 (7) [back to overview]Cumulative Incidence of Treatment Failure
NCT01309997 (7) [back to overview]Number of Patients Achieving Improvement in Cutaneous Sclerosis
NCT01309997 (7) [back to overview]Patients Who Were Able to Taper Corticosteroids
NCT01309997 (7) [back to overview]Baseline Histopathologic Score in the Two Treatment Arms
NCT01309997 (7) [back to overview]Patients With Any Percentage Decline in Any Grade of Sclerosis Without Increase in Percentage of Higher Grades of Sclerosis in Other Areas on the Vienna Skin Scale
NCT01312818 (2) [back to overview]Number of Subjects Who Achieved Complete Remission of Their Disease
NCT01312818 (2) [back to overview]Number of Subjects Experiencing Drug Related Adverse Events
NCT01319981 (3) [back to overview]Number of Patients With Complete Remission at One Year
NCT01319981 (3) [back to overview]Overall Survival
NCT01319981 (3) [back to overview]Complete Response Duration
NCT01392469 (7) [back to overview]Geometric Mean Ratio of Dose Normalized AUCtau for Sildenafil Before and After Imatinib Administrations
NCT01392469 (7) [back to overview]Geometric Mean Ratio of Dose Normalized Cmax for Sildenafil Before and After Imatinib Administrations
NCT01392469 (7) [back to overview]Geometric Mean Ratio of Dose Normalized Maximum Plasma Concentration (Cmax) for Bosentan Before and After Imatinib Administrations
NCT01392469 (7) [back to overview]Dose Normalized AUCtau of Imatinib and CGP74588 (Active Metabolite of Imatinib)
NCT01392469 (7) [back to overview]Number of Participants With At Least One or More Adverse Events (AEs)
NCT01392469 (7) [back to overview]Dose Normalized Cmax of Imatinib and CGP74588 (Active Metabolite of Imatinib)
NCT01392469 (7) [back to overview]Geometric Mean Ratio of Dose Normalized Area Under the Curve From Time Zero to Tau (AUCtau) for Bosentan Before and After Imatinib Administrations
NCT01392495 (1) [back to overview]Number of Patients With Adverse Events, Serious Adverse Events and Deaths
NCT01593254 (5) [back to overview]Time to Molecular Response (MR)^4.5
NCT01593254 (5) [back to overview]Overall Survival (OS)
NCT01593254 (5) [back to overview]Percentage of Patients Achieving Major Molecular Response (MMR) After 12 Months of CML Treatment
NCT01593254 (5) [back to overview]Progression Free Survival (PFS)
NCT01593254 (5) [back to overview]Median Time to Major Molecular Response (MMR)
NCT01650805 (3) [back to overview]Complete Cytogenetic Response (CCyR) Rate
NCT01650805 (3) [back to overview]Major Molecular Response (MMR) Rate at 12 Months
NCT01650805 (3) [back to overview]<10% BCR-ABL^IS Rate
NCT01673009 (1) [back to overview]Percent Change From Baseline in Tumor Volume at 6 Months
NCT01781975 (6) [back to overview]Change in HbA1c Levels Over Time
NCT01781975 (6) [back to overview]Number of Severe Hypoglycemic Events
NCT01781975 (6) [back to overview]Number of Adverse Events
NCT01781975 (6) [back to overview]Area Under the Stimulated C-peptide Curve (AUC) Mean Over the First 2 Hours of a 4 Hour Mixed Meal Tolerance Test at the 1 Year Visit
NCT01781975 (6) [back to overview]Area Under the Stimulated C-peptide Curve (AUC) Mean Over 4 Hours at 24 Months
NCT01781975 (6) [back to overview]Change in Insulin Dose (Units/kg) Over Time
NCT01795716 (1) [back to overview]Area Under Curve (AUC) Time Frame: Predose, 0.5,1,1.5,2,3,5,8,12,24,48,72hours Post-dose
NCT01827930 (8) [back to overview]Rate of BCR-ABL Undetectable
NCT01827930 (8) [back to overview]Time to the First BCR-ABL Undetectable
NCT01827930 (8) [back to overview]Molecular Response at 3, 6, 9 and 12 Months
NCT01827930 (8) [back to overview]Rate of Decline of 2-log of the BCR-ABL Transcript Rate at 3 ,6, 9 and 12 Months From Baseline - Randomised Study
NCT01827930 (8) [back to overview]Time to Complete Molecular Response (CMR) and Major Molecular Response (MMR)
NCT01827930 (8) [back to overview]Overall Survival
NCT01827930 (8) [back to overview]Percentage of Patients Presenting a Decline of the BCR-ABL Transcript Rate at 12 Months From Baseline - Randomised Study
NCT01827930 (8) [back to overview]Progression-free Survival
NCT02127372 (4) [back to overview]Phase 1 - Maximum Tolerated Dose (MTD) of STI571
NCT02127372 (4) [back to overview]Phase II - Radiographic Response
NCT02127372 (4) [back to overview]Phase 1 - Maximum Tolerated Dose (MTD) of Docetaxel and Cisplatin
NCT02127372 (4) [back to overview]Phase 2: 1 Year Survival
NCT02130557 (16) [back to overview]Kaplan-Meier Estimate of Probability of Retaining Complete Cytogenetic Response (CCyR) at Month 48
NCT02130557 (16) [back to overview]Cumulative Incidence of Event Free Survival (EFS) Events
NCT02130557 (16) [back to overview]Summary of Trough Plasma Concentration by Presence of Grade 3 or Higher Adverse Events (AEs) of Bosutinib
NCT02130557 (16) [back to overview]Summary of Trough Plasma Concentration by Presence of Grade 1 or Higher Adverse Events (AEs) of Bosutinib
NCT02130557 (16) [back to overview]Summary of Trough Plasma Concentration by Complete Cytogenetic Response (CCyR) of Bosutinib
NCT02130557 (16) [back to overview]Number of Participants With Treatment-Emergent Adverse Events by National Cancer Institute Common Terminology Criteria for AEs (NCI CTCAE) (Version 4.0)
NCT02130557 (16) [back to overview]Summary of Trough Plasma Concentration by Major Molecular Response (MMR) of Bosutinib
NCT02130557 (16) [back to overview]Number of Participants With Laboratory Test Abnormalities Based on National Cancer Institute Common Terminology Criteria for AEs (NCI CTCAE) Version 4.03
NCT02130557 (16) [back to overview]Percentage of Participants With Major Molecular Response (MMR) Up to Month 18
NCT02130557 (16) [back to overview]Percentage of Participants With Major Molecular Response (MMR) at Month 12
NCT02130557 (16) [back to overview]Percentage of Participants With Complete Cytogenetic Response (CCyR) Up to Month 12
NCT02130557 (16) [back to overview]Overall Survival (OS) Rate
NCT02130557 (16) [back to overview]Number of Participants With Vital Signs Abnormalities
NCT02130557 (16) [back to overview]Number of Participants With Clinically Significant Electrocardiogram (ECG) Abnormalities
NCT02130557 (16) [back to overview]Number of Participants With Adverse Events (AEs) Leading to Study Drug Discontinuation
NCT02130557 (16) [back to overview]Kaplan-Meier Estimate of Probability of Retaining Major Molecular Response (MMR) at Month 48
NCT02257541 (3) [back to overview]Phase Ib Study: Number of Participants With Dose-Limiting Toxicities
NCT02257541 (3) [back to overview]Phase Ib Portion: Response Rate (RR)
NCT02257541 (3) [back to overview]Phase Ib Study: Response Rate (RR)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Diarrhea of Patients at 6 Months (After Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Diarrhea of Patients at Baseline (Before Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Fatigue of Patients at 6 Months (After Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Fatigue of Patients at Baseline (Before Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Sleep Status of Patients at 6 Months (After Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Patient-reported Health Status Related to Sleep Status of Patients at Baseline (Before Stopping Tyrosine Kinase Inhibitors (TKIs)
NCT02269267 (7) [back to overview]Number of Patients With Chronic Myeloid Leukemia (CML) Who Develop Molecular Recurrence After Discontinuing TKIs.
NCT02272777 (1) [back to overview]Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)
NCT02644525 (1) [back to overview]Percent of Baseline Loa Loa Microfilariae
NCT03023046 (5) [back to overview]Event-free Survival
NCT03023046 (5) [back to overview]Number of Participants With Complete Measurable Residual Disease (MRD) Response Rate
NCT03023046 (5) [back to overview]Number of Participants With Adverse Events
NCT03023046 (5) [back to overview]Number of Participants With Morphological Complete Response Rate
NCT03023046 (5) [back to overview]Overall Survival
NCT03112603 (24) [back to overview]Rate of Participants With Clinically Relevant Improvement of the Modified Lee cGvHD Symptom Scale Score
NCT03112603 (24) [back to overview]Vz/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]Tmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]t1/2 of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]Percentage of Participants With a ≥ 50% Reduction in Daily Corticosteroid Dose
NCT03112603 (24) [back to overview]Percentage of Participants Successfully Tapered Off of All Corticosteroids
NCT03112603 (24) [back to overview]Cumulative Incidence of Non-relapse Mortality (NRM)
NCT03112603 (24) [back to overview]Cumulative Incidence of Malignancy Relapse/Recurrence (MR)
NCT03112603 (24) [back to overview]Cmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]CL/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]Change From Baseline in Functional Assessment of Cancer Therapy - Bone Marrow Transplantation (FACT-BMT)
NCT03112603 (24) [back to overview]Change From Baseline in EQ-5D-5L
NCT03112603 (24) [back to overview]AUClast of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]AUCinf of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses
NCT03112603 (24) [back to overview]Utilization of Medical Resources
NCT03112603 (24) [back to overview]Rate of FFS at Study Completion
NCT03112603 (24) [back to overview]Rate of Failure-free Survival (FFS)
NCT03112603 (24) [back to overview]Overall Survival (OS)
NCT03112603 (24) [back to overview]ORR at the End of Cycle 3
NCT03112603 (24) [back to overview]Number of Participants With Any Treatment-emergent Adverse Event (TEAE)
NCT03112603 (24) [back to overview]Efficacy of Ruxolitinib Versus Investigator's Choice Best Available Therapy (BAT) in Participants With Moderate or Severe Steroid Refractory Chronic Graft Versus Host Disease (SR-cGvHD) Assessed by Overall Response Rate (ORR) at the Cycle 7 Day 1 Visit
NCT03112603 (24) [back to overview]Duration of Response Through Study Completion
NCT03112603 (24) [back to overview]BOR During Cross-over Treatment With Ruxolitinib
NCT03112603 (24) [back to overview]Best Overall Response (BOR) at Cycle 7 Day 1
NCT03131999 (2) [back to overview]Serum VEGF-D
NCT03131999 (2) [back to overview]Adverse Events
NCT03589326 (1) [back to overview]Number of Participants With Minimal Residual Disease (MRD)-Negative Complete Remission (CR) at The End of Induction Phase
NCT03891901 (20) [back to overview]White Blood Cell Count
NCT03891901 (20) [back to overview]Number of Myelomonocytic Cells in the Blood
NCT03891901 (20) [back to overview]Maximum Concentration (Cmax) of Imatinib
NCT03891901 (20) [back to overview]Maximum Concentration (Cmax) of Imatinib
NCT03891901 (20) [back to overview]Half-life (T1/2) of Imatinib
NCT03891901 (20) [back to overview]Half-life (T1/2) of Imatinib
NCT03891901 (20) [back to overview]Elimination Rate Constant (Ke) of Imatinib
NCT03891901 (20) [back to overview]Elimination Rate Constant (Ke) of Rifabutin
NCT03891901 (20) [back to overview]Frequency of Grade 3 or 4 Adverse Events (AEs)
NCT03891901 (20) [back to overview]Frequency of Serious Adverse Events (SAEs)
NCT03891901 (20) [back to overview]Half-life (T1/2) of Isoniazid
NCT03891901 (20) [back to overview]Half-life (T1/2) of Rifabutin
NCT03891901 (20) [back to overview]Maximum Concentration (Cmax) of Rifabutin
NCT03891901 (20) [back to overview]Area Under the Curve (AUC) for Imatinib
NCT03891901 (20) [back to overview]Maximum Concentration (Cmax) of Isoniazid
NCT03891901 (20) [back to overview]Area Under the Curve (AUC) for Imatinib
NCT03891901 (20) [back to overview]Elimination Rate Constant (Ke) of Imatinib
NCT03891901 (20) [back to overview]Area Under the Curve (AUC) for Isoniazid
NCT03891901 (20) [back to overview]Area Under the Curve (AUC) for Rifabutin
NCT03891901 (20) [back to overview]Elimination Rate Constant (Ke) of Isoniazid
NCT05286528 (3) [back to overview]Overall Survival Rate: Type of Second Line TKI
NCT05286528 (3) [back to overview]Overall Survival Rate: Type of First Line TKI
NCT05286528 (3) [back to overview]Overall Survival Rate: All Participants
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Major Cytogenetic Response After 6 and 12 Months of Treatment.

"Cytogenetic response in terms of the percentage of Ph chromosome positive metaphases in bone marrow is defined as follows:~Complete* (0% Ph-positive cells) Partial* (1-34%) Minor (35-95%) None (96-100%).~*Major cytogenetic response includes complete and partial cytogenetic response." (NCT00015847)
Timeframe: 6 and 12 months after treatment

InterventionParticipants (Number)
Imatinib Mesylate18

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Complete Cytogenetic Response at 6 and 12 Months (Phase II)

"Cytogenetic response in terms of the percentage of Ph chromosome positive metaphases in bone marrow is defined as follows:~Complete* (0% Ph-positive cells) Partial* (1-34%) Minor (35-95%) None (96-100%)." (NCT00015847)
Timeframe: At 6 and 12 months during phase II

InterventionParticipants (Number)
Imatinib Mesylate13

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Peak Concentration (Cmax)

Peak concentration (cmax) is a pharmacokinetic measure defined as the highest concentration of a drug measured after the drug is administered. The cmax of imatinib mesylate on day 1 of course 1 is reported. Two milliliter (0.5 ml for children under the age of 5) blood samples were collected immediately prior to imatinib mesylate administration on Day 1 of Course 1 and at the following timepoints following drug administration: 0.5, 1, 1.5, 2, 4, 10 and 12 hours after the morning dose. (NCT00021229)
Timeframe: Day 1 of Course 1

Interventionµg/ml (Mean)
Stratum I: Radiation + Imatinib Mesylate1.3
Stratum IIA: Imatinib Mesylate2.6
Stratum IIB: Imatinib Mesylate1.3

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Pre-treatment Basic Fibroblast Growth Factor Values From Plasma

This study attempted to investigate in an exploratory manner the effect of biological markers on tumor growth. Basic fibroblast growth factor (bFGF) may play a role in tumor development by helping tumor vessels establish and grow. Blood (plasma) was drawn from participants before treatment to measure the baseline plasma bFGF values. (NCT00021229)
Timeframe: Pre-treatment

Interventionpg/ml (Mean)
Stratum I: Radiation + Imatinib Mesylate8.69
Stratum IIA: Imatinib Mesylate32.3
Stratum IIB: Imatinib Mesylate11.3

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Pre-treatment Basic Fibroblast Growth Factor Values From Urine

This study attempted to investigate in an exploratory manner the effect of biological markers on tumor growth. Basic fibroblast growth factor (bFGF) may play a role in tumor development by helping tumor vessels establish and grow. Urine was collected from participants before treatment to measure the baseline urine bFGF values. (NCT00021229)
Timeframe: Pre-treatment

Interventionpg/ml (Mean)
Stratum I: Radiation + Imatinib Mesylate5665
Stratum IIA: Imatinib Mesylate10322
Stratum IIB: Imatinib Mesylate5312

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Pre-treatment Vascular Endothelial Growth Factor From Urine

This study attempted to investigate in an exploratory manner the effect of biological markers on tumor growth. Vascular endothelial growth factor (VEGF) may play a role in tumor development by helping tumor vessels establish and grow. Urine was collected from participants before treatment to measure the baseline urine VEGF values. (NCT00021229)
Timeframe: Pre-treatment

Interventionpg/ml (Mean)
Stratum I: Radiation + Imatinib Mesylate79
Stratum IIA: Imatinib Mesylate86.1
Stratum IIB: Imatinib Mesylate45.3

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Pre-treatment Vascular Endothelial Growth Factor Values From Plasma

This study attempted to investigate in an exploratory manner the effect of biological markers on tumor growth. Vascular endothelial growth factor (VEGF) may play a role in tumor development by helping tumor vessels establish and grow. Blood (plasma) was drawn from participants before treatment to measure the baseline plasma VEGF values. (NCT00021229)
Timeframe: Pre-treatment

Interventionpg/ml (Mean)
Stratum I: Radiation + Imatinib Mesylate119.9
Stratum IIA: Imatinib Mesylate155.2
Stratum IIB: Imatinib Mesylate78.2

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Change From Baseline in Volume FLAIR at Two Weeks After Completion of Radiation

This study attempted to investigate in an exploratory manner the effect of radiation (RT) on changes in various neuroimaging variables in pediatric brainstem gliomas (stratum I). Neuroimaging changes may have some association with outcome (response, survival, etc.). Volume FLAIR is one parameter obtained from standard magnetic resonance imaging (MRI) studies of the brain. Volume FLAIR was obtained at baseline (pre-radiation) and within two (+/- one) weeks after completion of RT. (NCT00021229)
Timeframe: Baseline and two weeks post completion of radiation

Interventioncubic centimeters (Mean)
Stratum I: Radiation + Imatinib Mesylate7.62

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Median Overall Survival

Overall Survival (OS) is defined as the interval from initiation of treatment to death or date of last contact for surviving patients. (NCT00021229)
Timeframe: Assessed before radiation therapy, before the first dose of imatinib, then every 8 weeks.

InterventionDays (Median)
Stratum I: Radiation + Imatinib Mesylate324.5

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Number of Participants in Phase I Stratum I With Dose Limiting Toxicities (DLT) Observed During First 8 Weeks (Courses 1 and 2) of Imatinib Therapy

The dose limiting toxicity (DLT) analysis population consists of phase I stratum I participants who developed DLT during the maximum tolerated dose (MTD) estimation period (course 1 and 2) or who completed the MTD estimation period (courses 1 and 2) without DLTs. DLTs observed during courses 1 and 2 were used to estimate the MTD. The estimated MTD based on the 23 participants who either had a DLT during course 1 or 2 or completed courses 1 and 2 without DLT is 265 mg/m2/day. (NCT00021229)
Timeframe: Day 1 of Imatinib Mesylate Therapy to Week 8

InterventionParticipants (Number)
Stratum I: Radiation + Imatinib Mesylate5

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Number of Participants in Phase I Stratum II With Dose Limiting Toxicities (DLT) Observed During First 8 Weeks (Courses 1 and 2) of Imatinib Therapy

The dose limiting toxicity (DLT) analysis population consisted of phase I stratum II participants who developed DLT during the maximum tolerated dose (MTD) estimation period (courses 1 and 2) or who completed the MTD estimation period (courses 1 and 2) without DLTs. DLTs observed during courses 1 and 2 were used to estimate the MTD. The estimated MTD based on the DLT analysis population of 20 in stratum IIA was 465 mg/m2/day. An MTD was not established in stratum IIB as no DLTs were observed at the higher dose levels of 620 and 800 mg/m2/day. (NCT00021229)
Timeframe: Day 1 of Imatinib Mesylate Therapy to Week 8

InterventionParticipants (Number)
Stratum IIA: Imatinib Mesylate2
Stratum IIB: Imatinib Mesylate0

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The Rate of Major Cytogenetic Response at 6 Months

Cytogenetic response is defined in terms of the percentage of Philadelphia (Ph) chromosome. Major cytogenetic response is defined as 0-34% Ph-positive cells. (NCT00022490)
Timeframe: 6 months

InterventionParticipants (Number)
Cytarabine/ Imatinib Mesylate5

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Percentage of Patients With Major Toxicity (Toxicity Grade ≥ 3)

Highest grade toxicity per subject was counted. Toxicities were graded using Common Toxicity Criteria (CTC) v 2.0. Grade refers to the severity of the toxicity, using Grades 1 through 5 with unique clinical descriptions of severity for a given toxicity based on this general guideline: Grade 1 Mild, Grade 2 Moderate, Grade 3 Severe, Grade 4 Life-threatening or disabling, Grade 5 Death related to toxicity. (NCT00028002)
Timeframe: Analysis occurs after all patients have been on study for at least 2 years. Measured from start of treatment to end of follow-up, to a maximum of 4.95 years.

Interventionpercentage of participants (Number)
Pre-surgeryPost-surgery
Imatinib Mesylate34.648.9

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FDG-PET as Biological Marker of Metabolic Response(MR) During Imatinib Mesylate (IM) Treatment, in Patients With GIST Who Are naı¨ve to Tyrosine Kinase Inhibitor Therapy

"evaluate FDG-PET as a non-invasive functional imaging tool to assess in situ tumor metabolism (as measured by the Standardized Uptake Values of FDG in the tumor) prior to and during the administration of IM. %change in SUVmax <1 indicate decreased tumor metabolism while values >1 indicated an increase in tumor metabolism.~Metabolic response by 18F-FDG PET was determined in accordance with the criteria of the European Organization for Research and Treatment of Cancer EORTC), with increases or decreases of more than 25% in SUVmax defining progressive metabolic disease (PMD) and partial metabolic response (PMR), respectively, and new lesions defining PMD." (NCT00028002)
Timeframe: change from baseline to 1 week post therapy

Interventionpercentage change in SUVmax (Mean)
PET Patricipants-59.4

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Rate of Disease Progression at 2 Years

Kaplan-Meier estimate of disease progression rate. Disease progression is determined by Response Evaluation Criteria in Solid Tumours criteria (RECIST). RECIST criteria is described here: http://ctep.cancer.gov/protocolDevelopment/docs/recist_guideline.pdf (NCT00028002)
Timeframe: From registration to two years

Interventionpercentage of participants (Number)
Imatinib Mesylate13.8

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Rates of Objective Response (Complete, Partial, and Stable)

The percentage of patients who achieved a complete, partial or stable response prior to surgery as assessed by Response Evaluation Criteria in Solid Tumours criteria (RECIST). RECIST criteria is described here: http://ctep.cancer.gov/protocolDevelopment/docs/recist_guideline.pdf. (NCT00028002)
Timeframe: Pretreatment and prior to surgery (at 4-10 weeks, based on surgery timing)

Interventionpercentage of participants (Number)
Complete ResponsePartial ResponseStable Disease
Imatinib Mesylate05.886.5

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Relapse Free Survival

Number of patients with relapsed disease within 1 Year post-transplant. Relapse is defined as the detection of > 5% blasts after a documented complete remission. (NCT00036738)
Timeframe: Assessed up to 1 year

InterventionParticipants (Count of Participants)
Treatment (Allogeneic Nonmyeloablative HSCT)3

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Overall Survival

Number of patients surviving up to five years post-transplant. (NCT00036738)
Timeframe: Assessed up to 5 years

InterventionParticipants (Count of Participants)
6 Months1 Year2 Years3 Years4 Years5 Years
Treatment (Allogeneic Nonmyeloablative HSCT)262419171613

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Leukemia-free Survival

Number of patients surviving in CR up to five years post-transplant. (NCT00036738)
Timeframe: Assessed up to 5 years

InterventionParticipants (Count of Participants)
6 Months1 Year2 Years3 Years4 Years5 Years
Treatment (Allogeneic Nonmyeloablative HSCT)191713111110

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Response To Induction Therapy With Hyper-CVAD Plus Imatinib Mesylate

"Complete Remission (CR): Defined as the presence of 5% or less blasts in the bone marrow, with a granulocyte count of 1.0 × 109/L or higher and a platelet count of 100 × 109/L and no extramedullary disease.~Partial Response (PR): As above for CR except for the presence of 6-25% marrow blasts.~Molecular CR: Same as for CR with RT-PCR negativity for bcr-abl.~Induction Death: Defined as death occurring after start of therapy without meeting the definition of CR or resistant disease." (NCT00038610)
Timeframe: Baseline to 6 months

Interventionparticipants (Number)
Complete RemissionPartial RemissionMolecular Complete RemissionInduction Death
Hyper-CVAD + Imatinib421171

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Disease-Free Survival Rate at 2-year and 5-year.

Disease-Free Survival (DFS) was calculated from the time of complete remission until relapse or death due to any cause. (NCT00038610)
Timeframe: Baseline to 2-year and 5-year

Interventionpercentage of participants (Number)
2-year DFS rate5-year DFS rate
Hyper-CVAD + Imatinib4943

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Overall Survival Rate at 2-year and 5-year.

Overall survival (OS) was calculated from the date of initiation of therapy until death. (NCT00038610)
Timeframe: Baseline to 2-year and 5-year

Interventionpercentage of participants (Number)
2-year OS rate5-year OS rate
Hyper-CVAD + Imatinib5743

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Participant Complete Hematologic Remission (CHR) Classified

Number of participants with Complete Hematologic Remission (CHR): normalization >4 weeks of bone marrow (<5% blasts), peripheral blood with WBC <10 x 109/L & no peripheral blasts, promyelocytes or myelocytes; disappearance all signs/symptoms disease. CHR further classified according to suppression of Philadelphia chromosome (Ph) by cytogenetics or i Fluorescence In Situ Hybridization (FISH): No cytogenetic response - Ph positive 100% of pretreatment value; Minor cytogenetic response - Ph positive 35-90% of pretreatment value; Partial cytogenetic response - Ph positive 1-34% of pretreatment value; Complete cytogenetic response - Ph positive 0%. Hematologic surveys twice per year with bone aspirations at discretion of treating physician. (NCT00038649)
Timeframe: Response to imatinib mesylate evaluated after completing 3 - 12 months of therapy.

Interventionparticipants (Number)
No cytogenetic responseMinor cytogenetic responsePartial cytogenetic responseComplete cytogenetic response
Gleevec014105

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Number of Participants With Molecular Response of Complete or Partial Hematologic Remission

Complete Hematologic Remission (CHR): normalization >4 weeks of bone marrow (<5% blasts), peripheral blood with White Blood Cells (WBC) <10 x 109/L & no peripheral blasts, promyelocytes or myelocytes; disappearance all signs/symptoms disease. Partial Hematologic Response (PHR) = CHR except persistence of immature cells (myelocytes, metamyelocytes), or splenomegaly < 50% of pretreatment, or thrombocytosis >450x109/L but <50% of pretreatment. Hematologic surveys twice per year with bone aspirations at discretion of treating physician. (NCT00038649)
Timeframe: Response to imatinib mesylate evaluated after completing 3 - 12 months of therapy.

Interventionparticipants (Number)
CHRPHR
Gleevec1100

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Duration of Response

Time from response to disease progression, measuring length of the response in those participants who responded. (NCT00038675)
Timeframe: From response evaluation (first evaluation following 2 months therapy) to disease progression or death or until disease progression whichever occurs first, up to 12 years and 5 months

InterventionMonths (Median)
Imatinib Mesylate68

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Number of Participants With a Complete Response (CR)

Acute myeloid leukemia (AML), Myelodysplastic Syndromes (MDS): CR=Normalization peripheral blood & bone marrow with 5% or less blasts; normo- or hypercellular marrow; Absolute Neutrophil Count (ANC) > 1.0 x 10^9/L, & platelet count >100 x 10^9/L; or CR marrow=As per CR but platelet count < 100 x 10^9/L. Agnogenic myeloid metaplasia (AMM) & CMML: CR=Absence of signs/symptoms of disease; White blood count between 1 to 10 x 10^9/L with no peripheral blasts, promyelocytes, or myelocytes and normalization of bone marrow (< 5% blasts in normocellular or hypercellular marrow) for 4+ weeks. PV: CR=normalization of hemoglobin/hematocrit without need for phlebotomies, disappearance all signs/symptoms of disease. HES: CR=disappearance of eosinophilia (NCT00038675)
Timeframe: after 2 months of therapy, up to 1 year.

Interventionparticipants (Number)
Acute LeukemiaChronic myeloproliferative disorders (CMPD)Chronic Myelomonocytic Leukemia (CMML)Essential ThrombocythemiaHypereosinophilic syndrome (HES)Systemic mastocytosis (SM)Myelodysplastic syndromes (MDS)MyelofibrosisPolycythemia Vera (PV)
Imatinib Mesylate002034012

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Overall Survival

Overall survival defined as time from registration to disease progression or death from any cause. (NCT00038675)
Timeframe: From the start of therapy to death or disease progression, assessed up to 12 years and 5 months

InterventionMonths (Median)
Imatinib Mesylate73.2

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5 Year Disease-free Survival for Autologous & Allogeneic Transplant Groups

Percentage of patients who achieved a complete remission (CR) and were alive and relapse free at 5 years. The 5-year progression free survival was estimated using the Kaplan Meier method. (NCT00039377)
Timeframe: 5 years from CR

Interventionpercentage of patients (Number)
Patients With HLA-matched Sibling Donor46
Patients Without HLA-matched Sibling Donors47

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5 Year Overall Survival for Autologous & Allogeneic Transplant Groups

Percentage of patients who were alive at 5 years. The 5-year progression free survival was estimated using the Kaplan Meier method. (NCT00039377)
Timeframe: 5 years from registration

Interventionpercentage of patients (Number)
Patients With HLA-matched Sibling Donor53
Patients Without HLA-matched Sibling Donors51

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Disease Free Survival

"Disease-free survival (DFS) was measured as the interval from achievement of complete remission (CR) until relapse or death, regardless of cause; patients alive and in CR were censored at last follow-up. DFS was estimated using the Kaplan Meier method.~A complete remission (CR) was defined as recovery of morphologically normal bone marrow and blood counts (i.e., neutrophils >= 1.5 x 10^9/L and platelets > 100 x 10^9/L) and no circulating leukemic blasts or evidence of extramedullary leukemia and persisting for at least one month." (NCT00039377)
Timeframe: Duration of treatment (up to 10 years)

Interventionyears (Median)
Entire Cohort1.7

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Overall Survival

Overall survival (OS) as the interval from the on-study date until death. OS was estimated using the Kaplan Meier method. (NCT00039377)
Timeframe: Duration of study (up to 10 years)

Interventionyears (Median)
Entire Cohort3.6

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Number of Participants Who Achieved a BCR-ABL Response at 12 Months

"BCR-ABL response is defined in two ways: complete molecular response (CMR) and major molecular response (MMR).~Complete Molecular Response is defined as a Bcr-Abl (a fusion of gene of Bcr and ABl genes) ratio ≤0.0032% on the International Scale Bcr = breakpoint cluster gene Abl = abelson proto-oncogene~MMR is defined as Bcr-Abl (A fusion gene of the breakpoint cluster region [Bcr] gene and Abelson proto-oncogene [Abl] genes) transcript ratio ≤0.1% (≥ 3 log reduction of BCR-ABL transcripts from a standardized baseline), as detected by reverse transcriptase polymerase chain reaction [RT-PCR] (performed centrally)." (NCT00039377)
Timeframe: 12 months

Interventionparticipants (Number)
Complete Molecular ResponseMajor Molecular Response
Entire Cohort94

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Concentration (Steady State) of Imatinib During Cycle One (Pharmacokinetics)

"Blood collected before and at 1,2,4 ad 24 hours after ingestion of imatinib on day 8 of cycle 1~result is the measurement of the before dosing on day 8 (trough level) and the 24 hour dosing day 8" (NCT00045734)
Timeframe: pre dosing on day 8 and 24 hour dosing day 8 of Pre-dosing Day 9

Interventionng/ml (Mean)
Day 8 Pre DosingDay 8 24 hour dosing
Treatment (Imatinib Mesylate)21292248

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Tumor Response as Assessed by MRI Using Macdonald Criteria

"The Macdonald criteria, roughly similarly to other systems, divides response into 4 types of response based on imaging (MRI) and clinical features~1: complete response; 2: partial response; 3:stable disease; 4:progression~Complete response imaging features: disappearance of all enhancing disease (measurable and non-measurable) sustained for at least 4 weeks; no new lesions clinical features; no corticosteroids; clinically stable or improved~Partial response imaging features: 50% or more decrease of all measurable enhancing lesions sustained for at least 4 weeks: no new lesions clinical features: stable or reduced corticosteroids; clinically stable or improved~Stable disease imaging features: does not qualify for complete response, partial response or progression clinical features: clinically stable~Progression imaging features: 25% of more increase in enhancing lesions; any new lesions clinical features: clinical deterioration" (NCT00045734)
Timeframe: Up to 5 years

Interventionparticipants (Number)
ProgressionStable
Treatment (Imatinib Mesylate)109

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Toxicity as Assessed by the Cancer Therapy Evaluation Program Common Toxicity Criteria (CTC) Version 2.0

percentage of patients who had grade 3 or grade 4 adverse events (NCT00045734)
Timeframe: Up to 5 years after completion of study treatment

Interventionpercentage of patients (Number)
Treatment (Imatinib Mesylate)2.3

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Progression-free Survival According to Response Evaluation Using Macdonald Criteria

"The Macdonald criteria, roughly similarly to other systems, divides response into 4 types of response based on imaging (MRI) and clinical features~1: complete response; 2: partial response; 3:stable disease; 4:progression~Complete response imaging features: disappearance of all enhancing disease (measurable and non-measurable) sustained for at least 4 weeks; no new lesions clinical features; no corticosteroids; clinically stable or improved~Partial response imaging features: 50% or more decrease of all measurable enhancing lesions sustained for at least 4 weeks: no new lesions clinical features: stable or reduced corticosteroids; clinically stable or improved~Stable disease imaging features: does not qualify for complete response, partial response or progression clinical features: clinically stable~Progression imaging features: 25% of more increase in enhancing lesions; any new lesions clinical features: clinical deterioration" (NCT00045734)
Timeframe: 3 years

Interventionmonths (Median)
Treatment (Imatinib Mesylate)2

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Determine Survival for Patients Treated With Imatinib Mesylate

survival determined from start of treatment to date of death (NCT00045734)
Timeframe: 3 years

Interventionmonths (Median)
Treatment (Imatinib Mesylate)16.8

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6 Months - Progression-free Survival According to Response Evaluation Using Macdonald Criteria

"The Macdonald criteria, roughly similarly to other systems, divides response into 4 types of response based on imaging (magnetic resonance imaging [MRI]) and clinical features~1: complete response; 2: partial response; 3:stable disease; 4:progression~Complete response imaging features: disappearance of all enhancing disease (measurable and non-measurable) sustained for at least 4 weeks; no new lesions clinical features; no corticosteroids; clinically stable or improved~Partial response imaging features: 50% or more decrease of all measurable enhancing lesions sustained for at least 4 weeks: no new lesions clinical features: stable or reduced corticosteroids; clinically stable or improved~Stable disease imaging features: does not qualify for complete response, partial response or progression clinical features: clinically stable~Progression imaging features: 25% of more increase in enhancing lesions; any new lesions clinical features: clinical deterioration" (NCT00045734)
Timeframe: At 6 months

Interventionpercentage of participants (Number)
Treatment (Imatinib Mesylate)29.4

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Percentage of Patients Progression-free

"The percentage of patient progression-free at 12 months, 18 months, and PFS will be estimated. Kaplan-Meier survival curves and logrank tests will be used to estimate progression-time distributions.~Progression is defined using response criteria (the neurologic examination and the MRI and/or CT), >25% increase in product of perpendicular diameters of contrast enhancement or mass or appearance of new lesions." (NCT00049127)
Timeframe: Time from study registration to date of disease progression or last follow-up, assessed up to 5 years

Interventionmonths (Mean)
Study 1 Arm C1.9
Study 2 Arm B4.0
Study 3 Arm E4.5

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Confirmed Response (i.e., an Objective Status of Complete Response (CR), Partial Response (PR), or Regression (REGR) on 2 Successive Evaluations at Least 4 Weeks Apart After the Start of Study Treatment).

"Complete Response (CR) is defined using response criteria (the neurologic examination and the Magnetic resonance imaging (MRI) and/or Computerized Tomography (CT)), total disappearance of all tumor with patient off corticosteroids or only on adrenal replacement maintenance.~Partial Response (PR) is defined using response criteria (the neurologic examination and the MRI and/or CT), >=50% reduction in product of perpendicular diameters of contrast enhancement or mass with no new lesions with the patient being on stable or decreased steroid dose.~Regression (REGR) is defined using response criteria (the neurologic examination and the MRI and/or CT), unequivocal reduction in size of contrast-enhancement or decrease in mass effect as agreed upon independently by primary physician and quality control physicians; no new lesions. Patient should be on stable or decreased steroid dose." (NCT00049127)
Timeframe: Up to 5 years

Interventionpercentage of confirmed responses (Number)
Study 1 Arm C0
Study 2 Arm B5.1
Study 3 Arm E0

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6-month Progression-free Survival (PFS), Defined as a Patient Being Alive and Progression-free 183 Days After the Date of Registration.

"The proportion of successes will be estimated using the Binomial point estimator (number of successes divided by the total number of evaluable patients) and the Binomial 90% confidence interval estimated using the Duffy-Santer algorithm.~Progression is defined using response criteria (the neurologic examination and the MRI and/or CT), >25% increase in product of perpendicular diameters of contrast enhancement or mass or appearance of new lesions." (NCT00049127)
Timeframe: 6 months

Interventionpercentage of patients (Number)
Study 1 Arm C33.35
Study 2 Arm B33.3
Study 3 Arm E25

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Overall Time to Death

Kaplan-Meier survival curves and logrank tests will be used to estimate survival distributions. (NCT00049127)
Timeframe: Time from date of registration to date of death due to any cause or last follow-up, assessed up to 5 years

Interventionmonths (Median)
Study 1 Arm C14.2
Study 2 Arm B16.6
Study 3 Arm E13.6

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Maximum Tolerated Dose (MTD) of Alemtuzumab (Phase I)

The maximum tolerated dose is defined as the highest alemtuzumab dose at which less than 40% of patients develop the dose limiting toxicity (DLT), where DLT is defined as the inability to proceed (due to medical complications) with the protocol treatment within six weeks of receiving the last dose of alemtuzumab. Groups of six patients will be enrolled into each cohort at the time of re-registration prior to starting Course IV. After a cohort has accrued 6 patients and at least 3 have completed the 2-6 week post alemtuzumab observation period without DLT, the incoming patients will be assigned to the next cohort in the table while the DLT and other toxicities continue to be assessed for the newly closed cohort. If less than 3 out of 6 enrolled patients in a cohort have completed the 2-6 week post alemtuzumab observation period without DLT, additional patients may continue to enroll in that same cohort, i.e., accrual will not be suspended while waiting for patient follow-up data. (NCT00061945)
Timeframe: 6 weeks

Interventionmg (Number)
Phase I - Alemtuzumab and Combination Chemotherapy30

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Minimal Residual Disease (MRD) During Treatment With Alemtuzumab (Phase II)

Minimal Residual Disease measures the presence of of circulating leukemia cells in the body. Patients that report a Complete Response (CR) during treatment are further tested to determine the presence of small amounts of circulating leukemia cells. Here we report the number of patients who were MRD negative. (NCT00061945)
Timeframe: 9 years 4 months

InterventionParticipants (Count of Participants)
Phase II - Alemtuzumab and Combination Chemotherapy16

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Disease-free Survival, for Only Complete Response Patients

Disease Free Survival (DFS) is defined as the time from a Complete Response (CR) until death or relapse. The date of last clinical assesment will be used as the censor date for patients with no death or relapse. The DFS will be estimated using the Kaplan-Meier method with confidence intervals presented. (NCT00061945)
Timeframe: 9 years 4 months

Interventionmonths (Median)
Phase I - Alemtuzumab and Combination Chemotherapy58.6
Phase II - Alemtuzumab and Combination Chemotherapy19.8

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Overall Survival

Overall Survival is defines as the time from registration to death due to any cause. It is estimated using the Kaplan-Meier method with confidence intervals presented. (NCT00061945)
Timeframe: 9 years 4 months

Interventionmonths (Median)
Phase I - Alemtuzumab and Combination Chemotherapy33.6
Phase II - Alemtuzumab and Combination Chemotherapy23.1

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Number of Participants Who Proceed to Course V Within 2-6 Weeks of the Last Dose of Alemtuzumab (Phase II)

The primary endpoint is the number of participants who are able to proceed to course V within two - six weeks of completion of course IV. (NCT00061945)
Timeframe: 8 months

Interventionparticipants (Number)
Phase II - Alemtuzumab and Combination Chemotherapy30

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Number of Participants Achieving Complete Remission

A complete remission (CR) requires the following: an absolute neutrophil count (segs and bands) > 1500/μl, no circulating blasts, platelets > 100,000/μl; bone marrow cellularity > 20% with trilineage hematopoiesis, and < 5% marrow blast cells, none of which appear neoplastic. All previous extramedullary manifestations of disease must be absent (e.g., lymphadenopathy, splenomegaly, skin or gum infiltration, testicular masses, or CNS involvement). (NCT00061945)
Timeframe: 9 years

Interventionparticipants (Number)
Phase I - Alemtuzumab and Combination Chemotherapy92
Phase II - Alemtuzumab and Combination Chemotherapy145

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Toxicity Summary

Toxicity assessed by Common Terminology Criteria for Adverse Events (CTCAE) version 2.0. Grade 3 and above adverse events possibly, probably or definitely related to treatment. (NCT00068380)
Timeframe: Up to 30 days post treatment

InterventionParticipants (Count of Participants)
Grade 3 : Alkaline phosphatase increasedGrade 3 : AnorexiaGrade 3 : ConstipationGrade 3 : FatigueGrade 3 : HyperglycemiaGrade 3 : Hemoglobin decreasedGrade 3 : HypoxiaGrade 3 : Abdominal painGrade 3 : HypophosphatemiaGrade 3 : HypokalemiaGrade 3 : HyponatremiaGrade 3 : Packed red blood cell transfusion
Treatment (Imatinib Mesylate)111111112113

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Time to Treatment Failure

Defined as the time from start of treatment to the discontinuation of treatment for any reason, including disease progression, treatment toxicity, patient preference, or death Will be summarized using the Kaplan-Meier product-limit estimators. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00068380)
Timeframe: From first day of treatment until discontinuation of treatment, assessed up to 30 days post treatment

InterventionMonths (Median)
Treatment (Imatinib Mesylate)0.98

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Response Rate

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by X-Ray, MRI or CT: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00068380)
Timeframe: Up to 6 years

Interventionpercentage of patients responding (Number)
Treatment (Imatinib Mesylate)0

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Overall Survival

Will be summarized using the Kaplan-Meier product-limit estimators. (NCT00068380)
Timeframe: From first day of treatment to time of death due to any cause, assessed up to 5 years post-treatment

InterventionMonths (Median)
Treatment (Imatinib Mesylate)3.25

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Progression-free Survival

Estimated using the product-limit method of Kaplan and Meier. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions. (NCT00068380)
Timeframe: From first day of treatment to the first observation of disease progression or death due to any cause, assessed up to 30 days post treatment

InterventionMonths (Median)
Treatment (Imatinib Mesylate)1.35

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Toxicity

Number of patients with Grade 3-5 adverse events that are related to study drug by given type of adverse event (NCT00070499)
Timeframe: Patients were assessed for adverse events monthly every 4 weeks for the first year, every 6 months for years 2 and 3, and annually for years 4 and 5.

,,,
InterventionParticipants with a given type of AE (Number)
ALT, SGPT (serum glutamic pyruvic transaminase)AST, SGOT (serum glutamic oxaloacetic trans.)Bilirubin (hyperbilirubinemia)Bronchospasm, wheezingCNS cerebrovascular ischemiaCPK (creatine phosphokinase)Cardiac-ischemia/infarctionColitisConduction abnor/Atrioventricular heart blockConstipationDehydrationDiarrheaDistention/bloating, abdominalDizzinessDyspnea (shortness of breath)Edema: head and neckEdema: limbEdema: trunk/genitalEdema: visceraFatigue (asthenia, lethargy, malaise)Febrile neutropeniaGGT (gamma-glutamyl transpeptidase)Glucose, serum-high (hyperglycemia)HematomaHemoglobinHepatobiliary/Pancreas-Other (Specify)Hot flashes/flushesHypertensionHypoxiaInfection with Grade 3 or 4 neutrophils - BloodInfection with Grade 3/4 neut - Lung (pneumonInfec with norm ANC or Grade 1 or 2 neut - ColonInf with no ANC or Grade 1/2 netLung (pneumonia)Infec with norm ANC or Grade 1 or 2 neut - ScrotumInfect with norm ANC or Grade 1 or 2 neut - SinusInf with no ANC or Grade 1/2 neut - Ur tract NOSInfection with unknown ANC - SinusLeft ventricular diastolic dysfunctionLeukocytes (total WBC)LymphopeniaMetabolic/Laboratory-Other (Specify)Mood alteration - depressionMucositis/stomatitis (clinical exam) - Oral cavityMuscle weak, not due to neurop. Whole body/generalNauseaNeuropathy: motorNeuropathy: sensoryNeutrophils/granulocytes (ANC/AGC)Pain - Abdomen NOSPain - BackPain - BonePain - Chest/thorax NOSPain - Extremity-limbPain - Head/headachePain - JointPain - MusclePain-Other (Specify)Pericardial effusion (non-malignant)Phosphate, serum-low (hypophosphatemia)PlateletsPleural effusion (non-malignant)Potassium, serum-high (hyperkalemia)Potassium, serum-low (hypokalemia)Prolonged QTc intervalProteinuriaPruritus/itchingPulmonary/Upper Respiratory-Other (Specify)Rash/desquamationRash: acne/acneiformRestrictive cardiomyopathyRetinal detachmentSodium, serum-high (hypernatremia)Syncope (fainting)Vaginal mucositisVision-blurred visionVomitingWatery eye (epiphora, tearing)Weight gain
Dasatinib110011231116007010013031120110120211011331000011183021031003122411110101001111113
High Dose Imatinib310000000006102021011110081001001100000210001200124131111300014000001040100001001
Standard Dose Imatinib A111003000001010200101000500000000001001101002008101001010006000000010000001100
Standard Dose Imatinib B32010000000201221001000050000000000000310020100151101032110111102002020010000000

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Two Year Relapse-free Survival

Relapse-free survival is measured from the date of documented (possibly unconfirmed) hematologic complete remission until loss of hematologic complete remission or death from any cause. Observations are censored at the date of last contact for patients last known to be alive with report of loss of hematologic complete remission. (NCT00070499)
Timeframe: every 3 months for the first year, every six months for years 2 and 3, annually for years 4 and 5

InterventionPercent of population (Number)
Standard Dose Imatinib A83
High Dose Imatinib97
Dasatinib96
Standard Dose Imatinib B95

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Hematologic Response

Hematologic response assesses whether patients' blood counts return to normal (NCT00070499)
Timeframe: 1 month after starting treatment

Interventionparticipants (Number)
Standard Dose Imatinib A63
High Dose Imatinib66
Dasatinib107
Standard Dose Imatinib B112

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2-year Overall Survival (OS)

Overall survival was measured from the date of registration to study until death from any cause with observations censored at the date of last contact for patients last known to be alive. (NCT00070499)
Timeframe: Every three months for the first year, every six months in years 2 and 3, and annually for years 4 and 5

InterventionPercent of population (Number)
Standard Dose Imatinib A89
High Dose Imatinib95
Dasatinib97
Standard Dose Imatinib B98

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Molecular Response Rate at 12 Months

Median value of baseline bcr-abl/bcr ratio from pretreatment was used as the baseline value for assessing each patient's molecular response. Molecular response criteria were: 1) not failed treatment on or before 12-month evaluation; 2) met criteria for hemalotogic response; 3) bcr-abl/bcr ration at 12-months must be 10,000 times smaller than the pretreatment ratio. (NCT00070499)
Timeframe: pretreatment and after 12 months of treatment

Interventionparticipants (Number)
Standard Dose Imatinib A5
High Dose Imatinib14
Dasatinib27
Standard Dose Imatinib B18

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MTD, Defined as One Dose Level Below the Dose That Induced DLT in at Least One Third of Patients at a Dose Level, Graded According to NCI CTCAE Version 3.0 (Phase I)

(NCT00074308)
Timeframe: Up to 28 days

Interventiondose level (Number)
Phase 1 = Dose Escalation2

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Response Rate at 8 Weeks, Evaluated Using RECIST (Phase II)

"Response and progression was evaluated in this study using Response Evaluation Criteria in Solid Tumors (RECIST).~Complete Response (CR): Disappearance of all target lesions. Partial Response (PR): At least 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD." (NCT00074308)
Timeframe: 8 weeks

InterventionParticipants (Count of Participants)
Phase 2 = Dose Expansion1

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Progression-free Survival at 16 Weeks (Phase II)

Progression Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. (NCT00074308)
Timeframe: 16 weeks

InterventionParticipants (Count of Participants)
Phase 2 = Dose Expansion8

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Tumor Response

RECIST 1.0 defines complete response as the disappearance of all target lesions and non-target lesions and no evidence of new lesions documented by two disease assessments at least 4 weeks apart. Partial response is defined as at least a 30% decrease in the sum of longest dimensions (LD) of all target measurable lesions taking as reference the baseline sum of LD. There can be no unequivocal progression of non-target lesions and no new lesions. Documentation by two disease assessments at least 4 weeks apart is required. In the case where the ONLY target lesion is a solitary pelvic mass measured by physical exam, which is not radiographically measurable, a 50% decrease in the LD is required. These patients will have their response classified according to the definitions stated above. Complete and partial responses are included in the objective tumor response rate. (NCT00075400)
Timeframe: CT scan or MRI if used to follow lesion for measurable disease every other cycle for the first 6 months; up to 5 years

Interventionpercentage of participants (Number)
Gleevec0

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Progression-free Survival (PFS) > 6 Months

Progression is defined according to RECIST v1.0 as at least a 20% increase in the sum of LD target lesions taking as reference the smallest sum LD recorded since study entry, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, global deterioration in health status attributable to the disease requiring a change in therapy without objective evidence of progression, or unequivocal progression of existing non-target lesions. (NCT00075400)
Timeframe: For those patients whose disease can be evaluated by physical examination, progression was assessed prior to each 28-day cycle. CT scan or MRI if used to follow measurable disease every other cycle for the first 6 months.

Interventionpercentage of participants (Number)
Gleevec4.3

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Overall Survival

The observed length of life from entry into the study to death or the date of last contact (NCT00075400)
Timeframe: From study entry to death or last contact, up to 5 years.

Interventionmonths (Median)
Gleevec4.1

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Duration of Progression Free Survival

Progression is defined according to RECIST v1.0 as at least a 20% increase in the sum of LD target lesions taking as reference the smallest sum LD recorded since study entry, the appearance of one or more new lesions, death due to disease without prior objective documentation of progression, global deterioration in health status attributable to the disease requiring a change in therapy without objective evidence of progression, or unequivocal progression of existing non-target lesions. (NCT00075400)
Timeframe: CT scan or MRI if used to follow lesion for measurable disease every other cycle for the first 6 months; up to 5 years

Interventionmonths (Median)
Gleevec1.6099

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Incidence of Adverse Effects as Assessed by CTCAE v 3.0

The frequency and severity of all toxicities are tabulated from submitted case report forms and summarized for review. (NCT00075400)
Timeframe: Each cycle during treatment and 30 days after treatment ends.

,,,,
InterventionParticipants (Count of Participants)
LeukopeniaNeutropeniaAnemiaAllergyHearingCardiovascularConstitutionalDermatologicEndocrineGastrointestinalGenitourinaryHemorrhageLymphaticsMetabolicNeuropathyOther neurologicOcularPainPulmonarySexual
Grade 02121722222271921522221718212121192222
Grade 1 (CTCAE v 3.0)21700193150032201211
Grade 2 (CTCAE v 3.0)019110611120121020200
Grade 3 (CTCAE v 3.0)00000010011011001000
Grade 4 (CTCAE v 3.0)00000000000001000000

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Confirmed Response Rate (Complete and Partial)

Number of participants with confirmed complete or partial response. Confirmed response (complete and partial) per Response Evaluation Criteria in Solid Tumors (RECIST) Criteria (V1.0). Complete Response (CR) is complete disappearance of all measurable and non-measurable disease; no new lesions; no disease related symptoms; and normalization of markers and other abnormal lab values. Partial response (PR) applies only to patients with at least one measurable lesion. PR is greater than or equal to 30% decrease under baseline of the sum of longest diameter of all target measurable lesions; no unequivocal progression of non-measurable disease and no new lesions. Confirmed response is two or more objective statuses a minimum of four weeks apart documented before progression or symptomatic deterioration. (NCT00087152)
Timeframe: 12 weeks

Interventionparticipants (Number)
Imatinib Mesylate & Capecitabine2

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Progression-free Survival at 6 Months

Percentage of participants progression-free at 6 months. Progression-free survival (PFS) measured from date of registration to first observation of progressive disease (per RECIST criteria (V1.0)), death due to any cause, or symptomatic deterioration. Kaplan-Meier was used to estimate progression-free survival (PFS) at six months. (NCT00087152)
Timeframe: Six months

Interventionpercentage of participants (Number)
Imatinib Mesylate & Capecitabine16

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Proportion of Patients Who Achieve a Clinical Response

Clinical response = Complete Response (absence of residual disease) or Partial Response defined as no new lesions (skin or oral), or no new visceral sites of involvement (or the appearance or worsening of tumor-associated edema or effusions); AND 50% or greater decrease in the number of lesions lasting for >4 weeks; OR Complete flattening of at least 50% of all previously raised lesions OR A 50% decrease in the sum of the products of the largest perpendicular diameters of the marker lesions (NCT00090987)
Timeframe: 20-24 weeks

Interventionproportion (Number)
Imatinib Mesylate (Gleevec)0.33

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Cytogenetic Response After Crossover

Cytogenetic response was based on the prevalence of Ph+ metaphases among cells in metaphase on a bone marrow sample (aspirate/biopsy). MCyR was defined as Complete CyR (0% Ph+ cells in metaphase in bone marrow) or Partial CyR (>0% to 35% Ph+ cells in metaphase in bone marrow). (NCT00103844)
Timeframe: every 12 week period out to 2 years and off-study timepoints; restricted to postcrossover measurements

,
InterventionParticipants (Number)
Major Cytogenetic Response (MCyR)Complete Cytogenetic Response (CCyR)Partial Cytogenetic Response (PCyR)
Dasatinib19154
Imatinib303

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Adverse Events (AEs), Serious Adverse Events (SAEs), Deaths and Hematologic Toxicities Prior to Crossover

AE=any new untoward medical occurrence or worsening of a pre-existing medical condition regardless of causal relationship with treatment. SAE=any untoward medical occurrence at any dose that: results in death; is life-threatening; requires or prolongs inpatient hospitalization; results in persistent or significant disability; is cancer; is congenital anomaly/birth defect; results in drug dependency/abuse; is an important medical event. Graded by National Cancer Institute Common Terminology Criteria for Adverse Events v3.0. (1=Mild, 2=Moderate, 3=Severe, 4=Life-threatening/disabling, 5=Death) (NCT00103844)
Timeframe: Continuously from baseline through 2 years

,
InterventionParticipants (Number)
Any Adverse Event (AE)Grade 3-4 AEsDrug-related AEsDrug-related Grade 3-4 AEsDeath within 30 days of last doseDrug-related Serious AEsAEs leading to discontinuationFluid Retention AEs - OverallFluid Retention AEs - Superficial EdemaFluid Retention AEs - Pleural EffusionFluid Retention AEs - OtherGrade 3-4 Hematologic Toxicity - AnemiaGrade 3-4 Hematologic Toxicity - ThrombocytopeniaGrade 3-4 Hematologic Toxicity - NeutropeniaGrade 3-4 Hematologic Toxicity - Leukopenia
Dasatinib10067946212823392025920586424
Imatinib45214419031021210047198

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Time to MCyR Prior to Crossover

Median time from first dosing date to date of MCyR (NCT00103844)
Timeframe: Baseline (within 4 weeks of Day 1), every 12 weeks, at crossover or off-study timepoints; restricted to precrossover measurements.

Interventionmonths (Median)
Dasatinib2.8
Imatinib2.8

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Time to CHR Prior to Crossover

Median time from first dosing date to date of CHR. CHR=all of the following criteria: white blood cell count ≤ institutional upper limit of normal; platelets < 450,000/mm³; no blasts or promyelocytes in peripheral blood; < 5% myelocytes plus metamyelocytes in peripheral blood; peripheral blood basophils ≤ 20%; no extramedullary involvement. Confirmed CHR is defined as CHR maintained at least 4 weeks after first documented at ≥ Day 14. Failure to maintain criteria of CHR was defined by 2 or more consecutive records of non-response. (NCT00103844)
Timeframe: Baseline (within 4 weeks of Day 1), weekly until Week 12, then every 12 weeks until crossover or off-study; restricted to precrossover measurements.

Interventionweeks (Median)
Dasatinib2.1
Imatinib2.1

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Number of Participants With Major Cytogenetic Response (MCyR) at Week 12

Cytogenetic response was based on the prevalence of Philadelphia chromosome positive (Ph+) metaphases among cells in metaphase on a bone marrow sample (aspirate/biopsy). MCyR was defined as Complete CyR (CCyR; 0% Ph+ cells in metaphase in bone marrow) or Partial CyR (PCyR; >0% to 35% Ph+ cells in metaphase in bone marrow). (NCT00103844)
Timeframe: Week 12

InterventionParticipants (Number)
Dasatinib36
Imatinib14

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Major Molecular Response (MMR)

Number of participants Achieving MMR. MMR is defined as ≤3 log reduction (ie, international ratio ≤0.1), in BCR-ABL levels from the standardized baseline value of BCR-ABL: Control Gene ratio. The international ratio is obtained by multiplying BCR-ABL: Control gene ratio by the lab-specific conversion factor. (NCT00103844)
Timeframe: Pretreatment, then after every 4 weeks for 12 weeks, then after every 12 week period out to 2 years; restricted to precrossover measurements.

Interventionparticipants (Number)
Dasatinib29
Imatinib6

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Duration of MCyR at 24 Months

Percentage of participants who achieved MCyR and did not progress at 24 months. (NCT00103844)
Timeframe: 24 Months

InterventionPercentage of Participants (Number)
Dasatinib90

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Complete Hematologic Response (CHR) at Any Time Prior to Crossover

Participants achieving CHR prior to crossover. CHR=all of the following criteria: white blood cell count ≤ institutional upper limit of normal; platelets < 450,000/mm³; no blasts or promyelocytes in peripheral blood; < 5% myelocytes plus metamyelocytes in peripheral blood; peripheral blood basophils ≤ 20%; no extramedullary involvement. Confirmed CHR is defined as CHR maintained at least 4 weeks after first documented at ≥ Day 14. Failure to maintain criteria of CHR was defined by 2 or more consecutive records of non-response. (NCT00103844)
Timeframe: Baseline (within 4 weeks of Day 1), weekly until Week 12 and then every 12 weeks until crossover or off-study; restricted to precrossover measurements.

InterventionParticipants (Number)
Dasatinib94
Imatinib40

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CHR After Crossover

Participants achieving CHR after crossover. CHR=all of the following criteria: white blood cell count ≤ institutional upper limit of normal; platelets < 450,000/mm³; no blasts or promyelocytes in peripheral blood; < 5% myelocytes plus metamyelocytes in peripheral blood; peripheral blood basophils ≤ 20%; no extramedullary involvement. Confirmed CHR is defined as CHR maintained at least 4 weeks after first documented at ≥ Day 14. Failure to maintain criteria of CHR was defined by 2 or more consecutive records of non-response. (NCT00103844)
Timeframe: Weekly for 12 weeks, then after every 12 week period out to 2 years; restricted to postcrossover measurements.

InterventionParticipants (Number)
Dasatinib37
Imatinib13

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Blood Sample Collection for Pharmacokinetic (PK) Analysis of Dasatinib

Number of participants from which blood samples were collected for population PK studies. (NCT00103844)
Timeframe: Day 8: pretreatment trough sample, a sample between 30 minutes and 3 hours following treatment, a sample between 5 and 8 hours following treatment, and a sample at 12 hours, prior to the next dose.

Interventionparticipants (Number)
Dasatinib78

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MCyR at Any Time Prior to Crossover

Cytogenetic response was based on the prevalence of Ph+ metaphases among cells in metaphase on a bone marrow sample (aspirate/biopsy). MCyR was defined as CCyR (0% Ph+ cells in metaphase in bone marrow) or PCyR (>0% to 35% Ph+ cells in metaphase in bone marrow). (NCT00103844)
Timeframe: Baseline (within 4 weeks of Day 1), every 12 weeks until crossover or off-study timepoints. Restricted to precrossover measurements.

,
InterventionParticipants (Number)
MCyR (CCyR + PCyR)CCyR (0% Ph+ cells)PCyR (>0% to 35% Ph+ cells)
Dasatinib544410
Imatinib1697

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Duration of MCyR at 12 Months and 18 Months

Percentage of participants who achieved MCyR and did not progress at 12 and 18 months. (NCT00103844)
Timeframe: 12 months, 18 months

,
Interventionpercentage of participants. (Number)
12 months18 months
Dasatinib9290
Imatinib7474

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Duration of Complete Hematologic Response (CHR)

Percentage of participants who achieved CHR and did not progress at specified time points. CHR=all of the following criteria: white blood cell count ≤ institutional upper limit of normal; platelets < 450,000/mm³; no blasts or promyelocytes in peripheral blood; < 5% myelocytes plus metamyelocytes in peripheral blood; peripheral blood basophils ≤ 20%; no extramedullary involvement. Confirmed CHR is defined as CHR maintained at least 4 weeks after first documented at ≥ Day 14. Failure to maintain criteria of CHR was defined by 2 or more consecutive records of non-response. (NCT00103844)
Timeframe: 12 months, 24 months

,
Interventionpercentage of participants (Number)
12 months24 months
Dasatinib9284
Imatinib8273

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Number of Participants With Adverse Experiences (AEs)

"Summary of participants who had adverse events (AEs), who discontinued treatment due to the AE, who had serious adverse events (SAEs), and who had SAEs that were related to treatments.~A serious adverse event is one that at any dose of the study drug or at any time during the period of observation:~Results in death;~Is life threatening;~Requires inpatient hospitalization or prolongation of existing hospitalization;~Results in persistent or significant disability/incapacity;~Is a congenital anomaly/birth defect;~Is medically important.~The Investigator assessed each AE for potential causal relationship between the event and study drug. An investigator assessment of possibly, probably or unknown relation is considered related." (NCT00114959)
Timeframe: up to 3 years

Interventionparticipants (Number)
AEsDiscontinued due to AESerious AEsSAEs considered related
Homoharringtonine + Imatinib Mesylate152127

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6 Month Progression Free Survival Rate

The percentage of patients with 6 months progression-free survival was estimated. Progression is defined, using RECIST, as a measurable increase in the smallest dimension of any target or non-target lesion, the appearance of new lesions, or the significant clinical deterioration related to progression of patient's disease. (NCT00115739)
Timeframe: 6 months

Interventionpercentage of patients (Number)
Imatinib (Gleevec) Tablets27

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6 Month Survival Rate

The percentage of patients still alive at 6 months was estimated. (NCT00115739)
Timeframe: 6 months

Interventionpercentage of patients (Number)
Imatinib (Gleevec) Tablets46

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Overall Response (Complete and Partial Response) Rate at 8 Weeks

The number of patients with Complete Response (CR), Partial Response (PR) and Stable Disease (SD) were determined at 8 weeks. (NCT00115739)
Timeframe: 8 weeks

Interventionparticipants (Number)
Number of Participants with CRNumber of Participants with PRNumber of Participants with SD
Imatinib (Gleevec) Tablets024

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Rate of Grade 3, Grade 4 and Grade 5 Toxicities Experienced by Patients With Anaplastic Thyroid Cancer Who Are Treated With Gleevec

Number of grade 3, grade 4 and grade 5 toxicities experienced by patients with anaplastic thyroid cancer who are treated with Gleevec. (NCT00115739)
Timeframe: Up to 30 days post treatment

Interventionevents (Number)
Number of Grade 3 Toxicities ReportedNumber of Grade 4 Toxicities ReportedNumber of Grade 5 Toxicities Reported
Imatinib (Gleevec) Tablets2900

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Estimated Rate of Overall Survival (OS) in Two Treatment Arms

OS was defined as time between randomization and death due to any cause during study treatment or during follow-up after discontinuation of treatment. Estimated rate of OS was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: 60 months over all and follow up period

,
InterventionPercent probability (Number)
12 Months24 Months36 Months42 Months48 Months60 Months
Imatinib 400 mg98.797.496.194.794.094.0
Imatinib 800 mg99.097.895.594.893.493.4

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Imatinib Pharmacokinetic Trough Plasma Concentration (Cmin) at Month 12

Imatinib PK trough plasma concentration (Cmin) was defined as any pre-dose Imatinib plasma concentration (NCT00124748)
Timeframe: Month 12

Interventionmg/mL (Mean)
Imatinib 400 mg1458.2
Imatinib 800 mg739.58

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Mean Actual Dose Intensity Per Day

The mean actual dose intensity per day from start of treatment up to last dose or discontinuation was evaluated up to Month 36. Actual dose intensity (mg/day) = total dose/time on treatment (periods of zero dose are included) (NCT00124748)
Timeframe: start of treatment to Month 36

Interventionmg/day (Mean)
Imatinib 400 mg399.3
Imatinib 800 mg643.3

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Percentage of Participants With Major Molecular Response (MMR) Rates at 12 Months

MMR is defined as Bcr-Abl (A fusion gene of the breakpoint cluster region [Bcr] gene and Abelson proto-oncogene [Abl] genes) transcript ratio ≤0.1% (≥ 3 log reduction of BCR-ABL transcripts from a standardized baseline), as detected by reverse transcriptase polymerase chain reaction [RT-PCR] (performed centrally). (NCT00124748)
Timeframe: 12 months

InterventionPercentage of participants (Number)
Imatinib 400 mg38.9
Imatinib 800 mg45.1

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Time to First Complete Cytogenetic Response

Cytogenetic response (CyR) is the percentage of Philadelphia positive metaphases (among at least 20 metaphase cells in Bone Marrow) with Complete Cytogenetic Response (CCyR) being 0 percent. Time to CCyR (months) = (date of first CCyR or censoring - date of randomization + 1) / 30.4375. Time to first CCyR was evaluated using the Kaplan-Meier method. (NCT00124748)
Timeframe: 60 months overall

InterventionMonths (Median)
Imatinib 400 mg10.8
Imatinib 800 mg5.8

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Time to First Complete Hematological Response (CHR)]

Complete Hematological Response (CHR) is defined is where all of the following criteria must be present for ≥4 weeks: White Blood Cell (WBC) count <10 x 109/L, Platelet count <450 x 109/L, Basophils <5%, No blasts and promyelocytes in Peripheral Blood (PB), (Myelocytes + metamyelocytes) < 5% in PB and No evidence of extramedullary involvement. Time to CHR (months) = (date of first CHR or censoring - date of randomization + 1) / 30.4375. Time to first CHR was evaluated using the Kaplan-Meier method. (NCT00124748)
Timeframe: 60 months overall

InterventionMonths (Median)
Imatinib 400 mg1.0
Imatinib 800 mg1.0

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Time to First Major Molecular Response

"MMR is defined as Bcr-Abl (A fusion gene of the breakpoint cluster region [Bcr] gene and Abelson proto-oncogene [Abl] genes) transcript ratio ≤0.1% (≥ 3 log reduction of BCR-ABL transcripts from a standardized baseline), as detected by reverse transcriptase polymerase chain reaction [RT-PCR] (performed centrally).~Time to MMR (months) = (date of first MMR or censoring - date of randomization + 1) / 30.4375. Time to first MMR was evaluated using the Kaplan-Meier method" (NCT00124748)
Timeframe: 42 months overall

InterventionMonths (Median)
Imatinib 400 mg13.6
Imatinib 800 mg8.4

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Estimated Rate of Progression Free Survival (PFS) in Two Treatment Arms

PFS on study which was defined as time between randomization and either (1) death due to any cause on treatment of during follow-up after discontinuation of treatment or (2) progression to accelerated phase (AP) or blast crisis (BC) on treatment during follow-up after discontinuation of study treatment. Estimated rate of PFS was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: 60 months over all and follow up period

,
InterventionPercent probability (Number)
12 Months24 Months36 Months42 Months48 Months60 Months
Imatinib 400 mg97.495.994.494.494.494.4
Imatinib 800 mg98.797.596.796.395.895.8

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Estimated Rate of Progression to Accelerated Phase (AC)/Blast Crisis (BC) in Two Treatment Arms

(Accelerated Phase/Blast Crisis) AP/BC was defined as time between randomization and either (1) (Chronic Myeloid Leukemia) CML-related death (if death was primary reason for discontinuation) or (2) progression to AP or BC (during treatment). Estimated rate of AC/BC was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: 60 months over all and follow up period

,
InterventionPercent probability (Number)
12 Months24 Months36 Months42 Months48 Months60 Months
Imatinib 400 mg97.495.995.295.295.295.2
Imatinib 800 mg99.097.997.597.097.097.0

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Estimated Rates of Progression Free Survival (PFS) on Treatment by Major Molecular Response (MMR)

A Landmark Kaplan-Meier analysis was performed for PFS at 42 months by MMR status at 6, 12, and 18 months to investigate their prognostic value. (NCT00124748)
Timeframe: 42 months

,
InterventionPercent probability (Number)
No MMR at 6 MonthsMMR at 6 MonthsNo MMR at 12 MonthsMMR at 12 MonthsNo MMR at 18 MonthsMMR at 18 Months
Imatinib 400 mg94.810093.210096.798.7
Imatinib 800 mg95.699.094.699.397.099.3

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Kaplan-Meier Estimates of Duration of First Complete Cytogenetic Response (CCyR)

Duration of CCyR was defined as the time between date of CCyR and the earliest of either (1) loss of CCyR OR (2) (Chronic Myeloid Leukemia) CML-related death or progression to (Accelerated Phase/Blast Crisis) AP/BC during study treatment. Estimated rate of duration of first CCyR was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: From first complete cytogenetic response to first confirmed loss or censoring

,
InterventionPercent probability (Number)
6 Months12 Months18 Months24 Months30 Months36 Months42 Months
Imatinib 400 mg99.198.298.298.298.298.298.2
Imatinib 800 mg99.297.897.396.896.895.995.9

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Kaplan-Meier Estimates of Duration of First Major Molecular Response Until Confirmed Loss

Duration of MMR (months) = (date of first confirmed loss or censoring - date of MMR + 1 ) / 30.4375. Estimated rate of duration of first MMR was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: From First major molecular response to first confirmed loss or censoring

,
InterventionPercent probability (Number)
3 Months6 Months9 Months12 Months15 Months18 Months21 Months24 Months30 Months36 Months42 Months
Imatinib 400 mg10098.397.495.693.892.890.989.988.585.185.1
Imatinib 800 mg96.390.790.288.487.586.185.183.682.581.177.9

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Percentage of Participants With Complete Cytogenetic Response (CCyR) Rate at 12, 24, 36, 42 Months

Cytogenetic response (CyR)is the percentage of Philadelphia chromosome positive metaphases (among at least 20 metaphase cells in bone marrow (BM)) with Complete Cytogenetic Response (CCyR) being 0 percent. (NCT00124748)
Timeframe: 12, 24, 36, 42 months

,
InterventionPercentage of Participants (Number)
12 months24 months36 months42 months
Imatinib 400 mg66.976.479.080.3
Imatinib 800 mg70.276.880.681.5

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Estimated Rate of Event Free Survival (EFS) in Two Treatment Arms

EFS on treatment was defined as time between randomization and either (1) death due to any cause during study treatment, (2) progression to accelerated phase (AP) or blast crisis (BC) on treatment, (3) loss of complete hematological response (CHR), or (4) loss of major cytogenic response (MCyR) while on treatment. Estimated rate of EFS was analyzed by Kaplan-Meier estimate (percent probability and 95% Confidence interval). (NCT00124748)
Timeframe: 60 months over all

,
InterventionPercent probability (Number)
12 Months24 Months36 Months42 Months48 Months60 Months
Imatinib 400 mg95.394.692.392.392.390.3
Imatinib 800 mg98.095.394.594.193.693.6

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Percentage of Patients With Undetectable Levels of Bcr-Abl (A Fusion Gene of the Breakpoint Cluster Region [Bcr] Gene and Abelson Proto-oncogene [Abl] Genes) Transcripts

"Undetectable levels or Complete molecular response is defined as Bcr-Abl ratio (%) on international scale (IS) <= 0.0032% (≥ 4.5 log reduction of BCR-Abl transcripts from a standardized baseline)." (NCT00124748)
Timeframe: 12 , 24, 36 and 42 months

,
InterventionPercentage of Partcipants (Number)
12 Months24 Months36 Months42 Months
Imatinib 400 mg4.511.512.714.6
Imatinib 800 mg4.710.313.212.5

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Percentage of Participants With Major Molecular Response (MMR) Rates at 24, 36, and 42 Months

MMR is defined as Bcr-Abl (A fusion gene of the breakpoint cluster region [Bcr] gene and Abelson proto-oncogene [Abl] genes) transcript ratio ≤0.1% (≥ 3 log reduction of BCR-ABL transcripts from a standardized baseline), as detected by reverse transcriptase polymerase chain reaction [RT-PCR] (performed centrally). (NCT00124748)
Timeframe: 24, 36 and 42 months

,
InterventionPercentage of participants (Number)
24 months36 months42 months
Imatinib 400 mg53.552.251.6
Imatinib 800 mg50.849.850.2

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Percentage of Participants With Complete Hematological Response (CHR) Rates at 12, 24, 36, and 42 Months

Complete Hematologic Response (CHR) is where all of the following criteria must be present for ≥4 weeks: White Blood Cell (WBC) count <10 x 109/L, Platelet count <450 x 109/L, Basophils <5%, No blasts and promyelocytes in Peripheral Blood (PB), (Myelocytes + metamyelocytes) < 5% in PB and No evidence of extramedullary involvement. (NCT00124748)
Timeframe: 12, 24, 36, and 42 months

,
InterventionPercentage of participants (Number)
12 months24 months36 months42 months
Imatinib 400 mg94.994.996.296.2
Imatinib 800 mg93.793.794.494.4

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Percentage of Participants With Progression Free Survival (PFS) During the Study Duration

PFS was defined as the time from the date of randomization to the date of the first documented progression according to the MacDonald criteria, or death due to any cause. MacDonald criteria are standard criteria in neurooncology. Tumor assessment was made according to the adapted MacDonald criteria based on the combined evaluation of 1) assessment of the MRI scan for measurable, evaluable, and new lesions (made by the independent external expert too), 2) overall assessment of neurological performance (made by the investigator), 3) concomitant steroid use (as reported by the investigator). (NCT00154375)
Timeframe: 6 months -1 year

,
InterventionPercentage of Participants (Number)
6 months12 months
Hydroxyurea Alone6.62.1
Imatinib Mesylate + Hydroxyurea (HU)5.32.1

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Progression-free Survival

Progression-free survival in months. Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00161213)
Timeframe: 4 years

Interventionmonths (Median)
Gemcitabine and Imatinib3.9

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Overall Survival

(NCT00161213)
Timeframe: 5 years

Interventionmonths (Median)
Gemcitabine and Imatinib6.23

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1-year Survival Rate

Percentage of subjects who survive up to 1 year (NCT00161213)
Timeframe: 5 years

Interventionpercentage of total evaluable subjects (Number)
Gemcitabine and Imatinib25.6

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Response Rate

"Response rate as defined by a best response of Stable Disease or better." (NCT00161213)
Timeframe: 5 years

Interventionpercentage of total evaluable subjects (Number)
Gemcitabine and Imatinib48.6

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Overall Survival (by Month)

Overall survival was defined as the time between start of treatment and death due to any reason. Overall survival for the participants was calculated by Kaplan-Meier estimates per month. The time was censored at the date of last contact for participants who discontinued treatment and were in survival follow-up. (NCT00171158)
Timeframe: From first dose until death of the patient, up to 14 years.

Interventionpercentage of participants (Number)
12 Months24 Months36 Months48 Months60 Months72 Months84 Months96 Months108 Months120 Months132 Months144 Months156 Months
Imatinib Mesylate (STI571)32.718.715.414.59.18.47.57.57.56.65.55.55.5

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Overall Survival

Overall survival was defined as the number of events of death, expressed as a percentage, from the start of treatment to death, due to any reason. (NCT00171158)
Timeframe: From first dose until death of the patient, up to 14 years.

Interventionpercentage of participants (Number)
Imatinib Mesylate (STI571)89.2

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Percentage of Participants With Cytogenetic Response (Complete Cytogenetic Response and Major Cytogenetic Response) to STI571

Response was evaluated from bone marrow aspirates and biopsy samples. Bone marrow cytogenetic studies were performed every 3 months during the core phase of the study, then twice yearly, then annually to evaluate Philadelphia chromosome positive (Ph+). Cytogenetic response was defined as the best response the participant achieved during study. Based on the percentage of Ph+ cells = (positive cells/ examined cells) x100, at each BM assessment the cytogenetic response was classified as: Complete Cytogenetic Response (CCyR):, 0% Ph+ cells; Partial Cytogenetic Response (PCyR):, >0 - 35% Ph+ cells; Minor: >35 - 65% Ph+ cells; and Minimal: >65 - 95% Ph+ cells, None: >95 % Ph+ cells and Not done: <20 metaphases were examined and/or response could not be assigned. Major Cytogenetic Response (MCyR) was defined as sum of the CCyR plus PCyR rates. (NCT00171223)
Timeframe: Up to 6 years after the start of treatment

,,
Interventionpercentage of participants (Number)
Complete Cytogenetic ResponseMajor Cytogenetic Response
Cytogenetic Failure37.263.8
Hematologic Failure29.645.4
Interferon-alpha Intolerance45.865.6

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Time to Complete Hematologic Response to STI571

Time to Complete Hematologic Response was defined for all participants with calculated confirmed complete hematologic response as the time until first documented response (which was confirmed >= 4 weeks). Complete hematological response was defined as normalization of peripheral blood counts (WBC and platelet count < ULN at the laboratory where the analysis was performed), with a normal WBC differential, and no immature granulocytes present, lasting for 4 weeks. (NCT00171223)
Timeframe: 12 months after the start of treatment

Interventionmonths (Median)
Hematologic Failure1.64
Cytogenetic Failure0.72
Interferon-alpha Intolerance0.72

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Percentage of Participants With Complete Hematologic Response to STI571

Hematologic response was evaluated from hematology measurements in the peripheral blood. Complete hematological response was defined as normalization of peripheral blood counts [WBC and platelet count < upper limit of normal (ULN) at the laboratory where the analysis was performed], with a normal WBC differential, and no immature granulocytes present, lasting for 4 weeks. (NCT00171223)
Timeframe: 12 months after the start of treatment

Interventionpercentage of participants (Number)
Hematologic Failure94.1
Cytogenetic Failure97.9
Interferon-alpha Intolerance91.7

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Duration of Complete Hematologic Response to STI571

Duration of hematologic response was defined as the time from the first documentation of the complete hematologic response to the date the loss of complete hematologic response is documented. Loss of complete hematological response was defined as a rising WBC count (increased to a level above the ULN at the laboratory where the analysis was performed confirmed by two samples obtained one month apart). The mean survival time and its standard error were underestimated because the largest observation was censored and the estimation was restricted to the largest event time. Complete hematological response was defined as normalization of peripheral blood counts (WBC and platelet count < ULN at the laboratory where the analysis was performed), with a normal WBC differential, and no immature granulocytes present, lasting for 4 weeks. (NCT00171223)
Timeframe: 12 months after the start of treatment

Interventionmonths (Mean)
Hematologic Failure19.3672
Cytogenetic Failure23.9389
Interferon-alpha Intolerance24.6818

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Percentage of Participants Alive Over Time Based on Kaplan-Meier Estimates

Overall survival was defined as the time from the first dose of STI571 to the death of the participant. If a participant is not known to have died, survival was censored at the time of last contact. Kaplan-Meier estimates of the percentage of participants at each time point was calculated. (NCT00171223)
Timeframe: 12, 24, 36, 48, 60, 72, 84, 96, 108, 120, 132, 144 and 156 months

,,
Interventionpercentage of participants (Number)
12 Months24 Months36 Months48 Months60 Months72 Months84 Months96 Months108 Months120 Months132 Months144 Months156 Months
Cytogenetic Failure98.993.691.587.183.879.779.779.178.47775.473.870.1
Hematologic Failure94.788.18478.473.370.168.566.563.36159.75755.5
Interferon-alpha Intolerance97.489.583.876.373.671.467.265.965.363.862.360.860.8

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Number of Participants With Grade 3 or 4 Eastern Cooperative Oncology Group (ECOG) Performance Status

The ECOG performance status was recorded at baseline and every 3 months during the core study. The ECOG Performance Scale has 5 grades. 0 = Fully active, able to carry out all pre-disease activities; 1 = Restricted in strenuous activity but ambulatory and able to carry out work of light or sedentary nature; 2 = Ambulatory and capable of all self-care but unable to carry out work activities. Active about 50% of waking hours; 3 = Capable of limited self-care, confined to bed/chair more than 50% of waking hours; 4 = Completely disabled; cannot carry on self-care. Totally confined to bed/chair. (NCT00171223)
Timeframe: Up to 9 months after the start of treatment

,,
InterventionParticipants (Count of Participants)
Grade 3Grade 4
Cytogenetic Failure00
Hematologic Failure10
Interferon-alpha Intolerance00

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Percentage of Participants With Cytogenetic Response in Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

Bone marrow (BM) cytogenetic analysis was required at baseline, after 12 weeks (visit 22) and after 24 weeks (visit 28) to evaluate Ph chromosome positivity. In several participants, this was also done after 4 and 8 weeks. Based on the percentage of Philadelphia chromosome positive (Ph+) cells = (positive cells/examined cells)x100, at each BM assessment the cytogenetic response was classified as: Complete, 0% Ph+ cells; Partial, >0 - 35% Ph+ cells; Minor, >35 - 65% Ph+ cells; Minimal, >65 - 95% Ph+ cells; None, >95% Ph+ cells; Not done: <20 metaphases were examined and/or response could not be assigned. Cytogenetic response was defined as confirmed complete or partial response. A BM sample was considered as assessable for cytogenetic response only if it contained ≥20 metaphases. However, an assessment of partial response was retained in a sample with <20 metaphases when it was immediately preceded or followed by a complete or partial response in another sample with ≥20 metaphases. (NCT00171249)
Timeframe: Up to 3 years after start of treatment

Interventionpercentage of participants (Number)
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg14.3
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg24.7

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Time to Response in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

Time to response was defined for all participants as the time until first documented response (which was confirmed ≥4 weeks later). (NCT00171249)
Timeframe: Up to 3 years after start of treatment

,
Interventionmonths (Median)
Hematologic responseCytogenetic response
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg0.952.83
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg0.992.96

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Overall Survival by Dose in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

To evaluate overall survival, all participants were followed after the last dose of study drug every month for the first three months and thereafter every three months until death. Overall survival was calculated for all participants as the time between start of treatment and death due to any reason. The time was censored at the date of last contact for participants who discontinued treatment and were in survival follow-up. For participants without survival follow-up information, the time was censored at last available visit/treatment date. (NCT00171249)
Timeframe: 12, 24, 36, 48, 60, 72, 84, 96, 108, 120, and 132 months after start of treatment

,
Interventionpercentage of participants (Number)
12 months24 months36 months48 months60 months72 months84 months96 months108 months120 months132 months
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg64.544.334.928.023.718.615.211.811.811.811.8
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg79.165.754.245.636.229.928.326.624.824.822.3

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Overall Survival by Disease

To evaluate overall survival, all participants were followed after the last dose of study drug every month for the first three months and thereafter every three months until death. Overall survival was calculated for all participants as the time between start of treatment and death due to any reason. The time was censored at the date of last contact for participants who discontinued treatment and were in survival follow-up. For participants without survival follow-up information, the time was censored at last available visit/treatment date. (NCT00171249)
Timeframe: 12, 24, 36, 48, 60, 72, 84, 96, 108, 120, 132, 144, and 156 months after start of treatment

,,,
Interventionpercentage of participants (Number)
12 months24 months36 months48 months60 months72 months84 months96 months108 months120 months132 months144 months156 months
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia74.458.84839.932.226.324.121.920.620.618.918.918.9
Acute Lymphoid Leukemia10.48.38.38.38.38.38.35.65.65.65.65.65.6
Acute Myeloid/Myelogenous Leukemia0000000000000
Lymphoid Blast Crisis12.5000000000000

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Duration of Response in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

Duration of response was defined as the time between first documented response (which was confirmed ≥4 weeks later) and the earliest date of the following: loss of response (when any of the criteria for response were no longer fulfilled); progression to blast crisis (≥30% blasts in peripheral blood or bone marrow, extramedullary involvement other than liver/spleen enlargement); discontinuation due to adverse event, laboratory abnormality, unsatisfactory therapeutic effect or death. (NCT00171249)
Timeframe: Up to 3 years after start of treatment

,
Interventionmonths (Median)
Hematologic responseCytogenetic response
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg16.4626.28
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg28.8127.63

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Time to Progression to Blast Crisis in Participants With Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

Progression to blast crisis was defined as ≥30% blasts in peripheral blood or bone marrow or as extramedullary involvement other than liver or spleen enlargement. (NCT00171249)
Timeframe: Up to 3 years after start of treatment

Interventionmonths (Median)
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg9.95
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg25.13

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Percentage of Participants With Hematologic Response in Accelerated Phase Chronic Myeloid/Myelogenous Leukemia

Hematologic response was evaluated from hematology measurements in the peripheral blood (PB) and bone marrow (BM) and assessments of extramedullary leukemic involvement (EMD) at physical examination. Response was defined as complete hematologic remission (CHR), no evidence of leukemia (NEL), or return to chronic phase (RTC). (NCT00171249)
Timeframe: Up to 3 years after start of treatment

Interventionpercentage of participants (Number)
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 400 mg64.9
Accelerated Phase Chronic Myeloid/Myelogenous Leukemia 600 mg74.7

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Overall Response Rate (ORR)

Defined as the proportion of patients with confirmed complete or partial response (CR or PR), recorded from date of treatment until date of recurrence or progressive disease, and assessed by RECIST v 1.1. (NCT00193180)
Timeframe: 18 months

Interventionpercentage of participants (Number)
Intervention16

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Overall Survival (OS)

Defined as the time from first protocol treatment to date of death due to any cause. (NCT00193180)
Timeframe: 18 months

Interventionmonths (Median)
Intervention15.4

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Progression Free Survival (PFS)

PFS defined as the length of time, in months, that patients were alive from date of first protocol treatment until worsening of disease, assessed by Response Evaluation Criteria in Solid Tumors (RECIST) v1.1. (NCT00193180)
Timeframe: 18 months

InterventionMonths (Median)
Intervention9.3

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Progression Free Survival (PFS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Worsening of Their Disease

(NCT00193258)
Timeframe: 18 months

Interventionmonths (Median)
Bevacizumab/Erlotinib/Imatinib8.9

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Overall Survival (OS), the Length of Time, in Months, That Patients Were Alive From Their First Date of Protocol Treatment Until Death

(NCT00193258)
Timeframe: 24 months

Interventionmonths (Median)
Bevacizumab/Erlotinib/Imatinib17.2

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Objective Response Rate (ORR), the Percentage of Patients Who Experience an Objective Benefit From Treatment

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR. (NCT00193258)
Timeframe: 18 months

Interventionpercentage of participants (Number)
Bevacizumab/Erlotinib/Imatinib17

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Percentage of Participants With a Reduction of BCR-ABL Transcript Level > 4.5 Log From the Start of From Initiation of Treatment

reduction of BCR-ABL transcript level > 4.5 Log from the start of from initiation of treatment (NCT00210119)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Imatinib Mesylate0

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Percentage of Participants With Molecular Response

"A patient is considered to be in molecular response if at least one of the following conditions is observed :~- a complete molecular response at 6 months defined by PCR negativation tested on twice~OR~- reduction of BCR-ABL transcript level > 2 Log from the start of from initiation of treatment" (NCT00210119)
Timeframe: 6 months

Interventionpercentage of participants (Number)
Imatinib Mesylate0

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Best Tumor Response (Core)

Best tumor response was based on the Southwestern Oncology Group (SWOG) criteria. Objective tumor response assessments were categorized according to the following criteria: complete response (CR), partial response (PR), no change or stable disease (SD), progression of disease (PD), unknown where the progression has not been documented and one or more measurable or evaluable sites have not been assessed (UNK), status after resection for progression (RP), status after resection for safety (RS), status after preventive resection (RPR), progressive after first resection (PDR) and not evaluable. Any tumor assessment after surgical resection for preventative reasons was treated like tumor assessments of UNK for calculation of best response. Tumor assessments with current objective status = RP, RS or PDR were treated like assessments with objective tumor status = PD n the calculation of best response. (NCT00237185)
Timeframe: Month 36

,
Interventionparticipants (Number)
Complete responsePartial responseStable diseaseProgressive diseaseNot evaluableUnknown
Imatinib Mesylate 400 mg049101220
Imatinib Mesylate 600 mg14913632

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Best Tumor Response (Core + Extension)

Best tumor response was based on the Southwestern Oncology Group (SWOG) criteria. Objective tumor response assessments were categorized according to the following criteria: complete response (CR), partial response (PR), no change or stable disease (SD), progression of disease (PD), unknown where the progression has not been documented and one or more measurable or evaluable sites have not been assessed (UNK), status after resection for progression (RP), status after resection for safety (RS), status after preventive resection (RPR), progressive after first resection (PDR) and not evaluable. Any tumor assessment after surgical resection for preventative reasons was treated like tumor assessments of UNK for calculation of best response. Tumor assessments with current objective status = RP, RS or PDR were treated like assessments with objective tumor status = PD n the calculation of best response. (NCT00237185)
Timeframe: Month 156

,
Interventionparticipants (Number)
Complete responsePartial responseStable diseaseProgressive diseaseNot evaluableUnknown
Imatinib Mesylate 400 mg149101120
Imatinib Mesylate 600 mg24813632

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Time to Onset of Response (Core + Extension)

Time to response was analyzed as time to event for all participants. Participants who did not meet the definition of confirmed PR/CR were censored at the time of their last progression-free tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to the date of the first tumor assessment that was later confirmed to be at least a partial response during the core and extension periods, up to 156 months.

Interventionmonths (Median)
Imatinib Mesylate 400 mg3
Imatinib Mesylate 600 mg3

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Time to Onset of Response (Core)

Time to response was analyzed as time to event for all participants. Participants who did not meet the definition of confirmed PR/CR were censored at the time of their last progression-free tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to the date of the first tumor assessment that was later confirmed to be at least a partial response during the core period, up to 36 months.

Interventionweeks (Median)
Imatinib Mesylate 400 mg13
Imatinib Mesylate 600 mg12

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Time to Treatment Failure (Core + Extension)

Time to treatment failure was analyzed as time to event for all participants. Participants who had neither progressed, died nor discontinued from the trial for any reason other than the condition no longer required therapy were censored for analysis at the time of their last tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to date of earliest occurrence of progression, death due to any cause, or discontinuation from the trial for any reason other than the condition no longer required therapy during the core and extension periods, up to 156 month.

Interventionmonths (Median)
Imatinib Mesylate 400 mg19
Imatinib Mesylate 600 mg19

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Time to Treatment Failure (Core)

Time to treatment failure was analyzed as time to event for all participants. Participants who had neither progressed, died nor discontinued from the trial for any reason other than the condition no longer required therapy were censored for analysis ate the time of their last tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to date of earliest occurrence of progression, death due to any cause, or discontinuation from the trial for any reason other than the condition no longer required therapy during the core period, up to 36 months.

Interventionweeks (Median)
Imatinib Mesylate 400 mg84
Imatinib Mesylate 600 mg84

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Time to Progression (Core + Extension)

Time to progression was analyzed as time to event for all participants. Participants who had neither progressed, died nor discontinued from the trial for any reason other than the condition no longer required therapy were censored for analysis at the time of their last tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to date of progression or death due to disease indication or discontinuation due to unsatisfactory therapeutic effect during the core and extension periods, up to 156 months.

Interventionmonths (Median)
Imatinib Mesylate 400 mg19.8
Imatinib Mesylate 600 mg25.5

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Progression Free Survival (PFS) (Core + Extension)

Progression free survival was analyzed as a time to event for each participant. If a participant had no event, then the PFS was censored at the last tumor assessment. (NCT00237185)
Timeframe: Date of first imatinib dose to earliest date of progression, resection due to safety/progression, death due to any cause or discontinuation due to unsatisfactory therapeutic effect during the core and extension periods, up to 156 months.

Interventionmonths (Median)
Imatinib Mesylate 400 mg19.3
Imatinib Mesylate 600 mg25.2

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Overall Survival (Core)

Overall survival was analyzed as time to event for all participants. Participants who did not die were censored at the last date known alive, which is the last date of any study medication, laboratory sample, tumor assessment, adverse event end date or date of last contact. (NCT00237185)
Timeframe: Date of first imatinib dose to the date of death during the core period, up to 36 months.

Interventionmonths (Median)
Imatinib Mesylate 400 mgNA
Imatinib Mesylate 600 mgNA

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Overall Survival (Core + Extension)

Overall survival was analyzed as time to event for all participants. Participants who did not die were censored at the last date known alive, which is the last date of any study medication, laboratory sample, tumor assessment, adverse event end date or date of last contact. (NCT00237185)
Timeframe: Date of first imatinib dose to the date of death during the core and extension periods, up to 156 months.

Interventionmonths (Median)
Imatinib Mesylate 400 mg55.9
Imatinib Mesylate 600 mg57.1

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Duration of Response (Core)

Duration of response was analyzed as time to event for all participants whose best response was at least a PR. The onset of response was the first tumor assessment that was subsequently confirmed to constitute at least a partial best response. The end of response was the first tumor assessment noting PD. (NCT00237185)
Timeframe: Date of confirmed best PR or CR to date of confirmed disease progression during the core period, up to 36 months.

Interventionweeks (Median)
Imatinib Mesylate 400 mg113
Imatinib Mesylate 600 mg123

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Duration of Response (Core + Extension)

Duration of response was analyzed as time to event for all participants whose best response was at least a PR. The onset of response was the first tumor assessment that was subsequently confirmed to constitute at least a partial best response. The end of response was the first tumor assessment noting PD. (NCT00237185)
Timeframe: Date of confirmed best PR or CR to date of confirmed disease progression during the core and extension periods, up to 156 months

Interventionmonths (Median)
Imatinib Mesylate 400 mg27
Imatinib Mesylate 600 mg30

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To Collect Matched Tumor Tissue of Trial Participants With Dermatofibrosarcoma Protuberans Before and After Treatment With Imatinib for Future Use in cDNA Microarray and Tissue Array Studies.

To obtain matched tumor tissue samples of trial participants dermatofibrosarcoma protuberans (DFSP)for the purpose of determining whether imatinib mesylate affects autocrine/paracrine stimulated signal transduction through the platelet-derived growth factor receptor pathway in DFSP by comparing the level of phosphorylated platelet-derived growth factor receptor beta (PDGFRB) in DFSP after up to 2 weeks of treatment with imatinib to the level of phosphorylated PDGFRB pre-treatment. (NCT00243191)
Timeframe: Prior to and after 2-weeks of imatinib therapy

Interventionpaired tumor tissue samples (Number)
Imatinib18

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Overall Time To Progression (TTP)

TTP is the amount of time from date of registration to date of first documentation of progression or symptomatic deterioration. For progression, one or more of the following must occur: (1) 20% increase in the sum of longest diameters of target measurable lesions over smallest sum observed (over baseline if no decrease during therapy) using the same techniques as baseline. (2) Increase in PSA by at least 25% from baseline in patients whose PSA did not decrease, and of 50% from nadir in patients whose PSA decreased with a confirmation 3 weeks later. (3) Unequivocal progression of non-measurable disease in the opinion of the treating physician (an explanation must be provided). (4) Appearance of any new lesion/site. (5) Death due to disease without prior documentation of progression and without symptomatic deterioration, which is defined as global deterioration of health status requiring discontinuation of treatment without objective evidence of progression. (NCT00251225)
Timeframe: Up to 24 months

Interventionmonths (Median)
Hormone Refractory Prostate Cancer Patients6.4

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Overall Survival (OS)

OS is the amount of time in months from the date of registration to the date of death from any cause. (NCT00251225)
Timeframe: Up to 60 months

Interventionmonths (Median)
Hormone Refractory Prostate Cancer Patients23.1

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Prostate-Specific Antigen (PSA) Response Rate

PSA response rate is the number of participants who experienced a best response of: complete response, CR (PSA less than or equal to 0.2 ng/mL, documented two or more times, a minimum of four weeks apart), partial response, PR (a decline in PSA by at least 50%, confirmed by a second PSA value four or more weeks later) or stable disease (does not qualify for CR, PR, Progression or Symptomatic Deterioration, at least 6 weeks after registration) / total number of analyzable patients. (NCT00251225)
Timeframe: Up to 12 months

Interventionpercentage of patients (Number)
Hormone Refractory Prostate Cancer Patients72.4

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Response: One Log Decrease in BCR-ABL

Molecular response defined as reduction by one log of the circulating peripheral blood for reverse transcription polymerase chain reaction (RT-PCR) transcripts of BCR-ABL (tumor-specific oncogenic fusion protein) after two consecutive measurements. RT-PCR performed at 3 month intervals. Response categorized as either 'No Decrease' or 'Decrease' if one log reduction in BCR-ABL detected. (NCT00267085)
Timeframe: 12 months

InterventionParticipants (Number)
DecreaseNo Decrease
CML Vaccine37

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2-year Relapse Free Survival Rate

(NCT00278876)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Imatinib Mesylate93.6

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2-year Overall Survival Rate

(NCT00278876)
Timeframe: 2 years

Interventionpercentage of participants (Number)
Imatinib Mesylate97.9

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Toxicity Profile

Number of patients who experienced toxicity from study treatment to evaluate the safety and tolerability of adjuvant imatinib (NCT00278876)
Timeframe: Monitoring of adverse events will be continued for at least 28days following the last dose of study treatment, up to 3 years.

Interventionparticipants (Number)
Imatinib Mesylate47

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Percentage of Patients Who Had Clinical Benefit

Patients who had clinical benefit were patients with a best response of complete response (CR), partial response (PR), or stable disease (SD) lasting for more than 6 months from the start of treatment until the first documented disease progression (PD) or death from any cause. (PD) was defined as ≥ 25% increase in size of the sum of the products of the largest perpendicular diameters of the target tumors compared to the smallest value recorded at or after baseline. SD was defined as insufficient tumor shrinkage to qualify for PR or CR and no increase in lesions which would qualify as PD. (NCT00290771)
Timeframe: Baseline to end of study (Month 24)

InterventionPercentage of participants (Number)
Imatinib 600 mg + Hydroxyurea 1000 mg9.9
Imatinib 1000 mg + Hydroxyurea 1000 mg6.0
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg8.2

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Percentage of Patients With an Objective Overall Response (OOR)

Patients with an OOR were those whose best response to treatment was a complete response (CR) or a partial response (PR) assessed with magnetic resonance imaging. A patient had a CR if the target tumors disappeared. A patient had a PR if there was a ≥ 50% reduction in the sum of the products of the largest perpendicular diameters of the target tumors compared to the baseline value. A best response of CR required at least 2 determinations of CR at least 4 weeks apart. A best response of PR required at least 2 determinations of PR or better at least 4 weeks apart (and not qualifying for CR). (NCT00290771)
Timeframe: Baseline to end of study (Month 24)

InterventionPercentage of participants (Number)
Imatinib 600 mg + Hydroxyurea 1000 mg3.8
Imatinib 1000 mg + Hydroxyurea 1000 mg3.0
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg3.5

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Percentage of Patients Surviving at Months 6, 12, and 24

Patients not known to have died were censored at the time of last survival follow-up. (NCT00290771)
Timeframe: Months 6, 12, and 24

,,
InterventionPercentage of participants (Number)
6 Months12 Months24 Months
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg50.029.713.9
Imatinib 1000 mg + Hydroxyurea 1000 mg50.931.320.3
Imatinib 600 mg + Hydroxyurea 1000 mg49.228.510.7

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Duration of Objective Overall Response (OOR)

Duration of OOR only included patients whose best overall response was complete response (CR) or partial response (PR). The start date was the date of the first documented response (CR or PR); the end date was the date of the first documented disease progression (PD) or death from any cause. (PD) was defined as ≥ 25% increase in size of the sum of the products of the largest perpendicular diameters of the target tumors compared to the smallest value recorded at or after baseline. If a patient had not progressed or died, the duration of OOR was censored at the time of the last OOR assessment. (NCT00290771)
Timeframe: Baseline to end of study (Month 24)

InterventionWeeks (Median)
Imatinib 600 mg + Hydroxyurea 1000 mg41.1
Imatinib 1000 mg + Hydroxyurea 1000 mg32.1
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg37.1

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Percentage of Patients With Progression-free Survival at Months 6 and 12

Progression-free survival (PFS) was defined as the time from the start of treatment to the date of the first documented disease progression (PD) or death due to any cause. (PD) was defined as ≥ 25% increase in size of the sum of the products of the largest perpendicular diameters of the target tumors compared to the smallest value recorded at or after baseline. If a patient had not progressed or died, progression-free survival was censored at the time of the last overall response assessment. (NCT00290771)
Timeframe: Months 6 and 12

,,
InterventionPercentage of participants (Number)
6 Months12 Months
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg10.65.3
Imatinib 1000 mg + Hydroxyurea 1000 mg9.93.3
Imatinib 600 mg + Hydroxyurea 1000 mg11.26.9

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Number of Patients With at Least 1 Adverse Event

An adverse event (AE) is any undesirable sign, symptom, or medical condition occurring after starting study drug even if the event is not considered to be related to study drug. Study drug refers to imatinib or hydroxyurea. The study treatment is the combination of these two study drugs. (NCT00290771)
Timeframe: Baseline to end of study (Month 24)

InterventionParticipants (Number)
Imatinib 600 mg + Hydroxyurea 1000 mg129
Imatinib 1000 mg + Hydroxyurea 1000 mg98
All Patients - Imatinib 600 or 1000 mg + Hydroxyurea 1000 mg227

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Percentage of Participants With On-study AEs of Special Interest

GI=gastrointestinal. AE=any new untoward medical occurrence or worsening of a preexisting medical condition that does not necessarily have a causal relationship with treatment. Grade 1=mild; Grade 2=moderate; Grade 3=severe and undesirable; Grade 4=life-threatening or disabling; Grade 5=death. Percentages based on the number of participants with a specific grade at baseline. Participants without on-study test values for a particular laboratory analyte are not included in the reporting of that analyte. (NCT00320190)
Timeframe: Months 1 to 12, continuously, and Months 12 to 24, continuously

,
InterventionPercentage of Participants (Number)
Fluid retention (Any grade)Fluid retention (Grades 3-5)Fluid retention: Superficial edema (Any grade)Fluid retention: Superficial edema (Grades 3-5)Fluid retention: Generalized edema (Any grade)Fluid retention: Generalized edema (Grades 3-5)Hemorrhage (Any grade)Hemorrhage (Grades 3-5)Hemorrhage: GI bleeding (Any grade)Hemorrhage: GI bleeding (Grades 3-5)Hemorrhage: Other bleeding (Any grade)Hemorrhage: Other bleeding (Grades 3-5)Diarrhea (Any grade)Diarrhea (Grades 3-5)Skin rash (Any grade)Skin rash (Grades 3-5)
Dasatinib, 100 mg5.30005.3000000026.3042.10
Imatinib, 800 mg38.57.730.807.77.715.407.707.7030.8015.40

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Time to Progression

Sample size of 40 patients per group was needed to detect an 8 month increase in time to progression with the combination (80% power, alpha =.05, 2-sided). (NCT00323063)
Timeframe: 5 years

Interventionmonths (Median)
Arm I (Gemcitabine Hydrochloride)2
Arm II (Gemcitabine Hydrochloride + Imatinib)2.5

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Response Rate (Complete and Partial Response)

Overall response rate was evaluated every 2 cycles (six weeks) for both groups using international criteria by the Response Evaluation Criteria in Solid Tumors (RECISTv1.0) for target lesions and were assessed by CT or MRI. Response rates were defined as complete response (CR), disappearance of all target lesions; partial response (PR), >=30% decrease in the sum of the longest diameter of target lesions. Overall response(OR) defined as OR=CR + PR (NCT00323063)
Timeframe: 5 years

Interventionpercentage of participants (Number)
Arm I (Gemcitabine Hydrochloride)9.1
Arm II (Gemcitabine Hydrochloride + Imatinib)9.1

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Time to Progression

(NCT00323362)
Timeframe: 2 years

Interventionmonths (Mean)
Gemcitabine Hydrochloride and Imatinib Mesylate2.77

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Percentage of Patients Who Meet Critieria for Response

"Response is considered Partial Response or Complete Response as per RECIST criteria.~Complete Response (CR): Disappearance of all target lesions Partial Response (PR): At least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD.~Progressive Disease (PD): At least a 20% increase in the sum of the LD of target lesions, taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions.~Stable Disease (SD): Neither sufficient shrinkage to qualify for PR nor sufficient increase to qualify for PD, taking as reference the smallest sum LD since the treatment started." (NCT00323362)
Timeframe: 2 years

Interventionpercentage of patients who responded (Number)
Gemcitabine Hydrochloride and Imatinib Mesylate0

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1-year Survival

Accrual duration is 2 years with an additional year for assessment of 1-year survival. Outcome measure time frame is about 3 years. (NCT00323362)
Timeframe: 3 years

Interventionpercentage of patients (Number)
Gemcitabine Hydrochloride and Imatinib Mesylate35

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Overall Survival

From date of registration (defined as date of randomization) to date of death due to any cause. Patients last known to be alive are censored at last date of contact. Note: median was not reached in the Imatinib arm due to limited follow-up data. (NCT00324987)
Timeframe: up to 7 years

Interventionmonths (Median)
Imatinib + Bevacizumab30
Imatinib0

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Progression Free Survival

From date of registration (defined as date of randomization) to date of first observation of progressive disease, death due to any cause or symptomatic deterioration. Patients last known to be alive and progression free are censored at last date of contact. Progression is defined as one or more of the following: 20% increase in the sum of longest diameters of target measurable lesions over smallest sum observed (over baseline if no decrease during therapy), provided at least one target lesion does NOT demonstrate uniform hypoattenuation over > 90% of maximal cross sectional area; unequivocal progression of non-measurable disease; appearance of new lesion/site that is not uniformly hypoattenuating; a hyperattenuating region within a previously cystic/uniformly hypoattenuating lesion will be considered progressive disease if hyperattenuating region is either >= 1 cm in longest diameter or round/oval and forms acute margins with border of target lesion; death due to disease. (NCT00324987)
Timeframe: Up to 7 years

Interventionmonths (Median)
Imatinib + Bevacizumab30
Imatinib81

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Median Time to Progression

(NCT00331409)
Timeframe: Time to progression

Interventionmonths (Median)
Everolimus and Imatinib Mesylate2.9

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Number of Participants With Adverse Events

"Toxicity assessments will be obtained as follows:~Cycle 1: Weeks 1,2,3 Cycle 2: Weeks 6,9 Cycle 3: Weeks 12, 15 Cycle 4: Weeks 18, 21 Cycle 5: Weeks 24, 27 Cycle 6+: Every visit during these cycles~Safety assessments will consist of evaluating adverse events and serious adverse events." (NCT00331409)
Timeframe: Duration of study, Up to 4 years

Interventionparticipants (Number)
Everolimus and Imatinib Mesylate19

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Number of Subjects That Demonstrated a Reduction in Tumor Measurements.

Number of subjects that received at least one post-baseline scan that demonstrated a reduction in sum target lesions per Response Evaluation Criteria in Solid Tumors (RECIST) criteria. (NCT00331409)
Timeframe: Up to 4 years

InterventionParticipants (Count of Participants)
Everolimus and Imatinib Mesylate5

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Overall Number of Participants Who Achieve a Response Rate (Complete Response, Partial Response, and Stable Disease) at 3 Months

(NCT00331409)
Timeframe: Up to 4 years

Interventionparticipants (Number)
Everolimus and Imatinib Mesylate18

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Progression-free Survival at 3 Months

(NCT00331409)
Timeframe: 3 months post 1st dose

Interventionmonths (Median)
Everolimus and Imatinib Mesylate2.9

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Number of Participants With Serious Adverse Events as a Measure of Safety (Second-line Treatment)

A serious adverse event is any experience that suggests a significant hazard, contraindication, side effect or precaution that: results in death, is life-threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or is medically significant (NCT00333840)
Timeframe: 144 months

InterventionParticipants (Number)
Imatinib to IFN-a + Ara-C2
IFN-a + Ara-C to Imatinib160

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Kaplan Meier Estimates of Event Free Survival (All Randomized Participants)

"Event-free survival is defined as the time between randomization and the earliest of any of the following events on treatment:~progression to Accelerated Phase (AP) or Blast Crisis (BC)~loss of Complete Hematological Response (CHR)~loss of Major Cytogenetic Response (MCyR) confirmed~loss of Major Cytogenetic Response (MCyR) unconfirmed~increase in white blood cell count (WBC) if approved by the Study Management Committee (SMC)~death (due to any cause when reported as primary reason for discontinuation of treatment).~Kaplan Meier estimates of the percentage of participants with Event Free Survival at the given time point was calculated. This outcome was measured in all randomized patients, regardless of whether crossover occurred, i.e., events that occurred in patients, who had crossed over, were attributed following crossover to the original randomized treatment." (NCT00333840)
Timeframe: 12,24,36,48,60,72,84,96,108,120,132 and 144 months

,
InterventionPercentage of participants (Number)
12 months (n = 553, 553)24 months (n = 505, 332)36 months (n = 448, 263)48 months (n = 415, 241)60 months (n = 395, 223)72 months (n = 376, 207)84 months (n = 352, 181)96 months (n = 334, 166)108 months (n = 301, 141)120 months (n = 269, 130)132 months (n = 257, 124)144 months (n = 143, 76)
IFN-a + Ara-C79.470.067.063.761.960.159.058.356.656.656.651.8
Imatinib (STI571)96.689.685.383.983.283.082.081.079.979.679.679.6

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Kaplan-Meier Estimates of Overall Survival (All Randomized Participants)

Overall survival was defined as the time between date of randomization and death due to any cause. The time was censored at last examination date for patients who were still being treated and at date of last contact for patients who discontinued treatment. Kaplan-Meier estimates of the percentage of participants at each time point was calculated. This outcome was measured in all randomized patients, regardless of whether crossover occurred, i.e., events that occurred in patients, who had crossed over, were attributed following crossover to the original randomized treatment. (NCT00333840)
Timeframe: 12,24,36,48,60,72,84,96,108,120,132 and 144 months

,
InterventionPercentage of participants (Number)
12 months (n = 553, 553)24 months (n = 542, 512)36 months (n = 518, 471)48 months (n = 492, 441)60 months (n = 475, 411)72 months (n = 461, 388)84 months (n = 446, 373)96 months (n = 430, 358)108 months (n = 391, 315)120 months (n = 368, 299)132 months (n = 356, 288)144 months (n = 250, 199)
IFN-a + Ara-C97.793.689.887.785.483.883.181.479.978.877.775.4
Imatinib (STI571)98.996.092.490.489.488.286.685.484.383.382.881.3

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Kaplan Meier Estimates of Time to Progression to Accelerated Phase (AP) or Blast Crisis (BC) (All Randomized Participants)

Time to progression to AP/BC is defined as the time between randomization and either of the following events on treatment: death (due to CML when reported as primary reason for discontinuation of treatment) or progression to Accelerated Phase or Blast Crisis and is censored at last examination date for patients without event. No data after discontinuation of study treatment was included. The Kaplan Meier estimates of the percentage of participants with survival without progression to AP/BC at the given time point was calculated. This outcome was measured in all randomized patients, regardless of whether crossover occurred, i.e., events that occurred in patients, who had crossed over, were attributed following crossover to the original randomized treatment. (NCT00333840)
Timeframe: 12,24,36,48,60,72,84,96,108,120,132 and 144 months

,
InterventionPercentage of participants (Number)
12 months (n = 553, 553)24 months (n = 513, 388)36 months (n = 461, 337)48 months (n = 431, 311)60 months (n = 409, 289 )72 months (n = 384, 265)84 months (n = 358, 236)96 months (n = 338, 220)108 months (n = 305, 189)120 months (n = 272, 175)132 months (n = 259, 165)144 months (n = 145, 94)
IFN-a + Ara-C92.990.087.984.783.583.182.482.482.482.482.482.4
Imatinib (STI571)98.595.794.093.192.792.792.792.492.192.192.192.1

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Percentage of Participants With Major Molecular Response (Second-line Treatment)

Major Molecular Response was determined using a quantitative polymerase chain reaction (PCR) laboratory test and was defined as BCR-ABL protein transcripts of ≤ 0.1% according to the international scale. (NCT00333840)
Timeframe: 12,24,36,48,60,72,84,96,108,120,132 and 144 months

InterventionPercentage of participants (Number)
12 months (n = 86)24 months (n = 62)36 months (n = 130)48 months (n = 216)60 months (n = 174)72 months (n = 146)84 months (n = 139)96 months (n = 138)108 months (n = 120)120 months (n = 84)132 months (n = 31)144 months
IFN-a + Ara-C to Imatinib51.269.478.581.986.291.186.387.090.085.790.3NA

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Percentage of Participants With Major Molecular Response (First-line Treatment)

Major Molecular Response was determined using a quantitative polymerase chain reaction (PCR) laboratory test and was defined as BCR-ABL protein transcripts of ≤ 0.1% according to the international scale. (NCT00333840)
Timeframe: 12,24,36,48,60,72,84,96,108,120,132 and 144 months

,
InterventionPercentage of participants (Number)
12 months (n= 305, 83)24 months (n= 102, 12)36 months (n= 68, 7)48 months (n= 305, 12)60 months (n= 316, 10)72 months (n= 292, 9)84 months (n= 247, 8)96 months (n= 228, 4)108 months (n= 233, 0)120 months (n= 204, 0)132 months (n= 168, 0)144 months (n= 1, 0)
IFN-a + Ara-C9.625.028.658.3100.088.987.5100.0NANANANA
Imatinib (STI571)50.269.676.577.088.088.091.992.593.693.192.3100.0

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Percentage of Participants With Event Free Survival Events (All Randomized Participants)

"Event-free survival is defined as the time between randomization and the earliest of any of the following events on treatment:~progression to Accelerated Phase (AP) or Blast Crisis (BC)~loss of Complete Hematological Response (CHR)~loss of Major Cytogenic Response (MCyR) confirmed~loss of Major Cytogenic Response (MCyR) unconfirmed~increase in white blood cell count (WBC) if approved by the Study Management Committee (SMC)~death (due to any cause when reported as primary reason for discontinuation of treatment).~The percentage of participants with Event Free Survival events in each category was calculated. This outcome was measured in all randomized patients, regardless of whether crossover occurred, i.e., events that occurred in patients, who had crossed over, were attributed following crossover to the original randomized treatment." (NCT00333840)
Timeframe: 144 months

,
InterventionPercentage of participants (Number)
Participants with eventsProgression to AP or BCLoss of CHRLoss of MCyR (confirmed)Loss of MCyR (unconfirmed)Increase of WBCDeath
IFN-a + Ara-C32.212.87.65.41.13.41.8
Imatinib (STI571)17.96.92.74.20.90.23.1

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Percentage of Participants With Best Cytogenetic Response (Second-line Treatment)

"Bone marrow aspirate was performed to evaluate cytogenetic results (percentage of Ph chromosome (Ph+) containing metaphases) and the amount of blasts and promyelocytes in bone marrow to establish cytogenetic response.~Major Cytogenetic Response= Complete Response or Partial Response. Complete Cytogenetic Response= 0 % of Ph+ metaphases (out of 20 metaphases). Partial Cytogenetic Response= > 0 and ≤ 35 % Ph+ metaphases (out of 20 metaphases). The percentage of participants with cytogenetic response in each category was calculated." (NCT00333840)
Timeframe: 144 months

,
InterventionPercentage of participants (Number)
Major Cytogenic ResponseComplete Cytogenic ResponsePartial Cytogenic Response
IFN-a + Ara-C to Imatinib86.081.05.0
Imatinib to IFN-a + Ara-C14.37.17.1

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Percentage of Participants With Best Cytogenetic Response (First-line Treatment)

"Bone marrow aspirate was performed to evaluate cytogenetic results (percentage of Philadelphia chromosome positive (Ph+) metaphases) and amount of blasts and promyelocytes in bone marrow to establish cytogenetic response.~Major Cytogenetic Response= Complete Response or Partial Response. Complete Cytogenetic Response= 0 % of Ph+ metaphases (out of 20 metaphases). Partial Cytogenetic Response= > 0 and ≤ 35 % of Ph+ metaphases (out of 20 metaphases). The percentage of participants with cytogenetic response in each category was calculated." (NCT00333840)
Timeframe: 144 months

,
InterventionPercentage of participants (Number)
Major Cytogenic ResponseComplete Cytogenic ResponsePartial Cytogenic Response
IFN-a + Ara-C23.311.611.8
Imatinib (STI571)89.082.86.1

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Number of Participants With Serious Adverse Events as a Measure of Safety (First-line Treatment)

A serious adverse event is any experience that suggests a significant hazard, contraindication, side effect or precaution that: results in death, is life-threatening, requires in-patient hospitalization or prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect or is medically significant (NCT00333840)
Timeframe: 144 months

InterventionParticipants (Number)
Imatinib (STI571)226
IFN-a + Ara-C163

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Overall Survival of Participants

This sample size would provide an estimate of the objective response rate (ORR) 95% confidence intervals for the ORR and CBR were calculated using the exact binomial method. Among patients with CR or PR as the best overall response, duration of response (DOR) was defined as the time from which measurement criteria were met for CR or PR until the date of progression. Progression-free survival (PFS) was defined as the time from study enrollment to disease progression or death from any cause, whichever occurred first. PFS data were censored at the time of removal from study. Overall survival (OS) was defined as the time from study registration to death from any cause. Information on vital status was collected following study completion through July 23, 2018 and was used in the determination of OS. Among patients with SD as the best overall response, duration of SD was defined as the time from study enrollment to disease progression or removal from study. (NCT00338728)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 182 months

Interventionmonths (Median)
Progression-free survival (PFS)Overall Survival (OS)
Letrozole and Imatinib Mesylate8.744.3

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Objective Response Rate (ORR)

Among participants with CR or PR as the best overall response, duration of response (DOR) was defined as the time from which measurement criteria were met for CR or PR until the date of progression. Progression-free survival (PFS) was defined as the time from study enrollment to disease progression or death from any cause, whichever occurred first. PFS data were censored at the time of removal from study. Overall survival (OS) was defined as the time from study registration to death from any cause. Information on vital status was collected following study completion through July 23, 2018 and was used in the determination of OS. Among patients with SD as the best overall response, duration of SD was defined as the time from study enrollment to disease progression or removal from study. (NCT00338728)
Timeframe: From the registration until disease progression, death, unacceptable toxicity, or withdraw of study consent, whichever occurred first assessed up to 182 months

InterventionParticipants (Count of Participants)
Complete Response (CR)Partial Response (PR)SD (including non-CR/Non-PD)>/=24 weeksSD (including non-CR/Non-PD)Progressive DiseaseNon-Evaluable
Letrozole and Imatinib Mesylate05168115

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Median Progression-free Survival (PFS)

Time in months from the start of study treatment to the date of first progression according to Macdonald criteria, or to death due to any cause. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00354913)
Timeframe: From the date of study treatment initiation to the date of the first documented progression or death from any cause, whichever came first, assessed up to 69 months.

Interventionmonths (Median)
Imatinib Mesylate+Hydroxyurea7

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Median Overall Survival (OS)

Time in months from the start of study treatment to date of death due to any cause. Patients alive at last follow-up are censored as of that follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00354913)
Timeframe: From the date of study treatment initiation to the date of death from any cause, assessed up to 69 months.

Interventionmonths (Median)
Imatinib Mesylate+Hydroxyurea66

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Objective Response Rate

Percentage of participants with an objective response (complete response or partial response). Per modified Macdonald criteria and assessed by MRI, complete response (CR) was the disappearance of all target lesions and partial response (PR) was a ≥50% decrease in the sum of the longest diameter of target lesions. Objective response = CR+PR. (NCT00354913)
Timeframe: 69 Months

Interventionpercentage of participants (Number)
Imatinib Mesylate+Hydroxyurea0

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Progression-free Survival at 6 Months

Percentage of participants surviving six months from the start of study treatment without progression of disease. PFS was defined as the time from the date of study treatment initiation to the date of the first documented progression according to the Macdonald criteria, or death due to any cause. (NCT00354913)
Timeframe: From the date of study treatment initiation to the date of the first documented progression or death from any cause, whichever came first, assessed up to 69 months. For each participant, PFS was assessed at 6 months after treatment initiation.

Interventionpercentage of participants (Number)
Imatinib Mesylate+Hydroxyurea61.9

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Adverse Events (AEs), Serious Adverse Events (SAEs), Deaths, and Discontinuations Due to AEs

An AE is defined as any new untoward medical occurrence or worsening of a pre-existing medical condition in a patient or clinical investigation subject administered an investigational (medicinal) product and that does not necessarily have a causal relationship with this treatment. An SAE is any untoward medical occurrence that at any dose results in death, is life-threatening, requires inpatient hospitalization or causes prolongation of existing hospitalization, results in persistent or significant disability/incapacity, is a congenital anomaly/birth defect, or is an important medical event. (NCT00362466)
Timeframe: From 2 weeks prior to randomization through Month 36. At least every 4 weeks until all study-related toxicities resolve to baseline, stabilize, or are deemed irreversible.

,
Interventionevents (Number)
AEsSAEsAEs leading to DiscontinuationDeaths
Dasatinib3000
Imatinib1000

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Number of Participants With Pain Progression

Pain progression defined as a 50% or more increase in MPQ-PPI score (0=no pain to 5=excruciating pain) or analgesic use from baseline for at least 3 consecutive weeks. Analgesic use scores were based on 1 point per non narcotic dose of medication and 4 points per dose of narcotic medication. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionParticipants (Number)
Sunitinib (Phase 3)14
Imatinib10

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Number of Participants With Pain Relief Response

Pain relief response defined as a 50% or more reduction in the McGill Pain Questionaire - Present Pain Intensity (MPQ-PPI) score (0=no pain to 5=excruciating pain) and/or analgesic use from baseline for at least 3 consecutive weeks. Analgesic use scores were based on 1 point per non narcotic dose of medication and 4 points per dose of narcotic medication. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionParticipants (Number)
Sunitinib (Phase 3)2
Imatinib4

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Number of Participants With Objective Response of Complete Response or Partial Response

Number of participants with objective response based assessment of confirmed complete response (CR) or partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as the disappearance of all target lesions. PR was defined as a greater than or equal to 30% decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionParticipants (Number)
Sunitinib (Phase 3)5
Imatinib2

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Duration of Response (DR)

"Time from start of first documentation of objective response(complete or partial response) that was subsequently confirmed to first documentation of objective tumor progression or death due to any cause, whichever occurred first.~Confirmed complete response (CR) and partial response (PR)according to Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as the disappearance of all target lesions. PR was defined as a greater than or equal to 30% decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions." (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionWeeks (Median)
Sunitinib (Phase 3)18.3
Imatinib19.8

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Euro Quality of Life (EQ-5D) - Health State Profile Utility Score - Imatinib Treatment Arm

"EQ-5D: participant rated questionnaire assessed health-related quality of life in terms of a single utility score. Health State Profile component rated current health for 5 domains: mobility, self-care, usual activities, pain and discomfort, and anxiety and depression; 1 indicated better health state (no problems); 3 indicated worst health state (eg, confined to bed). Scoring formula developed by EuroQol Group assigned utility value for each domain in the profile. Score was transformed and results in a total score ranged 0.21 to 1.000; higher score indicated a better health state." (NCT00372567)
Timeframe: Days 1 and 28 of each cycle

InterventionScores on a scale (Mean)
Cycle 1 (n=22)Cycle 2 (n=23)Cycle 3 (n=18)Cycle 4 (n=18)Cycle 5 (n=17)Cycle 6 (n=12)Cycle 7 (n=12)Cycle 8 ( (n=11)Cycle 9 (n=7)Cycle 10 (n=7)Cycle 11 (n=3)
Imatinib0.800.850.820.860.830.840.810.680.860.860.88

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Euro Quality of Life (EQ-5D)- Visual Analog Scale (VAS) - Sunitinib Treatment Arm

EQ-5D: participant rated questionnaire assessed health-related quality of life in terms of a single index value. The VAS component rated current health state on a scale from 0 (worst imaginable health state) to 100 (best imaginable health state); higher scores indicated a better health state. (NCT00372567)
Timeframe: Days 1 and 28 of each cycle

InterventionScores on a Scale (Mean)
Cycle 1 (n=30)Cycle 2 (n=27)Cycle 3 (n=21)Cycle 4 (n=23)Cycle 5 (n=16)Cycle 6 (n=16)Cycle 7 (n=12)Cycle 8 (n=11)Cycle 9 (n=7)Cycle 10 (n=6)Cycle 11 (n=3)Cycle 12 (n=2)
Sunitinib (Phase 3)78.1377.1978.5280.1784.2585.8178.2584.7382.5781.0081.0086.50

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Euro Quality of Life (EQ-5D)- Visual Analog Scale (VAS) - Imatinib Treatment Arm

EQ-5D: participant rated questionnaire assessed health-related quality of life in terms of a single index value. The VAS component rated current health state on a scale from 0 (worst imaginable health state) to 100 (best imaginable health state); higher scores indicated a better health state. (NCT00372567)
Timeframe: Days 1 and 28 of each cycle

InterventionScores on a scale (Mean)
Cycle 1 (n=22)Cycle 2 (n=22)Cycle 3 (n=20)Cycle 4 (n=18)Cycle 5 (n=15)Cycle 6 (n=11)Cycle 7 (n=12)Cycle 8 (n=10)Cycle 9 (n=7)Cycle 10 (n=7)Cycle 11 (n=3)
Imatinib75.4173.6472.8576.1468.9368.2767.0863.7074.6476.8675.33

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Euro Quality of Life (EQ-5D) - Health State Profile Utility Score- Sunitinib Treatment Arm

"EQ-5D: participant rated questionnaire to assess health-related quality of life in terms of a single utility score. Health State Profile component rated current health for 5 domains: mobility, self-care, usual activities, pain and discomfort, and anxiety and depression; 1 indicated better health state (no problems); 3 indicated worst health state (eg, confined to bed). Scoring formula developed by EuroQol Group assigned utility value for each domain in profile. Score was transformed and results in a total score ranged 0.21 to 1.000; higher score indicated a better health state." (NCT00372567)
Timeframe: Days 1 and 28 of each cycle

InterventionScores on a scale (Mean)
Cycle 1 (n=30)Cycle 2 (n=27)Cycle 3 (n=21)Cycle 4 (n=23)Cycle 5 (n=16)Cycle 6 (n=16)Cycle 7 (n=12)Cycle 8 (n=11)Cycle 9 (n=6)Cycle 10 (n=5)Cycle 11 (n=3)Cycle 12 (n=2)
Sunitinib (Phase 3)0.900.840.840.850.890.900.840.830.760.780.830.93

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Time to Tumor Response (TTR)

Time from date of randomization to first documentation of objective tumor response (partial or complete response). Confirmed complete response (CR) and partial response (PR) according to Response Evaluation Criteria in Solid Tumors (RECIST). CR was defined as the disappearance of all target lesions. PR was defined as a greater than or equal to 30% decrease in the sum of the longest dimensions of the target lesions taking as a reference the baseline sum longest dimensions. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionWeeks (Median)
Sunitinib (Phase 3)4.1
Imatinib40.1

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Time to Treatment Failure (TTF)

TTF included death for any reason, treatment termination due to intolerable toxicity, or withdrawal of consent, whichever occurred first. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionMonths (Median)
Sunitinib (Phase 3)8.2
Imatinib6.3

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Time to Pain Relief Response (TTPR)

Pain relief response defined as a 50 percent (%) or more reduction in the McGill Pain Questionaire - Present Pain Intensity (MPQ-PPI) score (0=no pain to 5=excruciating pain) and/or analgesic use from baseline for at least 3 consecutive weeks. Analgesic use scores were based on 1 point per non narcotic dose of medication and 4 points per dose of narcotic medication. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionDays (Median)
Sunitinib (Phase 3)34.0
Imatinib22.0

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Time to Pain Progression (TTPP)

TTPP is the number of days from randomization to the first documentation of pain progression (defined as a 50% or more increase in MPQ-PPI score [0=no pain to 5=excruciating pain] or analgesic use from baseline for at least 3 consecutive weeks). Analgesic use scores were based on 1 point per non narcotic dose of medication and 4 points per dose of narcotic medication. (NCT00372567)
Timeframe: Day 28 of Cycle 1 up to 26

InterventionDays (Median)
Sunitinib (Phase 3)22.0
Imatinib99.0

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Progression-Free Survival (PFS)

Time from randomization to the first documentation of tumor progression or death due to any cause in the absence of documented tumor progression, whichever was earlier. (NCT00372567)
Timeframe: Baseline, Week 5, and every 8 weeks until Year 2

InterventionMonths (Median)
Sunitinib8.6
Imatinib6.4

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Overall Survival (OS)

Time from date of randomization to the date of death. In the absence of confirmation of death, survival time was censored to the last date the participant was known to be alive. (NCT00372567)
Timeframe: Baseline up to 2 years

InterventionMonths (Median)
Sunitinib (Phase 3)12.9
ImatinibNA

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Overall Response Rate (Complete and Partial Responses) as Assessed by RECIST Criteria

Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR (NCT00408460)
Timeframe: Baseline, Week 4 of courses 2, 4 and 6

InterventionParticipants (Count of Participants)
Treatment (Enzyme Inhibitor, Chemotherapy)11

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Overall Survival

(NCT00408460)
Timeframe: Every 3 months for 5 years

Interventionmonths (Median)
Treatment (Enzyme Inhibitor, Chemotherapy)7.3

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Time to Tumor Progression

Progression is defined using Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0), as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00408460)
Timeframe: Baseline and every 2 months post treatment until the date of first documented tumor progression or date of death from any cause, whichever came first, assessed up to 5 years.

Interventionmonths (Median)
Treatment (Enzyme Inhibitor, Chemotherapy)3.6

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Number of Participants With Immunologic Response

Immunologic Response (immune response) is defined as an increase of ≥ 0.5 PR1-HLA-A2 [human leukocyte antigen-A2 (HLA-A2)] tetramer cells / μl at the time of either the 3rd or 4th vaccination compared to the pre study absolute PR1-HLA-A2 tetramer cells / μl. Participants receive a total of 4 vaccinations over a period of 18 weeks (i.e., one vaccination each on weeks 0, 3, 6, and 18). Participants assessed after 3rd and 4th vaccination for immunologic response. (NCT00415857)
Timeframe: Period of 18 weeks (i.e., one vaccination each on weeks 0, 3, 6, and 18).

Interventionparticipants (Number)
PR1 + Imatinib0
PR1 + Imatinib + Interferon0

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Molecular Response Rate

Molecular response rate is number of respondents compared to total participants. Molecular Response is defined as a greater than a one-log reduction of Breakpoint Cluster Region-Abelson Murine Leukemia (BCR-ABL) transcript levels by quantitative polymerase chain reaction (PCR) from the baseline level at the time vaccination was initiated, or a disappearance of BCR-ABL transcripts, as measured by reverse transcription polymerase chain reaction (RT-PCR), occurring within 6 months from the last vaccination. Participants receive a series of 4 vaccinations administered at 3-week intervals and the fourth (final) vaccination administered 3 months after the third vaccination with blood draw to test PCR following every 3 months to test the level of leukemia in the blood and to see if disease is responding to the vaccine. (NCT00415857)
Timeframe: Baseline to 18 weeks, up to 6 months post final vaccination for overall study participation period.

Interventionpercentage of participants (Number)
PR1 + Imatinib0
PR1 + Imatinib + Interferon0

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Response Rate (Major and Complete Cytogenetic Response)

Rate is defined as number of participants with response of Major and Complete cytogenetic response out of total study participants. Response evaluated at one and 3 months from start of therapy, then every 3 months in patients with response, for one year, then every 6-12 months. Responses classified according to suppression of Philadelphia (Ph) chromosome by cytogenetic analysis: a) Complete cytogenetic response - Not Ph positive; b) Major cytogenetic response - Ph positive 1-34% of pretreatment value; c) Minor cytogenetic response - Ph positive 35-65% of pretreatment value; d) Minimal cytogenetic response - Ph positive 65-99% of pretreatment value; e) No cytogenetic response - Ph positive 100% of pretreatment value. (NCT00415909)
Timeframe: Evaluated at baseline (pretreatment) up to 12 months

Interventionpercentage of participants (Number)
Baseline1 Month3 Months12 Months
TALL-104 + IM0673333

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Overall Clinical Benefit

Overall Clinical Benefit was measured as the sum of complete response (CR), partial response (PR), and stable disease (SD). (NCT00424385)
Timeframe: up to 20 weeks

Interventionpercentage of evaluable participants (Number)
Imatinib + Sorafenib Cohort 0 & 120

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Number of Patients Experiencing Dose Limiting Toxicities (DLT's)

Eligible patients were enrolled in one of 4 cohorts, where each cohort allowed 3 evaluable patients to be on study, patients withdrawn from treatment for reasons other than toxicity were not considered evaluable. If one of the three evaluable patients experienced a dose limiting toxicity (DLT) the cohort was expanded to 6 evaluable patients. Patients will receive both study drugs on escalated dosing schedule until the maximum of 400 mg PO BID is reached for both drugs or toxicity is established. If 2 out of six evaluable patients experience a dose limiting toxicity this would show that the Maximum Tolerated Dose (MTD) was the dose from the prior cohort. (NCT00424385)
Timeframe: up to 20 weeks

Interventionparticipants (Number)
Imatinib + Sorafenib Cohort 01
Imatinib + Sorafenib Cohort 12

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Time to Disease Progression (TTP)

Medium TTP is 2 months (range 1-5). 10 patients were evaluable for disease progression for these patients occurred between 1-5 months after starting the study. The TTP was calculated per protocol. For radiographic assessment Response Evaluation Criteria in Solid Tumors (RECIST) was used. Complete response = disappearance of all lesions. Partial response (PR)=30% or greater decrease in sum of longest diameter of measureable lesions SD. Lesions have no sufficient decrease for progressive disease and no sufficient increase to meet Progressive Disease (PD). PD more than 20% increase in sum of longest diameter of measurable lesions or 2 or more new bone mets. prostate-specific antigen (PSA) assessment for patients with measurable disease, PSA progression in the absence of measurable disease progression will not be considered progressive disease. (NCT00424385)
Timeframe: up to 5 cycles, an average of 20 weeks, from the day of first treatment until the date of the last dose of study drug

Interventionmonths (Median)
Imatinib + Sorafenib Cohort 0 & 12

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Overall Survival

Overall survival (OS) is defined as the time from study entry to death or date last known alive. (NCT00424515)
Timeframe: Patients were followed long-term every 3 months until first progression, death or lost to follow-up. Median survival follow-up was 10.6 months (range 3.7-27.1).

Interventionmonths (Median)
Amplified KIT11.9
Mutated KIT12.9

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Best Overall Response

Best overall response (BOR) on treatment was based on RECIST 1.0 criteria. For target lesions, complete response (CR) is complete disappearance of all target lesions and partial response (PR) is at least a 30% decrease in the sum of longest diameter (LD) of target lesions, taking as reference baseline sum LD. CR or PR confirmation required within 4 weeks. Progressive disease (PD) is at least a 20% increase in the sum LD of target lesions from smallest sum LD as reference or the appearance of one or more new lesions. Stable disease (SD) is neither meeting PR or PD. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. CR is disappearance of all non-target lesions. (NCT00424515)
Timeframe: Disease was evaluated radiologically at baseline, after 6-weeks, and at 2-month intervals on treatment. Mean treatment duration was 4 months (range 1-11; amplified/mutated 3m/ 6m).

,
Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgressive Disease
Amplified KIT0029
Mutated KIT0733

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Time to Progression

Time to progression (TTP) based on the Kaplan-Meier method is defined as the duration of time from study entry to documented disease progression (PD) requiring removal from the study. Per RECIST 1.0 criteria: progressive disease (PD) is at least a 20% increase in the sum of longest diameter (LD) of target lesions taking as reference the smallest sum LD recorded since the treatment started or the appearance of one or more new lesions. PD for the evaluation of non-target lesions is the appearance of one or more new lesions and/or unequivocal progression of non-target lesions. (NCT00424515)
Timeframe: Disease was evaluated radiologically at baseline, after 6-weeks, and at 2-month intervals on treatment and every 3 months long-term. Mean treatment duration was 4 months (range 1-11; amplified/mutated 3m/ 6m).

Interventionmonths (Median)
Amplified KIT3.4
Mutated KIT3.9

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Time to Progression-free Survival

Progression-free survival, defined as the time from first administration of study drugs to the first PSA value of a PSA non-responder. Responders will be censored with date of PSA response for the analysis. The median time to PSA progression free survival was not achieved (NCT00427999)
Timeframe: every 4 weeks up to 24 weeks

Interventiondays (Median)
STI571+ Pioglitazone+ Etoricoxib + Dexamethasone + TreosulfaneNA

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Overall Survival Rate

Overall survival (OS) is defined as time from randomization to death from any cause or last date known alive. The median time to overall survival rate was not achieved (NCT00427999)
Timeframe: every 4 weeks up to 24 weeks

Interventiondays (Median)
STI571+ Pioglitazone+ Etoricoxib + Dexamethasone + TreosulfaneNA

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Quality of Life Assessed With EORTC-30

Health-related quality of life was assessed with the European Organization for the Research and Treatment of Cancer Quality of Life Questionnaire Core 30 (EORTC-30) questionnaire and was presented descriptively. The EORTC QLQ-C30 is a questionnaire including following sub-scales: global health status, functional scales (physical functioning, role functioning, emotional functioning, cognitive functioning, and social activity), symptom scales (fatigue, nausea and vomiting, and pain) and single items (dyspnoea, insomnia, appetite loss, constipation, diarrhoea and financial difficulties). Scores are averaged for each scale and transformed to 0-100 scale; higher score indicates better quality of life on global health status and functional scales and worse quality of life on symptom scales and financial difficulty scale. (NCT00427999)
Timeframe: baseline and Final Visit (week 24)

Interventionscores on a scale (Mean)
Baseline: financial difficulties (n=49)Baseline: appetite loss (n=50)Baseline: dyspnea (n=49)Baseline: constipation (n=50)Baseline: role functioning (n=50)Baseline: insomnia (n=49)Baseline: cognitive functioning (n=49)Baseline: diarrhea (n=50)Baseline: physical functioning (n=50)Baseline: pain (n=50)Baseline: emotional functioning (n=49)Baseline: social functioning (n=49)Baseline: fatigue (n=50)Baseline: global health status (n=49)Baseline: nausea & vomiting (n=50)Final Visit: financial difficulties (n=42)Final Visit: appetite loss (n=43)Final Visit: dyspnea (n=43)Final Visit: constipation (n=43)Final Visit: role functioning (n=43)Final Visit: insomnia (n=42)Final Visit: cognitive functioning (n=43)Final Visit: diarrhea (n=43)Final Visit: physical functioning (n=43)Final Visit: pain (n=43)Final Visit: emotional functioning (n=43)Final Visit: social functioning (n=43)Final Visit: fatigue (n=43)Final Visit: global health status (n=43)Final Visit: nausea & vomiting (n=43)
STI571+ Pioglitazone+ Etoricoxib + Dexamethasone + Treosulfane11.616.020.414.074.034.087.19.381.732.364.672.432.960.026.019.024.038.86.255.431.781.813.266.726.061.864.046.051.044.6

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PSA Response Rate

To investigate the effect of a treatment with Imatinib mesylate, Pioglitazone , Etoricoxib, and Dexamethasone in combination with metronomic chemotherapy (Treosulfane) on the PSA response rate in patients with hormone refractory prostate cancer. A patient will be defined as a responder if a PSA decline of at least 50%, which must be confirmed by a second PSA value 4 weeks later, is observed. A patient will be defined as a non-responder if PSA has not decreased during treatment. Non-response is defined as a 25% increase over the baseline on-study which is confirmed (equal or more) by a second value 4 weeks apart. The absolute increase must account for > 5 ng/ml. (NCT00427999)
Timeframe: up to 24 weeks

Interventionparticipants (Number)
PSA responder - NoPSA responder - Yes
STI571+ Pioglitazone+ Etoricoxib + Dexamethasone + Treosulfane3823

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Time to PSA Response

Time to PSA response, defined as the time from first administration of study drugs to the first PSA value of a confirmed PSA response. Non-responders will be censored with date of final visit/premature discontinuation for the analysis. Median time to PSA response was not achieved (NCT00427999)
Timeframe: every 4 weeks up to 24 weeks

Interventiondays (Median)
STI571+ Pioglitazone+ Etoricoxib + Dexamethasone + TreosulfaneNA

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Percentage of Participants Reaching Overall Survival

Overall survival from diagnosis (NCT00458848)
Timeframe: At 60 months

Interventionpercentage of patients (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy48.8

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Number of Patients Reaching Complete Hematological Response After Induction Therapy

(NCT00458848)
Timeframe: At the end of induction, day +50

Interventionparticipants (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy49

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Percentage of Participants Reaching Disease Free Survival

(NCT00458848)
Timeframe: At 60 months

Interventionpercentage of participants (Number)
Philadelphia Positive, Imatinib Only in Induction Therapy45.8

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Objective Response Rate

Response will be evaluated in this study using the new international criteria proposed by the RECIST Committee. A Simon two-stage minimax design will be employed. (NCT00470470)
Timeframe: Every 6 weeks for the first 3 courses and then every 12 weeks thereafter

Interventionparticipants (Number)
Complete ResponsePartial ResponseStable DiseaseProgression of Disease
Treatment (Enzyme Inhibitor Therapy)13147

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Time to Progression

Progression will be evaluated in this study using the new international criteria proposed by the RECIST Committee. Time to progression will be estimated using the Kaplan-Meier method. (NCT00470470)
Timeframe: Time from the treatment start to the date of disease progression

Interventionweeks (Mean)
Treatment (Enzyme Inhibitor Therapy)12

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Number of Responders With Confirmed Best Overall Response of Complete Response (CR) or Partial Response (PR) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set

The best overall response (CR/PR) must be confirmed by at least two determinations at least 4 weeks apart before progression. Using modified RECIST criteria, a Complete Response is defined as disappearance of all lesions, and a Partial Response is defined as either 1) at least a 30% decrease in the sum of the longest diameter of target lesions and no new lesions or progression of non-target lesions or 2) disappearance of all target lesions but persistence of one or more non-target lesion(s). (NCT00471328)
Timeframe: Up to 34 months

InterventionParticipants (Number)
Control/Cross Over to Nilotinib1

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Progression-free Survival (PFS) From Central Radiology Review Based on Primary Analysis (Data Cut-off: June, 2008)

Progression-free survival (PFS) is the time from date of randomization to the date of first documented progression or death due to any cause. If a participant has not had an event, progression-free survival is censored at the time of last adequate tumor assessment. Progression is defined according to Modified Response Evaluation Criteria in Solid Tumors (modified RECIST) criteria as at least a 20% increase in the sum of the longest diameter of target lesions, worsening of the non-target lesions or the appearance of one or more new lesions. (NCT00471328)
Timeframe: Up to 16 months

Interventiondays (Median)
Nilotinib109.0
Control/Cross Over to Nilotinib111.0

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Progression-free Survival (PFS) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set

PFS is defined as the time from the first date of cross-over to nilotinib therapy from the control arm to the date of the first observation of documented disease progression. Tumor assessment was based on the local investigator's measurement using Modified Response Evaluation Criteria in Solid Tumors (modified RECIST) criteria. Progression is defined according to modified RECIST criteria as at least a 20% increase in the sum of the longest diameter of target lesions, worsening of the non-target lesions or the appearance of one or more new lesions. (NCT00471328)
Timeframe: Up to 34 months

Interventiondays (Median)
Control/Cross Over to Nilotinib84

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Overall Survival for Treatment Crossover Analysis Set

For patients who crossed-over to nilotinib from the control arm, the overall survival was the time from the first dose date of nilotinib after switching from control arm to the date of death due to any cause. If death was not observed, the OS was censored at the latest date the patient was known to be alive. (NCT00471328)
Timeframe: Up to 34 months

Interventiondays (Median)
Control/Cross Over to Nilotinib231

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Overall Survival During Core and Extension Phases of the Study

Overall survival (OS) is defined as the time from date of randomization to date of death due to any cause. If a participant is not known to have died, survival will be censored at the date of last contact. This analysis included both Core and Extension data as well as survival follow up data. (NCT00471328)
Timeframe: Up to 50 months (including core, extension and follow up period)

Interventiondays (Median)
Nilotinib361
Control/Cross Over to Nilotinib300

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Overall Survival Based on Primary Analysis (Data Cut-off:June, 2008)

Overall survival (OS) is defined as the time from date of randomization to date of death due to any cause. If a participant is not known to have died, survival will be censored at the date of last contact. (NCT00471328)
Timeframe: Up to 16 months

Interventiondays (Median)
Nilotinib332.0
Control/Cross Over to Nilotinib280.0

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Overall Clinical Benefit (Complete Response [CR]/Partial Response [PR] or Stable Disease [SD]) From Central Radiology Review Based on Primary Analysis (Data Cut-off: June, 2008)

The overall clinical benefit includes the best overall responses of CR, PR, or SD. The best overall responses of CR/PR must be confirmed by at least two determinations at least 4 weeks apart before progression. The best overall response of SD must have at least one SD (or better) at least 6 weeks (or 6 months or 12 months as applicable) after randomization but before progression. (NCT00471328)
Timeframe: Up to 16 months

,
InterventionPercentage of Participants (Number)
CR/PR/SDCR/PR/SD lasting > 6 monthsCR/PR/SD lasting > 12 months
Control/Cross Over to Nilotinib44.61.20
Nilotinib52.77.30.6

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Overall Clinical Benefit (Complete Response [CR]/Partial Response [PR] or Stable Disease [SD]) From Local Investigator's Assessment Based on Treatment Crossover Analysis Set

The overall clinical benefit includes the best overall responses of CR, PR, or SD. The best overall responses of CR/PR must be confirmed by at least two determinations at least 4 weeks apart before progression. The best overall response of SD must have at least one SD (or better) at least 6 weeks (or 6 months or 12 months as applicable) after randomization but before progression. (NCT00471328)
Timeframe: Up to 34 months

InterventionPercentage of Participants (Number)
CR/PR/SDCR/PR/SD lasting > 6 monthsCR/PR/SD lasting > 12 months
Control/Cross Over to Nilotinib37.37.56.0

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Number of Responders With Confirmed Best Overall Response of Complete Response (CR) or Partial Response (PR) From Central Radiology Review During Primary Analysis (Data Cut-off: June, 2008)

The best overall response is the best response recorded from randomization until disease progression. The CR/PR must be confirmed by at least two determinations at least 4 weeks apart before progression. Using modified RECIST criteria, a Complete Response is defined as disappearance of all lesions, and a Partial Response is defined as either 1) at least a 30% decrease in the sum of the longest diameter of target lesions and no new lesions or progression of non-target lesions or 2) disappearance of all target lesions but persistence of one or more non-target lesion(s). (NCT00471328)
Timeframe: Up to 16 months

InterventionParticipants (Number)
Nilotinib1
Control/Cross Over to Nilotinib0

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Rate of a ≥ 4 Log Reduction in BCR-ABL Transcripts in Nilotinib Treatment Arms With Imatinib

Molecular response of <=0.01% is defined as BCR-ABL ratio (%) on IS <= 0.01% (corresponds to >=4 log reduction of BCR-ABL transcripts from standardized baseline value) (NCT00471497)
Timeframe: at 6, 12, 24, 36, 48, 60, 72, 84, 96, 108 and 120 months

,,
InterventionPercentage of participants (Number)
Molecular response of <=0.01% at 6 monthsMolecular response of <=0.01% at 12 monthsMolecular response of <=0.01% at 24 monthsMolecular response of <=0.01% at 36 monthsMolecular response of <=0.01% at 48 monthsMolecular response of <=0.01% at 60 monthsMolecular response of <=0.01% at 72 monthsMolecular response of <=0.01% at 84 monthsMolecular response of <=0.01% at 96 monthsMolecular response of <=0.01% at 108 monthsMolecular response of <=0.01% at 120 months
Imatinib 400 mg QD1.13.910.214.119.831.127.229.028.332.228.3
Nilotinb 300 mg BID8.912.124.529.433.047.944.342.939.740.435.5
Nilotinib 400 mg BID5.78.922.123.829.943.445.240.638.134.933.8

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Rate of Complete Cytogenetic Response (CCyR) on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)

Rate of CCyR is defined as the percentage of participants in complete cytogenetic response (CCyR). CcyR is defined as 0% of Ph+ metaphases in the bone marrow. (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD72.9
Nilotinb 300 mg BID73.1
Nilotinib 400 mg BID66.7

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Rate of Major Molecular Response (MMR) on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)

Rate of MMR is defined as the percentage pf participants in MMR (reduction of ≥ 3 logs in BCR-ABL transcripts compared to the standardized baseline established in IRIS, or ≤ 0.1% BCR-ABL/ABL % by international scale and measured by real-time quantitative polymerase chain reaction (RQ-PCR)) (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD64.6
Nilotinb 300 mg BID73.1
Nilotinib 400 mg BID66.7

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Rate of Hematologic Response on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)

Rate of hematologic response is defined as the percentage of participants in complete hematologic response (defined as the following present for at least 4 weeks: WBC count <10 x 109/L, Platelet count <450 x 109/L, Basophils <5%, No blasts and promyelocytes in peripheral blood, Myelocytes + metamyelocytes < 5% in peripheral blood, No evidence of extramedullary disease, including spleen and liver). (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD83.3
Nilotinb 300 mg BID84.6
Nilotinib 400 mg BID66.7

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Actual Dose-intensity

Actual dose intensity is defined as total dose over time on treatment (NCT00471497)
Timeframe: approx. 11 years

Interventionmg/day (Median)
Imatinib 400 mg QD400.0
Nilotinb 300 mg BID591.1
Nilotinib 400 mg BID758.9

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Duration of CCyR

Duration of CCyR is defined as the time from date of first documented CCyR to the earliest date of loss of CCyR. (NCT00471497)
Timeframe: up to 72 months

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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All Collected Deaths

On treatment deaths were collected from first patient first visit up to 28 days after study treatment discontinuation (approx. 11 years). Patients with cancer were also followed up for overall survival until the end of the trial (to collect any deaths occurring more than 28 days after study drug discontinuation). In this study, one death was collected after randomization but before the participant received study drug. (NCT00471497)
Timeframe: From FPFV up to 28 days post treatment (approx. 11 years), From FPFV to LPLV (approx. 12 years)

,,
Interventiondeaths (Number)
On-treatment deathsTotal deaths
Imatinib 400 mg QD429
Nilotinb 300 mg BID1032
Nilotinib 400 mg BID523

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Duration of Both a ≥ 4 and ≥ 4.5 Log Reduction in BCR-ABL Transcripts

It is defined as the time from the date of first documented BCR-ABL ratio of ≤ 0.01% and ≤ 0.0032% to the earliest of the following: Loss of BCR-ABL ratio of ≤ 0.01% and ≤ 0.0032%, respectively, CML-related death or progression to AP/BC during study treatment. The time will be censored at last molecular assessment (PCR) date for patients for whom none of the above events is reported. (NCT00471497)
Timeframe: approx. 11 years

,,
InterventionMonths (Median)
duration of first molecular response of <=0.01%duration of first molecular response of <=0.0032%
Imatinib 400 mg QDNANA
Nilotinb 300 mg BIDNANA
Nilotinib 400 mg BIDNANA

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Percentage of Participants With MMR at 12 Months Between All 3 Arms by Sokal Risk Group With Imputation

MMR is defined as the percentage of participants in MMR (reduction of ≥ 3 logs in BCR-ABL transcripts compared to the standardized baseline established in IRIS, or ≤ 0.1% BCR-ABL/ABL % by international scale and measured by real-time quantitative polymerase chain reaction (RQ-PCR)) at 12 months. (NCT00471497)
Timeframe: 12 months

,,
InterventionPercentage of participants (Number)
Sokal risk group = LowSokal risk group = Interm.Sokal risk group = High
Imatinib 400 mg QD26.022.816.7
Nilotinb 300 mg BID40.850.541.0
Nilotinib 400 mg BID53.440.032.1

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Pharmacokinetics: Cmin

Cmin is defined as the minimum serum concentration after dose (NCT00471497)
Timeframe: any day after day 8 up to cycle 12 (each cycle = 28 days) and after at least 3 consecutive days without dose interruption or dose modification at pre-dose (0 hour), 1 hour, 2 hours, 3 hours, 5 hours, 8 hours, and 12 hours after dose administration

Interventionng/mL (Median)
Nilotinb 300 mg BID1430
Nilotinib 400 mg BID915

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Rate of a ≥ 4.5 Log Reduction in BCR-ABL Transcripts in Nilotinib Treatment Arms With Imatinib

This is the molecular response of <=0.0032% is defined as BCR-ABL ratio (%) on IS <= 0.0032% (corresponds to >=4.5 log reduction of BCR-ABL transcripts from standardized baseline value) (NCT00471497)
Timeframe: at 6, 12, 24, 36, 48, 60, 72, 84, 96, 108 and 120 months

,,
InterventionPercentage of participants (Number)
Molecular response of <=0.0032% at 6 monthsMolecular response of <=0.0032% at 12 monthsMolecular response of <=0.0032% at 24 monthsMolecular response of <=0.0032% at 36 monthsMolecular response of <=0.01032 at 48 monthsMolecular response of <=0.0032% at 60 monthsMolecular response of <=0.0032% at 72 monthsMolecular response of <=0.0032% at 84 monthsMolecular response of <=0.01% at 96 monthsMolecular response of <=0.0032% at 108 monthsMolecular response of <=0.0032% at 120 months
Imatinib 400 mg QD0.00.42.88.110.219.818.019.123.324.021.2
Nilotinb 300 mg BID3.54.612.413.816.332.331.231.631.931.927.0
Nilotinib 400 mg BID1.45.07.812.117.129.528.828.832.428.125.6

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Time to Both a ≥ 4 and ≥ 4.5 Log Reduction in BCR-ABL Transcripts

Time to BCR-ABL ratio of ≤ 0.01% and ≤ 0.0032% is defined as: date of first BCR-ABL ratio of ≤ 0.01% and ≤ 0.0032% - date of randomization +1. (NCT00471497)
Timeframe: up to 84 months

,,
InterventionMonths (Median)
time to first molecular response of <=0.01%time to first molecular response of <=0.0032%
Imatinib 400 mg QD30.4637.29
Nilotinb 300 mg BID19.3832.46
Nilotinib 400 mg BID22.7035.94

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Rate of Complete Cytogenetic Response (CCyR) in Nilotinib Treatment Arms With Imatinib at 12 Months and Beyond 12 Months

"CCyR is defined as 0% Ph+ metaphases based on at least 20 metaphases from bone marrow cytogenetics. Patients with no CCyR as the best response by any specific time point, all missing cytogenetic evaluations by that time point or Ph- at baseline are combined as Nocomplete cytogenetic response." (NCT00471497)
Timeframe: 12, 24, 36, 48, 60, 72 months (M)

,,
InterventionPercentage of participants (Number)
CCyR at M12CCyR at M24CCyR at M36CCyR at M48CCyR at M60CCyR at M72
Imatinib 400 mg QD55.561.514.111.32.51.8
Nilotinb 300 mg BID70.266.09.28.92.81.8
Nilotinib 400 mg BID68.766.212.813.52.82.8

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Rate of Hematologic Response

Rate of hematologic response is defined as the percentage of participants in complete hematologic response (defined as the following present for at least 4 weeks: WBC count <10 x 109/L, Platelet count <450 x 109/L, Basophils <5%, No blasts and promyelocytes in peripheral blood, Myelocytes + metamyelocytes < 5% in peripheral blood, No evidence of extramedullary disease, including spleen and liver). (NCT00471497)
Timeframe: 12 months, 24 months, Overall on Core study (approx. 11 years)

,,
InterventionPercentage of participants (Number)
Complete hematologic response (CHR) by M12CHR by M24CHR Overall
Imatinib 400 mg QD93.393.694.0
Nilotinb 300 mg BID90.190.892.2
Nilotinib 400 mg BID89.090.490.7

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Rate of MMR at 6 Months and Beyond in All 3 Treatment Arms

MMR is defined as the percentage of participants in MMR (reduction of ≥ 3 logs in BCR-ABL transcripts compared to the standardized baseline established in IRIS, or ≤ 0.1% BCR-ABL/ABL % by international scale and measured by real-time quantitative polymerase chain reaction (RQ-PCR)) at 6 months and beyond up to 120 months based on final data. (NCT00471497)
Timeframe: 6, 12, 24, 36, 48, 60, 72, 84, 96, 108 and 120 months

,,
InterventionPercentage of participants (Number)
MMR at M6MMR at M12MMR at M24MMR at M36MMR at M48MMR at M60MMR at M72MMR at M84MMR at M96MMR at M108MMR at M120
Imatinib 400 mg QD12.022.337.538.543.849.141.740.337.537.536.4
Nilotinb 300 mg BID33.044.761.759.259.962.852.550.046.143.337.9
Nilotinib 400 mg BID29.543.159.157.355.261.257.750.946.340.239.1

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Time to Progression to AP/BC

Time to progression to AP/BC is defined as the time from the date of randomization to the date of event defined as the first documented disease progression to AP/BC or the date of CML related death. (NCT00471497)
Timeframe: approx. 11 years

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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Rates of Durable MMR at 24 Months Between All 3 Arms

Durable MMR at 24 months is defined as having MMR both at 12 months and at 24 months, and with no documented loss of MMR between these 12 month and 24 month time points. (NCT00471497)
Timeframe: 24 months

InterventionPercentage of participants (Number)
Imatinib 400 mg QD20.5
Nilotinb 300 mg BID41.8
Nilotinib 400 mg BID39.1

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Rate of Major Molecular Response (MMR) at 12 Months Between Two Nilotinib Arms

MMR is defined as the percentage of participants in MMR (reduction of ≥ 3 logs in BCR-ABL transcripts compared to the standardized baseline established in IRIS, or ≤ 0.1% BCR-ABL/ABL % by international scale and measured by real-time quantitative polymerase chain reaction (RQ-PCR)) at 12 months based on 12-month cut-off interim data. (NCT00471497)
Timeframe: 12 months

InterventionPercentage of participants (Number)
Nilotinb 300 mg BID44.3
Nilotinib 400 mg BID42.7

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Time to First MMR

Time to MMR is defined as time from date of randomization to the date of the first documented MMR in nilotinib treatment arms, compared to imatinib in adult patients with Ph+ CML in CP. (NCT00471497)
Timeframe: up to 84 months

InterventionMonths (Median)
Imatinib 400 mg QD14.13
Nilotinb 300 mg BID8.31
Nilotinib 400 mg BID8.53

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Time to Complete Cytogenic Response (CCyR)

Time to CCyR is defined as the time from the date of randomization to the date of first documented CCyR (NCT00471497)
Timeframe: 24 months

InterventionMonths (Median)
Imatinib 400 mg QD8.5
Nilotinb 300 mg BID5.7
Nilotinib 400 mg BID5.7

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Progression-free Survival (PFS)

Progression-free survival is defined as the time from the date of randomization to the date of event defined as the first documented disease progression to AP/BC or the date of death from any cause occurring in the core or extension study, or during the follow-up period after discontinuation of core or extension study (NCT00471497)
Timeframe: approx. 11 years

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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Rate of a ≥ 4 Log Reduction in BCR-ABL Transcripts on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)

Molecular response of <=0.01% is defined as BCR-ABL ratio (%) on IS <= 0.01% (corresponds to >=4 log reduction of BCR-ABL transcripts from standardized baseline value) (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD43.8
Nilotinb 300 mg BID57.7
Nilotinib 400 mg BID33.3

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Rate of ≥ 4.5 Log Reduction in BCR-ABL Transcripts on Nilotinib 400 mg BID Therapy After Insufficient Response During Core Treatment and Switch to Extension Phase (Extension)

Molecular response of <=0.0032% is defined as BCR-ABL ratio (%) on IS <= 0.0032% (corresponds to >=4.5 log reduction of BCR-ABL transcripts from standardized baseline value) (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD35.4
Nilotinb 300 mg BID38.5
Nilotinib 400 mg BID33.3

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Presence of Newly Observed BCR-ABL Mutations in Patients Post-baseline and Correlate With Response to Treatment With Imatinib and Nilotinib (Extension)

This is the percentage of patients with any emergent mutation on extension treatment. The mutation comprised of T315T, less sensitive to nilotinib, unknown and sensitive to nilotinib. (NCT00471497)
Timeframe: Overall for Extension study for approx. 10 years

InterventionPercentage of participants (Number)
Imatinib 400 mg QD20.8
Nilotinb 300 mg BID11.5
Nilotinib 400 mg BID33.3

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Pharmacokinetics: Tmax

Tmax is defined as the sampling time when maximum measured serum concentration occurs (NCT00471497)
Timeframe: any day after day 8 up to cycle 12 (each cycle = 28 days) and after at least 3 consecutive days without dose interruption or dose modification at pre-dose (0 hour), 1 hour, 2 hours, 3 hours, 5 hours, 8 hours, and 12 hours after dose administration

Interventionhour (h) (Median)
Nilotinb 300 mg BID1.47
Nilotinib 400 mg BID1.50

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Pharmacokinetics: Cmax

Cmax is defined as the maximum serum concentration after dose (NCT00471497)
Timeframe: any day after day 8 up to cycle 12 (each cycle = 28 days) and after at least 3 consecutive days without dose interruption or dose modification at pre-dose (0 hour), 1 hour, 2 hours, 3 hours, 5 hours, 8 hours, and 12 hours after dose administration

Interventionng/mL (Median)
Nilotinb 300 mg BID1555
Nilotinib 400 mg BID1440

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Pharmacokinetics: AUC0-last

AUC0-last is defined as area under concentration-time curve from time zero to the last measurable sample, calculated by log-linear trapezoidal method (NCT00471497)
Timeframe: any day after day 8 up to cycle 12 (each cycle = 28 days) and after at least 3 consecutive days without dose interruption or dose modification at pre-dose (0 hour), 1 hour, 2 hours, 3 hours, 5 hours, 8 hours, and 12 hours after dose administration

Interventionh.ng/mL (Median)
Nilotinb 300 mg BID14446
Nilotinib 400 mg BID11689

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Overall Survival (OS)

OS is defined as the time from the date of randomization to the date death. Up to 10 calendar years of follow up from the date when the last patient randomized received the first dose of study drug in all active treatment arms of adult patients with Ph+ CML CP. (NCT00471497)
Timeframe: approx. 11 years

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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Major Molecular Response Rate (MMR) at 12 Months Between All 3 Arms - With Imputation

MMR is defined as the percentage of participants in MMR (reduction of ≥ 3 logs in BCR-ABL transcripts compared to the standardized baseline established in IRIS, or ≤ 0.1% BCR-ABL/ABL % by international scale and measured by real-time quantitative polymerase chain reaction (RQ-PCR)) at 12 months. (NCT00471497)
Timeframe: Baseline, 12 months

InterventionPercentage of participants (Number)
Imatinib 400 mg QD22.3
Nilotinb 300 mg BID44.3
Nilotinib 400 mg BID42.7

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Event-free Survival (EFS)

Event-free survival is defined as the time from the date of randomization to the date of first occurrence of any of the following: death due to any cause (if death is the primary reason for discontinuation), progression to AP or BC, loss of PCyR, loss of CCyR, loss of CHR (NCT00471497)
Timeframe: approx. 11 years

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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Duration of MMR

Duration of MMR for patients with MMR is defined as the time between date of MMR and the earliest of the following: loss of MMR, CML-related death or progression to AP/BC during study treatment The time will be censored at last molecular assessment (PCR) date for patients for whom none of the above events is reported. (NCT00471497)
Timeframe: approx. 11 years

InterventionMonths (Median)
Imatinib 400 mg QDNA
Nilotinb 300 mg BIDNA
Nilotinib 400 mg BIDNA

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Number of Patients With Adverse Events (AEs), Serious Adverse Events (SAEs) and Death During the Core

In this analysis patients with all (serious and non -serious) adverse events, and death were reported. See Safety Section. (NCT00477269)
Timeframe: 6 months

,
Interventionparticipants (Number)
Paients with AE(s)DeathSAE(s)
Placebo29311
STI57127312

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Number of Patients With Adverse Events (AEs), Serious Adverse Events (SAEs) and Death During the Extension

In this analysis patients with all (serious and non -serious) adverse events, and death were reported. See Safety Section. (NCT00477269)
Timeframe: 72 months

Interventionparticipants (Number)
Any AE(s)DeathSAE(s)
All Patients22416

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Blood Gas Measurement - PvO2 at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including PvO2 levels at baseline and Study completion Week 24. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline n=14,14Week 24 n=11,11
Placebo34.7032.65
STI57133.1635.56

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Blood Gas Measurement - pH at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including pH levels at baseline and Study completion Week 24. The pH scale measures how acidic or basic a substance is. It ranges from 0 to 14. A pH of 7 is neutral. A pH less than 7 is acidic, and a pH greater than 7 is basic. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionpH scale (Mean)
Baseline n=24,23Week 24 n=17,17
Placebo7.447.46
STI5717.437.44

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Blood Gas Measurement - PaO2 at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including PaO2 levels at baseline and Study completion Week 24. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline n=22,21Week 24 n=16,17
Placebo63.7570.13
STI57163.3672.49

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Blood Gas Measurement - PaCO2 at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including PaCO2 levels at baseline and Study completion Week 24. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline n=23,21Week 24 n=16,17
Placebo30.0230.23
STI57132.7033.36

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Blood Gas Measurement - Arterial Saturation at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including Arterial Saturation levels at baseline and Study completion Week 24. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
Interventionpercentage of saturation (Mean)
Baseline n=19,16Week 24 n=14,15
Placebo91.8191.78
STI57187.9992.89

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Mean Pulmonary Artery Pressure (PAP) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including right Pulmonary Arterial Pressure (PAP). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline breathing ambient air (n=27,28)Baseline every 2 mins breathing NO (1st) (n=20,20)Baseline every 2 mins breathing NO (2nd) (n=17,18)Baseline 5 mins after NO administration (n=20,14)Baseline 15 mins after NO administration(n=19,19)Week 24 breathing ambient air (n=20,22)Week 24 every 2 mins breathing NO (1st) (n=10,13)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=10,12)Week 24 15 mins after NO administration (n=10,14)
Placebo59.255.753.356.956.555.555.153.957.557.2
STI57161.761.658.160.960.352.550.946.247.048.1

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Change From Baseline of Six Minute Walk Test - Number of Stops at Different Time Periods

The Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Number of stops were recorded for each patient. (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
Interventionnumber of stops (Mean)
Day 32 (n=25,27)week 8 (n=23,24)week 12 (n=22,24)week 16 (n=19, 23)week 20 (n=19, 21)study completion Week 24 (n=21, 12)
Placebo0.10.00.30.00.3-0.1
STI571-0.2-0.2-0.3-0.3-0.4-0.3

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Borg Score-Systolic Blood Pressure During the Six Minutes Walk Test at Different Time Periods

Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. During the walk the patient was connected to a portable pulse oximeter via a finger probe. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Systolic blood pressure (mmHg) were recorded before the test at resting, at the end of the test and two minutes after the end of the test (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline: Resting (n= 26, 28)Baseline: End of Test (n= 21, 26)Baseline: 2 minutes after end of test (n=25, 27)Day 32: Resting (n= 25, 27)Day 32: End of Test (n= 22, 22)Day 32: 2 minutes after end of test (n= 25, 26)Week 8: Resting (n= 22, 24)Week 8: End of Test (n= 19, 20)Week 8: 2 minutes after end of test (n= 23, 24)Week 12: Resting (n= 22, 23)Week 12: End of Test (n= 17, 19)Week 12: 2 minutes after end of test (n= 20, 22)Week 16: Resting (n= 19, 22)Week 16: End of Test (n= 15,18)Week 16: 2 minutes after end of test (n= 19, 22)Week 20: Resting (n= 19, 20)Week 20: End of Test (n= 16,17)Week 20: 2 minutes after end of test (n= 19, 20)Week 24: Resting (n= 20, 21)Week 24: End of Test (n= 16, 17)Week 24: 2 minutes after end of test (n= 20, 19)
Placebo104.6118.3110.4106.0122.3113.8107.3119.9114.5107.7118.8115.9105.7119.8112.6109.1119.9115.1108.2116.8111.1
STI571111.3119.9120.0111.4126.5119.6108.9124.6115.2106.5122.2115.9106.7117.2114.6106.5122.4115.5110.6126.9118.2

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Borg Score-Oxygen Saturation(SaO2) During the Six Minutes Walk Test at Different Time Periods

Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. During the walk the patient was connected to a portable pulse oximeter via a finger probe. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. The test was terminated if the patient became too distressed or if their SaO2% fell below 60%. (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
InterventionPercentage of Oxygen Saturation (Mean)
Baseline: Resting (n= 28, 29)Baseline: End of Test (n= 28, 28)Baseline: 2 minutes after end of test (n=26, 26)Day 32: Resting (n= 25, 28)Day 32: End of Test (n= 25, 28)Day 32: 2 minutes after end of test (n= 25, 26)Week 8: Resting (n= 23, 25)Week 8: End of Test (n= 23, 24)Week 8: 2 minutes after end of test (n= 23, 23)Week 12: Resting (n= 22, 25)Week 12: End of Test (n= 20, 24)Week 12: 2 minutes after end of test (n= 19, 22)Week 16: Resting (n= 19, 24)Week 16: End of Test (n= 18, 23)Week 16: 2 minutes after end of test (n= 19, 19)Week 20: Resting (n= 19, 22)Week 20: End of Test (n= 18, 21)Week 20: 2 minutes after end of test (n= 19, 21)Week 24: Resting (n= 20, 22)Week 24: End of Test (n= 20, 21)Week 24: 2 minutes after end of test (n= 20, 21)
Placebo93.487.992.092.487.292.793.287.993.193.989.694.294.188.193.393.787.693.494.389.394.8
STI57194.387.993.094.589.094.895.190.994.495.189.892.795.087.994.694.087.593.895.589.994.8

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Borg Score-Heart Rate (HR) During the Six Minutes Walk Test at Different Time Periods

Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. During the walk the patient was connected to a portable pulse oximeter via a finger probe. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Heart Rate (bpm) were recorded before the test at resting, at the end of the test and two minutes after the end of the test (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
Interventionbeats per minute (bpm) (Mean)
Baseline: Resting (n= 28, 29)Baseline: End of Test (n= 28, 29)Baseline: 2 minutes after end of test (n=26, 26)Day 32: Resting (n= 25, 28)Day 32: End of Test (n= 25, 28)Day 32: 2 minutes after end of test (n= 25, 26)Week 8: Resting (n= 23, 25)Week 8: End of Test (n= 23, 24)Week 8: 2 minutes after end of test (n= 23, 23)Week 12: Resting (n= 22, 25)Week 12: End of Test (n= 20, 25)Week 12: 2 minutes after end of test (n= 19, 22)Week 16: Resting (n= 19, 24)Week 16: End of Test (n= 18, 23)Week 16: 2 minutes after end of test (n= 19, 21)Week 20: Resting (n= 19, 22)Week 20: End of Test (n= 18,22)Week 20: 2 minutes after end of test (n= 19, 21)Week 24: Resting (n= 20, 22)Week 24: End of Test (n= 20, 21)Week 24: 2 minutes after end of test (n= 20, 21)
Placebo87.9112.394.183.6113.190.681.1110.388.985.1113.089.484.4117.985.580.2118.087.383.6116.888.9
STI57180.8106.384.280.7108.489.280.3109.585.376.5105.383.876.5102.885.875.3109.283.379.5110.287.9

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Mean Cardiac Output (CO) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Cardiac Output (CO). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionL/min (Mean)
Baseline breathing ambient air (n=27,28)Baseline every 2 mins breathing NO (1st) (n=19,20)Baseline every 2 mins breathing NO (2nd) (n=17,18)Baseline 5 mins after NO administration (n=19,14)Baseline 15 mins after NO administration(n=18,19)Week 24 breathing ambient air (n=20,22)Week 24 every 2 mins breathing NO (1st) (n=10,13)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=10,12)Week 24 15 mins after NO administration (n=10,14)
Placebo4.094.224.434.714.474.354.674.624.654.46
STI5714.204.023.984.203.874.904.804.794.634.48

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Mean Heart Rate (HR) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Heart Rate (HR). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
Interventionbeats per minute (bpm) (Mean)
Baseline breathing ambient air (n=27,28)Baseline every 2 mins breathing NO (1st) (n=20,19)Baseline every 2 mins breathing NO (2nd) (n=17,17)Baseline 5 mins after NO administration (n=19,15)Baseline 15 mins after NO administration(n=18,19)Week 24 breathing ambient air (n=20,22)Week 24 every 2 mins breathing NO (1st) (n=9,13)Week 24 every 2 mins breathing NO (2nd) (n=8,11)Week 24 5 mins after NO administration (n=9,12)Week 24 15 mins after NO administration (n=10,14)
Placebo84.984.483.384.385.183.082.582.879.382.9
STI57177.375.975.273.276.276.676.376.675.773.2

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Blood Gas Measurement - Venous Saturation at Baseline and Study Completion

The right heart catheter assessment was performed to assess Blood Gas Measurements in pulmonary hypertension, including Venous Saturation levels at baseline and Study completion Week 24. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
Interventionpercentage of saturation (Mean)
Baseline n=17,14Week 24 n=13,13
Placebo60.8457.00
STI57157.9665.11

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Mean Pulmonary Artery Wedge Pressure (PAWP) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Pulmonary Arterial Wedge Pressure (PAWP). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline breathing ambient air (n=26,28)Baseline every 2 mins breathing NO (1st) (n=20,17)Baseline every 2 mins breathing NO (2nd) (n=17,16)Baseline 5 mins after NO administration (n=19,12)Baseline 15 mins after NO administration(n=18,17)Week 24 breathing ambient air (n=19,22)Week 24 every 2 mins breathing NO (1st) (n=9,13)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=10,12)Week 24 15 mins after NO administration (n=10,14)
Placebo7.67.77.87.88.18.610.210.010.310.4
STI5719.09.59.49.59.68.47.97.07.16.7

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Number of Patients With Pulmonary Hypertension (PAH) Assessd by World Health Organization (WHO) Classification on Physical Activity

PAH assessed according to the WHO classification: Class I Patients with PAH but without resulting limitation of physical activity. Ordinary physical activity does not cause undue dyspnea or fatigue, chest pain or near syncope. Class II Patients with PAH resulting in slight limitation of physical activity. They are comfortable at rest. Ordinary physical activity causes undue dyspnea or fatigue, chest pain or near syncope. Class III Patients with PAH resulting in marked limitation of physical activity. They are comfortable at rest. Less than ordinary activity causes undue dyspnea or fatigue, chest pain or near syncope. Class IV Patients with PAH with inability to carry out any physical activity without symptoms. These patients manifest signs of right heart failure. Dyspnea and/or fatigue may even be present at rest. Discomfort is increased by any physical activity. (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion

,
Interventionnumber of participants (Number)
Baseline: WHO Class IV (n=27,30)Baseline: WHO Class III (n=27,30)Baseline: WHO Class II (n=27,30)Day 32: WHO Class IV (n=27,30)Day 32: WHO Class III (n=27,30)Day 32: WHO Class II (n=27,30)Week 8: WHO Class IV (n=24,27)Week 8: WHO Class III (n=24,27)Week 8: WHO Class II (n=24,27)Week 12: WHO Class IV (n=23,27)Week 12: WHO Class III (n=23,27)Week 12: WHO Class II (n=23,27)Week 16: WHO Class IV (n=22,27)Week 16: WHO Class III (n=22,27)Week 16: WHO Class II (n=22,27)Week 16: WHO Class I (n=22,27)Week 20: WHO Class IV (n=19,24)Week 20: WHO Class III (n=19,24)Week 20: WHO Class II (n=19,24)Week 20: WHO Class I (n=19,24)Week 24: WHO Class IV (n=21,25)Week 24: WHO Class III (n=21,25)Week 24: WHO Class II (n=21,25)
Placebo1227321612061179118711149021310
STI5712141131113391201211011110010811128

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Mean Pulmonary Vascular Resistance (PVR) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Pulmonary Vascular Resistance (PVR). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. PVR calculated according to the equation:PVR = (PAP - PCWP)/CO (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
Interventiondyn*s/cm^5 (Mean)
Baseline breathing ambient air (n=27,27)Baseline every 2 mins breathing NO (1st) (n=19,17)Baseline every 2 mins breathing NO (2nd) (n=17,16)Baseline 5 mins after NO administration (n=19,11)Baseline 15 mins after NO administration(n=18,16)Week 24 breathing ambient air (n=19,21)Week 24 every 2 mins breathing NO (1st) (n=9,14)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=10,12)Week 24 15 mins after NO administration (n=10,14)
Placebo1118.31067.9982.81160.41132.91017.01000.61033.6987.81042.5
STI5711124.41180.91064.61131.51181.9729.9706.9687.4717.2776.1

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Borg Score-Diastolic Blood Pressure During the Six Minutes Walk Test at Different Time Periods

Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. During the walk the patient was connected to a portable pulse oximeter via a finger probe. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Diastolic blood pressure (mmHg) were recorded before the test at resting, at the end of the test and two minutes after the end of the test (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline: Resting (n= 26, 28)Baseline: End of Test (n= 21, 26)Baseline: 2 minutes after end of test (n=25, 27)Day 32: Resting (n= 25, 27)Day 32: End of Test (n= 22, 22)Day 32: 2 minutes after end of test (n= 25, 26)Week 8: Resting (n= 22, 24)Week 8: End of Test (n= 19, 20)Week 8: 2 minutes after end of test (n= 23, 24)Week 12: Resting (n= 22, 23)Week 12: End of Test (n= 17, 19)Week 12: 2 minutes after end of test (n= 20, 22)Week 16: Resting (n= 19, 22)Week 16: End of Test (n= 15,18)Week 16: 2 minutes after end of test (n= 19, 22)Week 20: Resting (n= 19, 20)Week 20: End of Test (n= 16,17)Week 20: 2 minutes after end of test (n= 19, 20)Week 24: Resting (n= 20, 21)Week 24: End of Test (n= 16, 17)Week 24: 2 minutes after end of test (n= 20, 19)
Placebo67.969.567.968.475.270.768.874.072.270.672.472.066.776.770.569.872.972.770.772.372.9
STI57168.275.171.669.678.272.567.774.871.265.575.673.167.772.771.467.272.971.969.774.171.3

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Change From Baseline of Six Minute Walk Test - Total Duration of Stops at Different Time Periods

The Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. If the patient stopped the duration of each stop was recorded. (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
Interventionminutes (Mean)
Day 32 (n=25,27)week 8 (n=23,24)week 12 (n=22,24)week 16 (n=19, 23)week 20 (n=19, 21)study completion Week 24 (n=21, 12)
Placebo0.120.070.190.060.120.03
STI571-0.06-0.03-0.03-0.03-0.05-0.02

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Change From Baseline of Six Minute Walk Test - Total Distance Walked at Different Time Periods

The Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Distance <500 meters suggests considerable exercise limitation; Distance 500-800 meters suggests moderate limitation; Distance >800 meters (with no rests) suggests mild or no limitation. (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
Interventionmeters (Mean)
Day 32 (n=25,27)week 8 (n=23,24)week 12 (n=22,24)week 16 (n=19, 23)week 20 (n=19, 21)study completion Week 24 (n=21, 12)
Placebo8.215.57.812.112.8-1.0
STI57110.217.02125.538.322.0

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Mean Systemic Vascular Resistance (SVR) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Systemic Vascular Resistance (SVR). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. SVR was calculated according to the equation: SVR = (Paorta - Pright atrium)/CO (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
Interventiondyn*s/cm^5 (Mean)
Baseline breathing ambient air (n=26,26)Baseline every 2 mins breathing NO (1st) (n=18,15)Baseline every 2 mins breathing NO (2nd) (n=16,14)Baseline 5 mins after NO administration (n=18,11)Baseline 15 mins after NO administration(n=17,15)Week 24 breathing ambient air (n=18,21)Week 24 every 2 mins breathing NO (1st) (n=9,13)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=9,12)Week 24 15 mins after NO administration (n=10,14)
Placebo1764.81769.71664.71666.61748.41667.91579.31592.51503.91629.3
STI5711674.41778.21807.31609.21976.31427.21344.21367.91419.71431.7

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Mean Systolic Arterial Pressure (SAP) at Baseline and Study Completion

The right heart catheter assessment was performed to assess several prognostic hemodynamic variables in pulmonary hypertension, including Systolic Arterial Pressure (SAP). Were assessed when the patient was in a stable hemodynamic rest state (as demonstrated by three consecutive Mean PAP and CO measurements within 10% of each other). PAP was assessed when the patient was breathing ambient air, every 2 minutes whilst breathing Nitric Oxide(NO) (1st and 2nd), 5 min after the end of NO administration, and 15 mins after the end of NO administration. (NCT00477269)
Timeframe: Baseline, and Study completion (Week 24)

,
InterventionmmHg (Mean)
Baseline breathing ambient air (n=26,28)Baseline every 2 mins breathing NO (1st) (n=20,19)Baseline every 2 mins breathing NO (2nd) (n=17,17)Baseline 5 mins after NO administration (n=21,15)Baseline 15 mins after NO administration(n=19,19)Week 24 breathing ambient air (n=20,22)Week 24 every 2 mins breathing NO (1st) (n=10,13)Week 24 every 2 mins breathing NO (2nd) (n=9,11)Week 24 5 mins after NO administration (n=9,12)Week 24 15 mins after NO administration (n=10,14)
Placebo108.2106.9105.4107.1106.9106.9102.9103.6104.0107.3
STI571110.3108.3109.9106.0109.5108.0103.9104.8103.4103.8

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Borg Score During the Six Minutes Walk Test at Different Time Periods

Borg Score during Six Minute Walk test was carried out along a course, such as a hospital corridor, measuring at least 20 meters delineated by markers. During the walk the patient was connected to a portable pulse oximeter via a finger probe. Patients were instructed to walk at a comfortable speed as far as they could manage in six minutes, resting whenever they needed to. Borg Score of Breathlessness was recorded using the following score of 0 to 10, how breathless do you feel? 0 is nothing at all and 10 is maximal breathlessness (NCT00477269)
Timeframe: Baseline, Day 32, Week 8, Week 12, Week 16, Week 20 and Study completion (Week 24)

,
Interventionscore on a scale (Mean)
Baseline: Resting (n= 26, 27)Baseline: End of Test (n= 27, 29)Baseline: 2 minutes after end of test (n=24, 26)Day 32: Resting (n= 25, 27)Day 32: End of Test (n= 25, 28)Day 32: 2 minutes after end of test (n= 25, 26)Week 8: Resting (n= 23, 24)Week 8: End of Test (n= 23, 25)Week 8: 2 minutes after end of test (n= 23, 24)Week 12: Resting (n= 22, 24)Week 12: End of Test (n= 22, 25)Week 12: 2 minutes after end of test (n= 22, 23)Week 16: Resting (n= 19, 23)Week 16: End of Test (n= 18, 23)Week 16: 2 minutes after end of test (n= 19, 23)Week 20: Resting (n= 19, 21)Week 20: End of Test (n= 18,22)Week 20: 2 minutes after end of test (n= 18, 20)Week 24: Resting (n= 20, 21)Week 24: End of Test (n= 20, 21)Week 24: 2 minutes after end of test (n= 20, 20)
Placebo0.433.021.080.483.071.060.382.320.580.462.920.650.502.830.700.673.110.750.402.930.67
STI5710.273.340.880.242.530.650.322.460.320.052.270.350.132.500.410.052.310.310.182.580.29

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Percentage of Participants Remaining in Confirmed Complete Cytogenetic Response (cCCyR)

"Cytogenetic response (CyR) is based on the prevalence of Philadelphia positive (Ph+) cells in metaphase from bone marrow (BM) sample. (Ideally, 25 metaphases but at least 20 metaphases from a BM sample were evaluated). Complete Cytogenetic Response (CCyR)=0% Ph+ cells in metaphase in BM. A cCCyR=those in which all measurements up to at least 28 days after the initial response show an equivalent or better CCyR.~Percentage of participants in cCCyR at years 2, 3, 4 and 5 was computed for all randomized participants who achieved cCCyR as measured from the time of first confirmation until the date of progression or death. Participants with cCCyR who neither progress nor die are censored on the date of their last cytogenetic assessment. Participants without cCCyR are considered to have progressed on Day 1." (NCT00481247)
Timeframe: Years 2, 3, 4 and 5

,
Interventionpercentage of participants (Number)
At Year 2At Year 3At Year 4At Year 5
Dasatinib98.096.995.693.1
Imatinib96.995.795.791.0

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Number of Participants With Grade 3/4 Abnormalities in On-study Laboratory Test Results

ULN=upper limit of normal. Grade 3=Severe AE; Grade 4=Life-threatening or disabling AE. Absolute neutrophil count: Grade 3 <1000-500/mm^3; Grade 4 <500/mm^3. Hemoglobin: Grade 3 <8.0-6.5 g/dL; Grade 4 <6.5 g/dL. Platelets: Grade 3 <50,000-25,000/mm^3; Grade 4 <25,000/mm^3. ALT/AST: Grade 3 >5.0-20*ULN; Grade 4 >20*ULN. Total bilirubin: Grade 3 >3-10*ULN; Grade 4 >10*ULN. Sample normal ranges (may vary by institution): ALT, Female: 7-30 U/L, Male: 10-55 U/L; AST, Female: 9-25 U/L, Male10-40 U/L; Total bilirubin: 0.0-1.0 mg/dL. Creatinine: Grade 3 >3.0-6.0*ULN; Grade 4 >6.0*ULN. Phosphate: Grade 3 <2.0-1.0 mg/dL; Grade 4 <1.0 mg/dL. Calcium: Grade 3 <7.0-6.0 mg/dL; Grade 4 <6.0 mg/dL. Potassium: Grade 3 <3.0-2.5 mmol/L; Grade 4 <2.5 mmol/L. (NCT00481247)
Timeframe: From date of last person, first visit to date of last person, last visit (approximately 8 years)

,
InterventionParticipants (Number)
Grade 3/4 Absolute neutrophil countGrade 3/4 HemoglobinGrade 3/4 PlateletsGrade 3/4 Alanine aminotransferase (ALT)Grade 3/4 Aspartate aminotransferase (AST)Grade 3/4 Total bilirubinGrade 3/4 CreatinineGrade 3/4 PhosphateGrade 3/4 CalciumGrade 3/4 Potassium
Dasatinib74355622331990
Imatinib61233743027978

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Time to Confirmed Complete Cytogenic Response (cCCyR) Overall

"The time to cCCyR for all randomized participants is defined as the time from the randomization date until criteria are first met for complete cytogenic response (provided it is confirmed later). The time to cCCyR analysis censors nonresponders who do not progress at their last cytogenetic assessments and nonresponders who progress at the maximum time of all randomized participants.~." (NCT00481247)
Timeframe: Day 1 to 5 years

InterventionMonths (Median)
Dasatinib3.1
Imatinib5.8

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Percentage of Participants With Progression-free Survival (PFS)

PFS was defined as the time from randomization until progression (any progression/death within 30 days of last dosing date, or between 30-60 days of last dosing prior to start of secondary therapy). Those who did not progress/die or who progressed/died after 60 days of last dose were censored at last on-study hematologic/cytogenetic assessment; those with progression/death 30-60 days of last dosing date and after start date of secondary therapy censored at last on-study hematologic/cytogenetic assessment prior to start of secondary therapy; those who had not received study treatment censored on date randomized. (NCT00481247)
Timeframe: Participants were followed-up for at least 5 years

InterventionPercentage of participants (Number)
Dasatinib88.9
Imatinib89.2

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Percentage of Participants With Overall Survival (OS)

OS was defined as the time from randomization to the date of death. If the participant had not died, survival was censored on last date the participant was known to be alive. (NCT00481247)
Timeframe: Participants were followed-up for at least 5 years

InterventionPercentage of participants (Number)
Dasatinib90.9
Imatinib89.6

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Percentage of Participants With Major Molecular Response (MMR) at Any Time

Molecular response was assessed using BCR-ABL transcript levels measured by realtime quantitative polymerase chain reaction. MMR is defined as a ratio BCR-ABL/ABL ≤0.1% on the international scale (ie, at least 3 log reduction from a standardized baseline value). (NCT00481247)
Timeframe: Planned total follow-up duration of 5 years

InterventionPercentage of participants (Number)
Dasatinib76.4
Imatinib64.2

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Number of Participants With Best Confirmed Complete Cytogenetic Response (cCCyR) Within 12 Months

Cytogenetic response (CyR) is based on the prevalence of Philadelphia positive (Ph+) cells in metaphase from bone marrow (BM) sample. (Ideally, 25 metaphases but at least 20 metaphases from a BM sample were evaluated). Complete Cytogenetic Response (CCyR)=0% Ph+ cells in metaphase in BM. A cCCyR=those in which all measurements up to at least 28 days after the initial response show an equivalent or better CCyR. (NCT00481247)
Timeframe: Pretreatment, every 3 months up to 12 months

InterventionParticipants (Number)
Dasatinib204
Imatinib177

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Time to Major Molecular Response (MMR) Overall

The time to MMR for all randomized participants is defined as the time from randomization date until measurement criteria are first met for MMR. The time to MMR analysis censors nonresponders who do not progress at their last molecular assessments and nonresponders who progress at the maximum time of all randomized participants. (NCT00481247)
Timeframe: Day 1 to 5 years

InterventionMonths (Median)
Dasatinib9.3
Imatinib15.0

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Participant Response Rate

Response rate to regimen defined as the number of complete or partial response divided by the total number of participants treated. Tumor response defined by Response Evaluation Criteria In Solid Tumors (RECIST). All complete and partial responses confirmed by a second assessment six weeks later. (NCT00485485)
Timeframe: At 6 weeks reconfirmed 6 weeks later

InterventionParticipants (Number)
Imatinib Mesylate + Docetaxel7

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Participants' With mCR Response to Post Transplant Imatinib Mesylate Therapy

Number of participants with response of molecular complete remission (mCR) to Imatinib Mesylate therapy as treatment for residual disease after transplant. Molecular remission is a complete remission with no evidence of disease in the blood cells and/or bone marrow using sensitive polymerase chain reaction (PCR) tests. (NCT00499889)
Timeframe: 1 Year

InterventionParticipants (Number)
Mesylate, Busulfan, Fludarabine + Antithymocyte Globulin10

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Participants' With mCR Response to Post Transplant DLI

Number of participants with response of molecular complete remission (mCR) to DLI as treatment for residual disease after transplant. Molecular remission is a complete remission with no evidence of disease in the blood cells and/or bone marrow using sensitive polymerase chain reaction (PCR) tests. (NCT00499889)
Timeframe: 1 year

InterventionParticipants (Number)
Mesylate, Busulfan, Fludarabine + Antithymocyte Globulin4

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Number of Participants in Complete Molecular Remission at 1 Year

Participants at 1 year in molecular remission, post transplant, post imatinib mesylate and donor lymphocyte infusion (DLI). Molecular remission is a complete remission with no evidence of disease in the blood cells and/or bone marrow using sensitive polymerase chain reaction (PCR) tests (this test is most commonly used in clinical trials). (NCT00499889)
Timeframe: Baseline to 1 year

Interventionparticipants (Number)
Mesylate, Busulfan, Fludarabine + Antithymocyte Globulin21

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Number of Participants Achieving Pathological Complete Response

Probability of response, defined as pathological complete remission based on tissue obtained at surgery. Pathological Complete Response (pCR): Patients without gross or microscopic evidence of residual disease at Radical Prostatectomy defined as pCR. (NCT00500110)
Timeframe: Every 3 months for 1 year, then every 6 months until disease progression or death

Interventionparticipants (Number)
Treatment0

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Number of Participants With Complete Response

Complete Response (CR): Disappearance lesions, no evidence new lesions documented by 2 disease assessments> 4 weeks apart. Partial Response (PR):>30% decrease in sum longest dimensions (LD) all target measurable lesions reference baseline sum of LD; No progression non-target lesions & no new lesions; Documentation by 2 disease assessments >4 weeks apart; Progressive Disease (PD) (ANY of following): >20% increase in sum LD of target lesions reference smallest sum LD or appearance of new lesions within 8 weeks of study entry; Unequivocal progression on existing non-target lesions, other than pleural effusions without cytological proof of neoplastic origin, within 8 weeks of study entry also considered increasing disease. Death due to disease without prior objective documentation of progression; Global deterioration in health attributable to disease requiring change in therapy without objective evidence of progression. Stable disease: Any condition not meeting above criteria. (NCT00506779)
Timeframe: 6 weeks to 18 weeks; Best response achieved since study entry where measurable disease defined as => 1 lesion accurately measured in at least 1 dimension (longest dimension to be recorded)

Interventionparticipants (Number)
Participants With Measurable Disease1
Participants With Non-Measurable Disease7

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Number of Participants Who Experienced Dose Limiting Toxicities (DLTs)

"Maximum Tolerated Dose (MTD) of Oral Imatinib Mesylate in Combination with Fixed Dose Paclitaxel where MTD of Imatinib Mesylate (mg/m^2 daily) to be determined with conventional 3+3 design, MTD is highest dose level in which 6 participants treated with at most 2 experiencing dose limiting toxicity (DLT). Study utilizes Common Terminology for Adverse Events Criteria (CTCAE) version 3.0 for adverse event reporting.~Following cohorts of 3 at lower dose levels until 1 of 3 patients experiences DLT; if 1 of 3 patients experiences DLT at dose level, enter 3 additional patients at dose level, if only 1 of 6 patients experiences DLT at dose level, proceed to next higher dose level with cohort of 3; If 2 of 3 or 3 of 6 patients experience DLT, MTD has exceeded. Once DLT exceeded, treat another 3 patients at previous dose if there were only 3 patients treated at that dose level. MTD is highest dose level in which treated 6 patients with at most 2 experiencing the DLT." (NCT00506779)
Timeframe: Evaluated at 3 weeks (one cycle)

Interventionparticipants (Number)
Imatinib Mesylate 400 mg0
Imatinib Mesylate 500 mg1
Imatinib Mesylate 600 mg2

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Cell Types That Contribute to the Gene Expression Changes Associated With Imatinib Therapy

To determine which cell types may be contributing to the gene expression changes associated with imatinib therapy, imatinib-responsive genes were isolated from from patient biopsies. From the total number of imatinib-responsive genes that were isolated, the percentage that came from endothelial cells, fibroblasts, B-cells, and multiple cell types was calculated. Reported values do not total to 100% because of rounding. (NCT00506831)
Timeframe: 6 months compared to baseline

Interventionpercentage of isolated genes (Number)
Endothelial cellsFibroblastsB-cellsMultiple cell types
Imatinib Mesylate1326852

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Percent Change in Modified Rodnan Skin Score at 6 Months Compared to Baseline

Modified Rodnan skin score (mRSS) on scale of 0 (no skin disease) to 51 severe skin disease. %change in mRSS=(score at 6 months - baseline score)/baseline score. Negative values indicate improvement in skin disease. Clinical important improvement defined as > 25% improvement. (NCT00506831)
Timeframe: 6 months compared to baseline

Interventionpercentage of change in MRSS (Mean)
Imatinib Mesylate-32

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Change in Scleroderma Health Assessment Questionnaire at 6 Months Compared to Baseline

Change in Health Assessment Questionnaire disability index at 6 months compared to baseline. The Questionnaire is comprised of a 20 question instrument pertaining to specific activities with possible integer responses of 0 (without any difficulty) to 3 (unable to do), and five additional scleroderma-specific visual analog scale (VAS) domains with possible values ranging from 0.0 to 15.0. The 20 questions are divided into eight domains. A mean score is calculated for each domain ranging from 0 to 3. A composite score is calculated by dividing the summed domain scores by the number of domains answered. The composite score is reported, falling between 0 and 3 on an ordinal scale. The scores are interpreted as 0 (no impairment in function) to 3 (maximal impairment of function). (NCT00506831)
Timeframe: 6 months compared to baseline

Interventionunits on a scale (Mean)
Imatinib Mesylate-.35

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Change in Pulmonary Function Tests at 6 Months Compared to Baseline

Change in % predicted Forced Vital Capacity (FVC) at 6 months compared to baseline. FVC is the volume of air that can forcibly be blown out after taking a full breath. FVC% predicted is defined as FVC% of the patient divided by the average FVC% in the population for any person of similar age, sex and body composition. (NCT00506831)
Timeframe: 6 months compared to baseline

InterventionFVC% predicted (Mean)
Imatinib Mesylate0

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Change in Dermal Thickness and Collagen Separation on Cutaneous Histopathology at 6 Months Compared to Baseline

(NCT00506831)
Timeframe: 6 months compared to baseline

Interventionmm (Number)
Imatinib Mesylate-.5

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Median Progression-free Survival (PFS) for Patients Less Than 60 Years of Age

"PFS measured from the date of Complete Response (CR) to the date of relapse or death. Progression defined as any of the following event: progression to accelerated phase or blast crisis, death, loss of CHR or MCyR, or in patients not achieving a CHR an increasing WBC despite appropriate therapeutic management~This outcome will be reported as median progression-free survival in months for participants less than 60 years of age." (NCT00509093)
Timeframe: up to 5 years from the End of Treatment

Interventionmonths (Median)
Imatinib Mesylate52.1

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Toxicity as Measured by NCI CTC v. 3.0

"Number of patients (%) experiencing an adverse event~See adverse events section for details" (NCT00509093)
Timeframe: 13 months from start of treatment

InterventionParticipants (Count of Participants)
Imatinib Mesylate30

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Percent of Participants Less Than 60 Years of Age With PFS at 8 and 13 Months Post-treatment

Percent of participants less than 60 years of age with PFS at 8 and 13 months post-treatment (NCT00509093)
Timeframe: at 8 and 13 months after treatment.

Interventionpercent of participants (Number)
at 8 months post treatmentat 13 months post treatment
Imatinib Mesylate76.254.5

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Percent of Participants 60 Years of Age or Older With PFS at 8 and 13 Months Post-treatment

Percent of participants 60 years of age or older with PFS at 8 and 13 months post-treatment (NCT00509093)
Timeframe: at 8 and 13 months after treatment.

Interventionpercent of participants (Number)
at 8 months post treatmentat 13 months post treatment
Imatinib Mesylate61.936.4

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Progression-free Survival for Patients 60 Years of Age and Older

Progression free survival will be measured from the date of Complete Response (CR) to the date of relapse or death. (NCT00509093)
Timeframe: up to 5 years from the End of Treatment

Interventionmonths (Median)
Imatinib Mesylate10.7

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Overall Response Rate (ORR)

ORR = participant proportion with responsive disease: Complete Response (CR): disappearance all clinically detectable malignant disease for at least 4 weeks, no new lesions; Partial Response (PR): >/= 50% decrease sum of products of perpendicular diameters of all measurable lesions for at least 4 weeks; Stable Disease: does not qualify for CR, PR or progression. Progressive Disease: a 25% or > increase in sum of products of measurable lesions over smallest sum observed, OR reappearance of lesion which had disappeared, OR appearance of new lesion/site. Response determined every 6 week cycle. (NCT00510653)
Timeframe: 6 weeks with re-evaluation every 6 weeks or until disease progression

Interventionparticipants (Number)
Complete ResponsePartial Response
Imatinib Mesylate00

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Change in Modified Rodnan Skin Score (MRSS)

No measures of dispersion was available as data were lost. The range of this measure is 0 to 51 and measures the extent of skin thickening with higher numbers representing thickening. (NCT00512902)
Timeframe: Baseline vs. Endpoint

Interventionunits on a scale (Mean)
Imatinib3.9

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Change in FVC (Forced Vital Capacity)

Measures the amount of air breathed out as a percent of predicted. (NCT00512902)
Timeframe: Baseline vs. Endpoint (1 year)

InterventionPercent predicted (Mean)
Imatinib1.74

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Change in DLco

DLCO (diffusing capacity or transfer factor of the lung for carbon monoxide (CO)) is the extent to which oxygen passes from the air sacs of the lungs into the blood. Commonly, it refers to the test used to determine this parameter. (NCT00512902)
Timeframe: Baseline vs. Endpoint (1 year)

InterventionPercent predicted (Mean)
Imatinib1.46

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Change in TLC (Total Lung Capacity)

No measures of dispersion was available for TLC as data were lost. This describes the total lung capacity as a percent of predicted. (NCT00512902)
Timeframe: Baseline vs. Endpoint (1 year)

InterventionPercent predicted (Mean)
Imatinib4.17

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Improvement in Indices of Pulmonary Function Measured by Change DLCO hb Adj % Predicted

This outcome measure includes patients with and without the presence of Interstitial Lung Disease (ILD). Diffusion capacity of the lungs for carbon monoxide (DLCO) measures how much oxygen travels from the alveoli of the lungs to the blood stream. DLCO is adjusted for hemoglobin as small changes in hemoglobin concentration can affect the carbon monoxide transfer. DLCO results are compared to normal values for a patient's height, age, sex, and ethnicity. A DLCO result that is at least 80% of the predicted value is considered normal. Improvement in DLCO hb adj % predicted is measured by Mean change (and 95% Confidence Interval) from Baseline mean to Month 12 mean (the average change in DLCO hb adj% from baseline to month 12). (NCT00555581)
Timeframe: 12 months

InterventionDLCO% (Mean)
400 mg Daily of Imatinib Mesylate5.5

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Improvement in Indices of Pulmonary Function Measured by Change in FVC % Predicted

This outcome measure includes patients with and without the presence of Interstitial Lung Disease (ILD). Forced vital capacity (FVC) is the amount of air that can be forcibly exhaled from the lungs after taking a deep breath. It is used to determine the severity of lung disease. Improvement in FVC % predicted is measured by Mean change (and 95% Confidence Interval) from Baseline mean to Month 12 mean. Results are compared to the predicted values that are calculated from a patients age, size, weight, and sex. Results are considered normal if FVC is 80 percent or more of the predicted value. Mean change in FVC % predicted is measured by the average change in FVC% percent predicted from baseline to month 12. (NCT00555581)
Timeframe: 12 months

InterventionFVC% (Mean)
400 mg Daily of Imatinib Mesylate6.4

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Improvement in the Modified Rodnan Skin Score

Improvement in the Modified Rodnan Skin Score (MRSS) is measured by Mean change (and 95% Confidence Interval) from Baseline mean to Month 12 mean.Measure Description: The Modified Rodnan Skin Score (MRSS) measures dermal skin thickness through the examination of 17 body areas: fingers, hands, forearms, arms, feet, legs, and thighs (in pairs), and face, chest, and abdomen. The skin score is 0 for uninvolved skin through 3 for severe thickening (hidebound skin). The total skin score is the sum of the skin scores of the individual areas. The minimum score is 0 and the maximum score is 51. A higher score indicates greater severity of disease. The mean change in MRSS represents the average change in total skin score from baseline to month 12. (NCT00555581)
Timeframe: 12 months

Interventionunits on a scale (Mean)
400 mg Daily of Imatinib Mesylate-6.6

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Scleroderma Health Assessment Questionnaire Disability Index

"The Scleroderma Health Assessment Questionnaire (SHAQ) consist of the Health Assessment Questionnaire (HAQ) and 8 other domains which include scales looking at pain, patient global assessment, vascular, digital ulcers, lung involvement, and gastrointestinal involvement. It addresses scleroderma related manifestations that contribute to disability. It is a quality of life measure. Each question is scored from 0 (without difficulty) to 3 (unable to do). Some domains in the SHAQ are visual analog scales that are measured first and then changed to a 0-3 scale.~The maximum from each category is added together and divided by the number of categories completed. Change in Scleroderma Health Assessment Questionnaire Disability Index (SHAQ-DI) is measured as Mean Change (and 95% Confidence Interval) from Baseline mean to Month 12 mean (the average change in SHAQ-DI from baseline to month 12)." (NCT00555581)
Timeframe: 12 months

Interventionunits on a scale (Mean)
400 mg Daily of Imatinib Mesylate0.02

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Change From Baseline at Month 12 in Short Form-36 (SF-36) Questionnaire:Mental Component Summary

The Short Form 36 (SF-36) is a validated 36 item questionnaire which measures quality of life across eight domains: physical functioning, role limitations due to physical health, role limitations due to emotional problems, energy/fatigue, emotional well-being, social functioning, pain, general health. The mental component score is composed of a subset of the 8 health domains. Each component is directly transformed into a 0 to 100 scale on the assumption that each question carries equal weight. A score of 0 is equal to maximum disability, and a score of 100 is equivalent to no disability.The SF-36 mental component can be obtained by looking at the mean average of all the emotionally relevant items. Change in Short Form 36 mental (SF-36 MC) is measured by Mean change (and 95 % Confidence Interval) from Baseline mean to Month 12 mean (the average change in SF-36 mental component from baseline to month 12). (NCT00555581)
Timeframe: 12 months

Interventionunits on a scale (Mean)
400 mg Daily of Imatinib Mesylate-6.6

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Change From Baseline at Month 12 in Short Form-36 (SF-36) Questionnaire: Physical Component Summary

The Short Form 36 (SF-36) is a 36 item questionnaire which measures quality of life across eight domains: physical functioning, role limitations due to physical health, role limitations due to emotional problems, energy/fatigue, emotional well-being, social functioning, pain, general health. The physical component score is composed of a subset of the 8 health domains.The SF-36 physical component can be obtained by looking at the mean average of all the physically relevant items. Each component is directly transformed into a 0 to 100 scale on the assumption that each question carries equal weight. A score of 0 is equal to maximum disability, and a score of 100 is equivalent to no disability. Change in Short Form 36 physical component (SF-36 PC) is measured by Mean change (and 95 % Confidence Interval) from Baseline mean to Month 12 mean (the average change in SF-36 physical component from baseline to month 12). (NCT00555581)
Timeframe: 12 months

Interventionunits on a scale (Mean)
400 mg Daily of Imatinib Mesylate6.8

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Cumulative Incidence of On-Treatment Transformation to Accelerated Phase (AP) or Blast Phase (BP) at 192 Weeks

"The cumulative incidence curve was generated based on the time from randomization to the first date of transformation to AP or BP while on study treatment adjusting for the competing risk of treatment discontinuation without transformation, for each participant.~Criteria for transformation to AP: 15 to 29% blasts; ≥30% blasts + promyelocytes; ≥20% basophils in blood or bone marrow; platelets <100*10^9/L (not related to therapy), in blood. Criteria for transformation to BP: ≥30% blasts in blood or bone marrow and extramedullary involvement other than liver or spleen (example: chloromas).~Time to transformation was calculated as weeks = ([date of first documented occurrence of the event - date of randomization] + 1)/7. If transformation was not obtained, censoring was at the last hematologic assessment or death (whichever was earliest). Participants who were not treated contributed time = 1 day/7. 95% confidence interval for the cumulative incidence is from Gray's method." (NCT00574873)
Timeframe: 192 weeks

InterventionPercentage of Participants (Number)
Bosutinib1.6
Imatinib4.4

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Kaplan-Meier Estimate of Probability of Retaining Complete Hematologic Response (CHR) at 192 Weeks

"The Kaplan-Meier curve was generated based on the first date of confirmed CHR until the first date of loss of CHR, objectively documented, for responders only. Participants without confirmed loss of response were censored at the last valid hematologic assessment.~CHR must have been of at least 4 weeks in duration confirmed by 2 assessments at least 4 weeks apart and was defined as follows: white blood cells ≤ institutional upper limit of normal, no peripheral blasts or promyelocytes, myelocytes + metamyelocytes <5% in blood, absolute neutrophil count ≥1.0*10^9/L, platelets ≥100 but <450*10^9/L unless related to therapy, <20% basophils in blood and no extramedually involvement (including hepato- or splenomegaly).~The medians have not been reached in either arm, as such, the premature estimated hazard ratio is provided. Four years rate was displayed since the majority of participants had first CHR by Year 1." (NCT00574873)
Timeframe: 192 weeks

InterventionPercentage of Participants (Number)
Bosutinib91.6
Imatinib86.0

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Percentage of Participants With Major Molecular Response (MMR) at Year 1

Molecular response was assessed using Bcr-Abl transcript levels measured by reverse transcriptase polymerase chain reaction (RT-PCR) from peripheral blood. A MMR was defined as a ratio Bcr-Abl/Abl less than or equal to (≤) 0.1% on the international scale (greater than or equal to [≥] 3 log reduction from standardized baseline in ratio of Bcr-Abl to Abl transcripts) with at least 3000 Abl analyzed. (NCT00574873)
Timeframe: Year 1 (48 weeks)

InterventionPercentage of Participants (Number)
Bosutinib38.0
Imatinib25.4

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Percentage of Participants With Complete Cytogenetic Response (CCyR) at Year 1

Cytogenetic Response (CyR) is based on the prevalence of Philadelphia chromosome positive (Ph+) metaphases among cells in metaphase on a bone marrow (BM) aspirate. CCyR was achieved when there was 0 percent (%) Ph+ metaphases among cells in a BM sample when at least 20 metaphases from a BM sample were analyzed, or less than (<) 1% breakpoint cluster region Abelson protooncogene (Bcr-Abl) fusion product among cells in a BM sample or peripheral blood sample when at least 200 cells were analyzed. (NCT00574873)
Timeframe: Year 1 (48 weeks)

InterventionPercentage of Participants (Number)
Bosutinib70.0
Imatinib68.3

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Kaplan-Meier Estimate of Probability of Retaining Derived MMR at 144 Weeks

"The Kaplan-Meier curve was generated based on the first date of MMR until the first date loss of MMR, objectively documented, for responders only. Participants without confirmed loss of response were censored at the last valid molecular assessment.~Molecular response was assessed using Bcr-Abl transcript levels measured by RT-PCR from peripheral blood. MMR is defined as a ratio Bcr-Abl/Abl ≤0.1% on the international scale (≥3 log reduction from standardized baseline in ratio of Bcr-Abl to Abl transcripts) with at least 3000 Abl analyzed.~The medians have not been reached in either arm, as such, the premature estimated hazard ratio is provided. Three years rate was displayed since the majority of imatinib participants had first MMR by Year 2." (NCT00574873)
Timeframe: 144 weeks

InterventionPercentage of Participants (Number)
Bosutinib94.7
Imatinib98.0

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Kaplan-Meier Estimate of Probability of Retaining CCyR at 192 Weeks

"The Kaplan-Meier curve was generated based the time from the first date of CCyR until the first date of confirmed loss of CCyR, objectively documented, for responders only. Participants without confirmed loss of CCyR were censored at the last valid cytogenetic assessment.~CyR is based on the prevalence of Ph+ metaphases among cells in metaphase on a bone marrow sample. CCyR was achieved when there was 0% Ph+ metaphases among cells in a BM sample when at least 20 metaphases from a BM sample were analyzed, or <1% Bcr-Abl fusion product among cells in a BM sample or peripheral blood sample when at least 200 cells were analyzed.~The medians have not been reached in either arm, as such, the premature estimated hazard ratio is provided. Four years rate was displayed since the majority of participants had first CCyR by Year 1." (NCT00574873)
Timeframe: 192 weeks

InterventionPercentage of Participants (Number)
Bosutinib92.9
Imatinib88.9

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Number of Participants With Non-response, Partial Response, Complete Response, and Remission Assessed by MRSS Values

The following MRSS categories were calculated for up to Week 48: Non-response: a reduction in MRSS <25%, Partial response: a reduction in MRSS between 25-<50%, Complete response: a reduction in MRSS between 50-<80%, Remission: a reduction in MRSS ≥80%. (NCT00613171)
Timeframe: Weeks 2, 4, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, and Week 48/End of Study (EOS)

InterventionParticipants (Count of Participants)
Week 272373437Week 472373437Week 672373437Week 872373437Week 1272373437Week 1672373437Week 2072373437Week 2472373437Week 2872373437Week 3272373437Week 3672373437Week 4072373437Week 4472373437Week 48/EOS72373437
Non-responseComplete ResponseRemissionPartial Response
STI57127
STI5710
STI57125
STI57124
STI5712
STI5711
STI57122
STI57115
STI57116
STI57113
STI5719
STI5713
STI5715
STI5718

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Change From Baseline in Modified Rodnan Skin Score (MRSS) at Each Time Point of Analysis

The efficacy of oral STI571 in participants with systemic sclerosis is defined by an improvement in MRSS. Skin thickness was assessed clinically in each of 17 body areas and scored using a 0-3 scale, where 0= normal, 1= mild thickness, 2= moderate thickness, and 3= severe thickness (maximum score 51). A higher score indicates greater severity of the disease. (NCT00613171)
Timeframe: Baseline, Weeks 2, 4, 6, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, and Week 48/End of Study (EOS)

Interventionunits on a scale (Mean)
BaselineWeek 2Week 4Week 6Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48/ EOS
STI57125.76.585.978.348.483.3412.7012.419.90-3.17-5.67-12.61-5.23-13.57-20.89

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Number of Participants With Adverse Events (AE's) and Serious Adverse Events (SAE's)

An AE is the appearance or worsening of any undesirable sign, symptom, or medical condition occurring after starting the study drug even if the event is not considered to be related to the study drug. An SAE is defined as an event that is fatal or life-threatening, results in persistent or significant disability/incapacity, constitutes a congenital anomaly/birth defect, requires inpatient hospitalization or prolongation of existing hospitalization, is medically significant, i.e., defined as an event that jeopardizes the patient or may require medical or surgical intervention to prevent one of the outcomes listed above. (NCT00613171)
Timeframe: Baseline to Week 48/EOS

InterventionParticipants (Count of Participants)
Participants Experiencing AE'sParticipants Experiencing SAE's
STI571275

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12-month Progression Free Survival (PFS)

Percentage of participants surviving twelve months from the start of cycle 1 without progression of disease. PFS was defined as the time from the cycle 1 start date to the date of the first documented progression according to modified Macdonald criteria, or to death due to any cause. (NCT00615927)
Timeframe: 12 months

Interventionpercentage of participants (Number)
Astrocytoma43.8
Oligodendroglioma34.4

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Median Overall Survival (OS)

Time in weeks from the start of cycle 1 to date of death due to any cause. Patients alive at last follow-up are censored as of that follow-up date. Median OS was estimated using a Kaplan-Meier curve. (NCT00615927)
Timeframe: Time in weeks from the start of cycle 1 to date of death due to any cause, assessed up to 156 weeks

Interventionweeks (Median)
AstrocytomaNA
OligodendrogliomaNA

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Median Progression-free Survival

Time in weeks from the start of cycle 1 to the date of first progression according to modified Macdonald criteria, or to death due to any cause. Patients alive who had not progressed as of the last follow-up had PFS censored at the last follow-up date. Median PFS was estimated using a Kaplan-Meier curve. (NCT00615927)
Timeframe: Time in weeks from the start of cycle 1 to the date of first progression according to modified Macdonald criteria or to death due to any cause, assessed up to 156 weeks

Interventionweeks (Median)
Astrocytoma43.5
Oligodendroglioma43.3

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Objective Response Rate

Number of participants with an objective response (complete response or partial response) based on modified Macdonald criteria. (NCT00615927)
Timeframe: 156 weeks

Interventionparticipants (Number)
Astrocytoma0
Oligodendroglioma0

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Safety and Tolerability of Gleevec + Hydroxyurea in Patients With Low-grade Gliomas

The number of patients experiencing any serious adverse event or other (non-serious) adverse event during the study participation. (NCT00615927)
Timeframe: 156 weeks

,
Interventionparticipants (Number)
Experienced any Serious Adverse EventExperienced any (non-serious) Adverse Event
Astrocytoma1028
Oligodendroglioma328

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Safety - Grade 3 or 4 Adverse Events

Number of reported grade 3 or 4 adverse events (NCT00667953)
Timeframe: through study completion, an average of 1 year

InterventionAdverse Events (Number)
Arm A:20

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Response

Response rate by RECIST (NCT00667953)
Timeframe: through study completion, an average of 1 year

InterventionParticipants (Count of Participants)
Arm A:1

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Percentage Change From Baseline in the Modified Rodnan Skin Score (mRSS) to Assess Skin Tethering

The modified Rodnan Skin Score is the accepted clinical measure of scleroderma skin activity. The investigator assessed the thickening of the skin using the modified Rodnan Skin Score through simple palpation on 17 different skin sites in the fingers, hands, forearms, arms, feet, legs, and thighs (bilaterally) and face, chest, and abdomen (singly). Skin thickness was assessed on a scale of 0 to 3; 0 representing normal skin and 3 being severe thickening. The sum of the individual scores can range from 0 (normal) to 51 (severe thickening in all 17 areas). Percentage change is calculated as the Month 4 Score - Baseline Score/Baseline Score * 100. A negative percentage change indicates improvement. (NCT00677092)
Timeframe: Baseline and Month 4

Interventionpercentage change in mRSS score (Mean)
Imatinib Mesylate Treatment-24

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Progression-Free Survival

"Progression-free survival based on the Kaplan-Meier method is defined as the duration of time from study entry to documented disease progression (PD) requiring removal from the study or death. Disease progression was assessed per International Workshop Criteria (IWC) [Cheson, et al. JCO 2007].~Per International Working Group response criteria in lymphoma progressive disease (PD) was defined as the appearance of new lesions; the sum of the product of the diameter (SPD) increasing ≥50% from nadir (smallest value seen during trial) in nodal target lesions overall; or, in any single nodal target lesion, a node with a short axis > 10 mm must increase > 50% in greatest transverse diameter or a node with short axis <10mm must increase by at least 50% to at least 15 mm x 15 mm or have a greatest transverse diameter greater than 15 mm." (NCT00684411)
Timeframe: Disease was evaluated radiologically at baseline, on treatment at weeks 8, 16, 24 and every 12 weeks thereafter, off treatment for 6 weeks or until death, whichever occurs first. Treatment duration was a median of 56 days (range 5-253 days).

Interventiondays (Median)
Imatinib Mesylate21

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Overall Survival

Overall survival is defined as the time from study entry to death or date last known alive. (NCT00684411)
Timeframe: Participants were followed long-term for survival for the earlier of 6 weeks from the end of treatment or death. Maximum follow-up was 288 days in this study cohort.

Interventiondays (Median)
Imatinib Mesylate154

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Overall Response Rate

"Overall response rate is defined as the proportion of patients who achieve complete remission (CR), complete remission/unconfirmed (CRu) or partial remission (PR) based on International Workshop Criteria (IWC) [Cheson, et al. JCO 2007].~Per the International Working Group response criteria in lymphoma (Cheson 2007) for target lesions assessed by CT: Complete response (CR): nodes that were greater than 15 mm in greatest transverse diameter at baseline shrank to less than 15 mm in greatest transverse diameter and those that were 11-15 mm in greatest transverse diameter but had a short axis diameter greater than 10 mm had a short axis diameter less than 10mm and a transverse diameter that remained less than 15 mm; partial response (PR) was defined as a decrease in the sum of the product of the diameter of target lesions by more than 50% but not fulfilling criteria for CR. Overall response was defined as CR+PR.~." (NCT00684411)
Timeframe: Disease was evaluated radiologically at baseline, weeks 8, 16, 24 and every 12 weeks thereafter on treatment. Treatment duration was a median of 56 days (range 5-253 days).

Interventionproportion of participants (Number)
Imatinib Mesylate0.0

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The Proportion of Patients at 1 Year With Treatment Efficacy Success

To be considered a treatment efficacy success at 1 year posttransplant, the patient's bone marrow must demonstrate complete hematological remission, absence of Philadelphia chromosomes, and not satisfy any of the criteria for treatment failure (>/= 1% aberrantly expressing marrow blasts by multiparameter flow cytometry, >5% BCR/ABL in marrow by fluorescent in situ hybridization, or >1 log rise in peripheral blood BCR/ABL by quantitative polymerase chain reaction (PCR) since day 80). (NCT00702403)
Timeframe: Up to 1 year

InterventionParticipants (Count of Participants)
By intention to treatExcluding early non-relapse deaths
Treatment (Prophylactic Inhibition of BCR-ABL Tyrosine Kinase)2929

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Survival

The proportion of study participants alive at 1, 2 and 3 years (NCT00702403)
Timeframe: Up to 3 years

InterventionParticipants (Count of Participants)
Overall Survival at 1 yearOveral Survival at 2 yearsOverall Survival at 3 years
Treatment (Prophylactic Inhibition of BCR-ABL Tyrosine Kinase)312828

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Number of Participants With Treatment Safety Failure

Safety and tolerability of nilotinib therapy in patients with imatinib-sensitive leukemia graded according to the National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events version 4.0. Treatment safety failure is defined for a patient with imatinib sensitive Ph+ leukemia as the inability to be able to deliver at least 400 milligrams per day of nilotinib in adults, and 230 milligrams/m2 per day in children, for at least 85% of the time interval between 81 and 365 days after transplant. The overall study will be considered successful if nilotinib is deliverable to more than 75% of the study participants at this minimum specified dose intensity. (NCT00702403)
Timeframe: Up to 365 days post-transplant

InterventionParticipants (Count of Participants)
Single Arm Nilotinib Relapse Prophylaxis13

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Patients Alive With Out Relapse

The proportion of study participants alive and without hematologic, cytogenetic or molecular evidence of BCR/ABL-positive leukemia at 1 year (NCT00702403)
Timeframe: Up to 1 year

InterventionParticipants (Count of Participants)
Single Arm Nilotinib Relapse Prophylaxis29

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Relapse

The proportion of patients with hematologic, cytogenetic or molecular relapse of BCR/ABL-positive leukemia (NCT00702403)
Timeframe: 1 and 3 years

InterventionParticipants (Count of Participants)
Proportion with relapse at 1 yearProportion with relapse at 3 years
Treatment (Prophylactic Inhibition of BCR-ABL Tyrosine Kinase)56

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Percent Change in Absolute Range of Motion (ROM) From Baseline to 6 Months

A change in ROM is 25% or greater from baseline. A partial response required improvement in 25% or more in ROM. Progression required 25% or greater loss of ROM.Patients with negative values in the Table are those who lost ROM. Percent improvement in ROM for 1-3 target joints. For patients with >1 target joint, the average ROM improvement was calculated. The average percentage change in ROM deficit from baseline to 6 months was obtained based on the number of degrees of ROM change (6 months)/total ROM deficit (baseline) at each joint. (NCT00702689)
Timeframe: 6 months

InterventionPercent change from baseline (Number)
Pt 2 6mo response% change in deficit from baselinePt 7 6mo response% change in deficit from baselinePt 8 6mo response% change in deficit from baselinePt10 6mo response% change in deficit from baselinePt12 6mo response% change in deficit from baselinePt13 6mo response% change in deficit from baselinePt14 6mo response% change in deficit from baselinePt15 6mo response% change in deficit from baselinePt16 6mo response% change in deficit from baselinePt17 6mo response% change in deficit from baselinePt18 6mo response% change in deficit from baselinePt19 6mo response% change in deficit from baselinePt20 6mo response% change in deficit from baseline
Imatinib Mesylate in Patients With cGVHD94351621166127223-25-23115

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Primary Range of Motion (ROM) Response

Progressive disease is defined as joint ROM: decrease of >25% in composite ROM score on 2 consecutive evaluations at least 2 weeks apart, but not greater than 4 weeks apart or steroid pulse: >1 steroid pulse per 3 month period if administered for sclerotic-type chronic graft versus host disease (ScGVHD). Response is joint ROM: increase of >25% in composite ROM score. Maximal response is a response with no further improvement over 2 sequential 3-month evaluations. Stable disease does not meet the criteria for progression, response, or maximal response. (NCT00702689)
Timeframe: 6 months

Interventionparticipants (Number)
Partial ResponseStable DiseaseProgressive Disease
Imatinib Mesylate in Patients With cGVHD572

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Total Chronic Graft Versus Host Disease (cGVHD) Provider Global Rating Score at Baseline and 6 Months

The provider global rating is a physician impression of severity of cGVHD symptoms from a scale of zero (no symptoms) to 10 (most severe GVHD symptoms possible). (NCT00702689)
Timeframe: Baseline and 6 months

InterventionProvider Global Rating Score (Number)
Patient #2 at BaselinePatient #2 at 6 MonthsPatient #3 at BaselinePatient #3 at 6 MonthsPatient #7 at BaselinePatient #7 at 6 MonthsPatient #8 at BaselinePatient #8 at 6 MonthsPatient #10 at BaselinePatient #10 at 6 MonthsPatient #12 at BaselinePatient #12 at 6 MonthsPatient #13 at BaselinePatient #13 at 6 MonthsPatient #14 at BaselinePatient #14 at 6 MonthsPatient # 15 at BaselinePatient #15 at 6 MonthsPatient #16 at BaselinePatient #16 at 6 MonthsPatient #17 at BaselinePatient #17 at 6 monthsPatient #18 at BaselinePatient #18 at 6 MonthsPatient #19 at BaselinePatient #19 at 6 MonthsPatient #20 at BaselinePatient #20 at 6 Months
Imatinib Mesylate in Patients With cGVHD543NA686754676476765468888588

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Total Skin Score at Baseline and 6 Months

Total skin score was graded by the National Institutes of Health Consensus Criteria. Skin score was calculated by dividing the total score by seven domains (skin, eye, oral, joint, gastrointestinal, hepatic, pulmonary) in men and 8 domains in women (previous domains noted plus gynecologic). Total skin score is a percentage of body surface area (BSA) involvement (range 0-100%). It was calculated from the sum of moveable body surface BSA and non-moveable BSA. Higher numbers = greater body surface area affected. (NCT00702689)
Timeframe: Baseline and 6 Months

Interventionunits on a scale (Number)
Patient # 2 - BaselinePatient # 2 - 6 monthsPatient # 3 - BaselinePatient # 3 - 6 monthsPatient # 7 - BaselinePatient # 7 - 6 monthsPatient # 8 - BaselinePatient # 8 - 6 monthsPatient # 10 - BaselinePatient # 10 - 6 monthsPatient # 12 - BaselinePatient # 12 - 6 monthsPatient # 13 - BaselinePatient # 13 - 6 monthsPatient # 14 - BaselinePatient # 14 - 6 monthsPatient # 15 - BaselinePatient # 15 - 6 monthsPatient # 16 - BaselinePatient # 16 - 6 monthsPatient # 17 - BaselinePatient # 17 - 6 monthsPatient # 18 - BaselinePatient # 18 - 6 monthsPatient # 19 - BaselinePatient # 19 - 6 monthsPatient # 20 - BaselinePatient # 20 - 6 months
Imatinib Mesylate in Patients With cGVHD66.65443.38NA66.2455.5353.155.2610.86.1221.2430.0679.262.2839.9640.571.4661.839.548.184.9685.1126.6424.321.1537.823.425.2

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Average Percentage Change in Range of Motion (ROM) Deficit

One or more joints were assessed for ROM deficit by a physiatrist with expertise in graft versus host disease and joint ROM. (NCT00702689)
Timeframe: 6 months

InterventionPercent change (Mean)
Imatinib Mesylate in Patients With cGVHD24.2

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Number of Participants With Adverse Events

Here is the number of participants with serious and non-serious adverse events assessed by the Common Terminology Criteria for Adverse Events (CTCAE v4.0). A non-serious adverse event is any untoward medical occurrence. A serious adverse event is an adverse event or suspected adverse reaction that results in death, a life-threatening adverse drug experience, hospitalization, disruption of the ability to conduct normal life functions, congenital anomaly/birth defect or important medical events that jeopardize the patient or subject and may require medical or surgical intervention to prevent one of the previous outcomes mentioned. (NCT00702689)
Timeframe: Date treatment consent signed to date off study, approximately, 41 months, 27 days

InterventionParticipants (Number)
Imatinib Mesylate in Patients With cGVHD20

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Change in Immunosuppression

Change in immunosuppression was defined by an increase or decrease in steroid use form baseline. (NCT00702689)
Timeframe: 6 months

Interventionparticipants (Number)
↓ Pred 20 mg everyday (qd )to 5 mg every other day↓ MPred 16 mg every other day(qod) to 4 mg qod↓ Pred:24mg every day(qd) to 20mg qdNo change↓ Tacro 2mg every am 1.5mg every pm to .5mg bidPred↓ 25mg qd to 15mg qd;Tacro↓ 2mg bid to 1mg bidPred↓ 2.5mg qd to 2.5mg every other day↓ Siro:2mg qd to 1 mg qdPred wean then ↑ 10 12.5mg bid;Tacro↑1.0 to 1.5bidMMF↓ 1g/bid to discontinued
Imatinib Mesylate in Patients With cGVHD1115111111

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Lung Function Score at Baseline and 6 Months

Lung function was graded by the National Institutes of Health Chronic Graft Versus Host Disease organ response criteria. The Lung function score = forced expiratory volume 1 (FEV1) score + carbon monoxide diffusing capacity (DLCO) score, with a possible range of 2 (better outcome)-12 (worst outcome). The percent predicted FEV1 and DLCO (adjusted for hematocrit but not alveolar volume) should be converted to a numeric score as follows: >80% =1; 70-79% = 2; 60-69% = 3; 50-59% = 4; 40-49% = 5; <40% = 6. (NCT00702689)
Timeframe: Baseline and 6 Months

Interventionunits on a scale (Number)
Patient #2 at BaselinePatient #2 at 6 MonthsPatient #3 at BaselinePatient #3 at 6 MonthsPatient #7 at BaselinePatient #7 at 6 MonthsPatient #8 at BaselinePatient #8 at 6 MonthsPatient #10 at BaselinePatient #10 at 6 MonthsPatient #12 at BaselinePatient #12 at 6 MonthsPatient #13 at BaselinePatient #13 at 6 MonthsPatient #14 at BaselinePatient #14 at 6 MonthsPatient # 15 at BaselinePatient #15 at 6 MonthsPatient #16 at BaselinePatient #16 at 6 MonthsPatient #17 at BaselinePatient #17 at 6 monthsPatient #18 at BaselinePatient #18 at 6 MonthsPatient #19 at BaselinePatient #19 at 6 MonthsPatient #20 at BaselinePatient #20 at 6 Months
Imatinib Mesylate in Patients With cGVHD229NA385633454455763256889922

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Disease Control Rate (DCR)

The Disease Control Rate (Complete Response(CR), Partial Response (PD) and Stable Disease (SD) rates for each treatment arm will be computed using the exact Clopper-Pearson interval estimation methodology. DCR is defined as the percentage of patients with a best overall response of • CR, i.e. at least two determinations of CR at least 4 weeks apart without loss of response between the determinations, • PR, i.e. at least two determinations of PR or better at least 4 weeks apart before progression (and not qualifying for a CR) and without loss of PR between the determinations, or • SD lasting at least 24 weeks, i.e. at least one SD or better response at least 24 weeks after randomization (and not qualifying for CR or PR). (NCT00751036)
Timeframe: every 2 months until 24 months (end of study)

,
InterventionPercentage of Patients (Number)
Disease Control Rate (CR, PR, or SD)Complete Response (CR)Partial Response (PR)Stable Disease (SD)Progressive Disease (PD)Unknown (UNK)
Imatinib47.806.541.337.015.2
Nilotinib54.22.14.247.925.020.8

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Time to Treatment Failure

TTF, defined as the time from date of randomization to the earliest of date of the first objective tumor progression, date of death due to any cause, or date of discontinuation due to reasons other than 'Protocol deviation' or 'Administrative problems'. (NCT00751036)
Timeframe: Time from date of radomization to the earliest date of the first objective tumor, death or discontinuation, assesed until 24 months.

InterventionDays (Median)
Nilotinib90.00
Imatinib112.00

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Progression-free Survival (PFS)

Progression-free survival (PFS) is the time from date of randomization to the date of first documented progression or death due to any cause. If a participant has not had an event, progression-free survival is censored at the time of last adequate tumor assessment. Progression is defined according to modified RECIST criteria as at least a 20% increase in the sum of the longest diameter of target lesions, worsening of the non-target lesions or the appearance of one or more new lesions. (NCT00751036)
Timeframe: 24 months

InterventionDays (Median)
Nilotinib111.00
Imatinib120.00

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Overall Survival (OS)

. OS is defined as the time from the date of randomization to the date of death due to any cause or the date of last contact prior to or on the date of data cutoff. The median time to overall survival and its associated 95 % CI will be derived, for each treatment arm, using the time to event analysis based on Kaplan-Meier methodology. (NCT00751036)
Timeframe: time from the date of randomization to the date of death due to any cause or the date of last contact prior to or on the date of data cutoff, assesed until 24 months.

InterventionDays (Median)
Nilotinib737
Imatinib594.00

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Rate of Confirmed Best Cumulative CMR

The rate of confirmed best cumulative CMR was defined as the number of participants who had confirmed CMR during the 24, 36 and 48 months post treatment after the randomization date. Participants who achieved confirmed best cumulative CMR during the first 12 months were considered responders. Participants who dropped out early or who did not provide sufficient data for any reason were considered to be non-responders. The definition of CMR is undetectable BCR-ABL (fusion gene formed between bcr gene from chromosome 22 and abl gene from chromosome 9) where BCR-ABL ratio in % international scale (IS) ≤ 0.00001 by RQ-PCR where there was no detectable BCR-ABL and 1) the test had a sensitivity of at least 4.5 logs below the standardized baseline; 2) RQ-PCR negativity was confirmed on the next RQ-PCR sample (usually 3 months later); and 3) the date of confirmed CMR was the date of the first of two negative results with sensitivity >4.5 logs. (NCT00760877)
Timeframe: 24 months, 36 month, 48 months

,
InterventionParticipants (Number)
24 months, Responders24 months, Non-responders36 months, Responders36 months, Non-responders48 months, Responders48 months, Non-responders
Imatinib119221822182
Nilotinib248029753272

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Rate of Confirmed Best Cumulative Complete Molecular Response (CMR)

The rate of confirmed best cumulative CMR was defined as the number of participants who had confirmed CMR during the first 12 months of treatment after the randomization date. Participants who achieved confirmed best cumulative CMR during the first 12 months were considered responders. Participants who dropped out early or who did not provide sufficient data for any reason were considered to be non-responders. The definition of CMR is undetectable BCR-ABL (fusion gene formed between bcr gene from chromosome 22 and abl gene from chromosome 9) where BCR-ABL ratio in % international scale (IS) ≤ 0.00001 by real-time quantitative polymerase chain reaction (RQ-PCR) where there was no detectable BCR-ABL and 1) the test had a sensitivity of at least 4.5 logs below the standardized baseline; 2) RQ-PCR negativity was confirmed on the next RQ-PCR sample (usually 3 months later); and 3) the date of confirmed CMR was the date of the first of two negative results with sensitivity >4.5 logs. (NCT00760877)
Timeframe: 12 months

,
InterventionParticipants (Number)
RespondersNon-responders
Imatinib697
Nilotinib1391

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Event-free Survival

Event-free survival was defined as the time from the date of randomization to the date of first occurrence of any of the following events on study treatment: loss of complete hematological response, confirmed loss of complete cytogenetic response (CCyR), confirmed loss of major molecular response (MMR), death from any cause during treatment, progression to the accelerated phase or blast crisis of chronic myelogenous leukemia (CML) per European Leukemia Network (ELN) criteria, whichever was earliest. (NCT00760877)
Timeframe: 48 months

InterventionMonths (Median)
NilotinibNA
ImatinibNA

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Overall Survival

Overall survival was defined as the time from the date of randomization to the date of death due to any cause at any time during the study, including the follow-up period after discontinuation of treatment. (NCT00760877)
Timeframe: 48 months

InterventionMonths (Median)
NilotinibNA
ImatinibNA

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Progression Free Survival (PFS)

PFS was defined as the time from the date of randomization to the date of the earliest documented progression-defining event as follows: transformation to blast crisis or accelerated phase disease, or death from any cause. (NCT00760877)
Timeframe: 48 months

Interventionmonths (Median)
NilotinibNA
ImatinibNA

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Number of Cross-over Participants With CMR

The definition of CMR is undetectable BCR-ABL (fusion gene formed between bcr gene from chromosome 22 and abl gene from chromosome 9) where BCR-ABL ratio in % international scale (IS) ≤ 0.00001 by RQ-PCR where there was no detectable BCR-ABL and 1) the test had a sensitivity of at least 4.5 logs below the standardized baseline; 2) RQ-PCR negativity was confirmed on the next RQ-PCR sample (usually 3 months later); and 3) the date of confirmed CMR was the date of the first of two negative results with sensitivity >4.5 logs. (NCT00760877)
Timeframe: 24 months, 36 months, 48 months

InterventionParticipants (Number)
24 months36 months48 months
Nilotinib369

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Time to Progression Free Survival (PFS)

PFS was defined as the time from the date of start of treatment to the date of the first documented progression or death due to any cause. Progression is defined as a 20% increase in the sum of the longest diameter of target lesions, or a measurable increase in a non-target lesion, or the appearance of new lesions (NCT00785785)
Timeframe: up to month 37

Interventionmonths (Median)
Nilotinib25.9
Imatinib29.7

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Duration of CCyR

Duration of CCyR was defined as time from the date of ransomization to the date of first loss of CCyR or death, whichever came first. (NCT00802841)
Timeframe: 24 months

InterventionMonths (Median)
NilotinibNA
Imatinib17.2

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Overall Survival (OS)

OS was defined as time from date of randomization to the date of the death. (NCT00802841)
Timeframe: 24 months

InterventionMonths (Median)
NilotinibNA
Imatinib25.7

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Time to CCyR

Time to CCyR was defined as time from date of randomization to date of first documented CCyR. (NCT00802841)
Timeframe: 24 months

InterventionMonths (Median)
Nilotinib5.55
Imatinib5.85

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Percentage of Participants With CCyr

CCyR was assessed from bone marrow samples. CCyr was defined as having 0% Philadelphia positive (Ph+) chromosome metaphases in bone marrow. (NCT00802841)
Timeframe: 12 and 24 months

,
InterventionPercentage of participants (Number)
12 months24 months
Imatinib55.861.1
Nilotinib53.151.0

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Percentage of Participants With Major Molecular Response (MMR)

MMR was defined as having a fusion gene of the Bcr and Abl genes of (BCR-ACL) less than or equal to 0.1% on the International Scale (IS). (NCT00802841)
Timeframe: 12 and 24 months

,
InterventionPercentage of participants (Number)
12 months24 months
Imatinib25.335.8
Nilotinib36.537.5

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Percentage of Participants With Complete Cytogenetic Response (CCyR)

CCyR was assessed from bone marrow samples. CCyr was defined as having 0% Philadelphia positive (Ph+) chromosome metaphases in bone marrow. (NCT00802841)
Timeframe: 6 months

InterventionPercentage of participants (Number)
Nilotinib50.0
Imatinib42.1

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Event-Free Survival (EFS)

EFS was defined as the time from the date of randomization to the date of the first occurrence of any of the following: loss of Complete Hematological Response (CHR), loss of Partial Cytogenetic Response (PCyR), loss of CCyR, death on treatment or progression to AP/BC. (NCT00802841)
Timeframe: 24 months

InterventionMonths (Median)
NilotinibNA
Imatinib24.3

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Progression-Free Survival (PFS)

PFS was defined as the time from the date of randomization to the date of documented disease progression to accelerated phase or blast crisis (AP/BC), or death due to any cause. (NCT00802841)
Timeframe: 24 months

InterventionMonths (Median)
NilotinibNA
ImatinibNA

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Progression-free-tolerance

This is defined as the percentage of participants who continued on treatment with no progression at 12 weeks since the start of treatment.A patient will be considered to have progression-free-tolerance if she does not drop out due to toxicity and does not have disease progression or die by the completion of 12 weeks on treatment. (NCT00840450)
Timeframe: 12 weeks

Interventionpercentage of participants (Number)
Paclitaxel and Imatinib Mesylate (Gleevec)75

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the Best Overall Clinical Response

This is defined as the percentage of participants who had either a complete response (CR) or a partial response (PR) as the best overall response according to Response Evaluation Criteria in Solid Tumors (RECIST) for measurable disease or CA-125 criteria for non-measurable disease. The response is evaluated at 12 weeks of treatment. (NCT00840450)
Timeframe: 12 weeks

Interventionpercentage of participants (Number)
Paclitaxel and Imatinib Mesylate (Gleevec)33

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Progression-free-survival at 12 Months

This defined as the percentage of participants who had progression free survival at 12 months from the beginning of the treatment. (NCT00840450)
Timeframe: up to 12 months

Interventionpercentage of participants (Number)
Paclitaxel and Imatinib Mesylate (Gleevec)17

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Time to PSA Progression

Time to PSA pregression is defined as the time at which therapy statred and ends when the PSA increased by 50% above the nadir confirmed on a second determination. (NCT00861471)
Timeframe: up to 2 years

Interventiondays (Mean)
Docetaxel +Gleevec188

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Percentage of Participants With Prostate Specific Antigen (PSA) Response

PSA response is defined as a greater than or equal to a 50% decrease in PSA from the baseline without clinical or radiologic evidence of progression according to the Response Evaluation Criteria in Solid Tumors (RECIST). PSA concentration was measured at baseline on day 1/cycle 1 before treatment, then day 1 of every cycle afterwards during therapy. (NCT00861471)
Timeframe: up to 9 months

Interventionpercentage of participants (Number)
Docetaxel +Gleevec50

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Percentage of Participants With Measurable Disease Response

Measurable disease response is defined as the number of participants whose best response is complete response or partial response over the number of patients with measurable desease according to the Response Evaluation Criteria in Solid Tumors (RECIST). (NCT00861471)
Timeframe: up to 2 years

Interventionpercentage of participants (Number)
Docetaxel +Gleevec20

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Median Overall Survival Time

Overall survival time is the time from the start of therapy till death. Median overall survival reported here is the time when 50% of the participants are alive. (NCT00861471)
Timeframe: up to 4 years

Interventionmonths (Median)
Docetaxel +Gleevec24.9

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Percentage of Participants With Greater or Equal to 80% PSA Reduction From Baseline Without Clinical or Radiologic Evidence of Progression

PSA was measured at baseline on day 1/cycle 1 before treatment, then day 1 of every cycle afterwards during therapy. (NCT00861471)
Timeframe: up to 9 months

Interventionpercentage of participants (Number)
Docetaxel +Gleevec16

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Recurrence-free Survival up to 60 Months

Recurrence-free survival assessment is based on the radiologic evidence and is defined as the time from the date of first dose of imatinib to the date of the first documented disease recurrence or death due to any cause (event). (NCT00867113)
Timeframe: Baseline up to 60 months

Interventionparticipants with an event (Number)
Subject with an eventEvent = disease recurrenceEvent=deathSubjects censored
Imatinib97282

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Overall Survival (OS) at 60 Months

Overall survival was defined as the time from the date of the first dose of study drug to the date of death. Subjects who were alive at the time of discontinuation/completion of the study were censored at the end of study date or end of treatment visit date if the subject refused to be followed post treatment. Full analysis set. (NCT00867113)
Timeframe: Baseline up to approximately 60 months

Interventionparticipants (Number)
subjects who diedsubjects censored
Imatinib388

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Kaplan-Meier Estimates for Recurrence-free Survival up to 60 Months

Recurrence-free survival (RFS) assessment is based on the radiologic evidence and is defined as the time from the date of first dose of imatinib to the date of the first documented disease recurrence or death due to any cause (event). RFS estimates were summarized using the Kaplan-Meier product-limit method (Kaplan 1958). Censoring rules for RFS with the earliest occurring rule used in the analysis: subjects without objective recurrence of disease who were alive at the time of their discontinuation from study were censored at the end of study date or end of treatment visit date if the subject refused to be followed post treatment and subjects recording antineoplastic therapy during the study were censored on the date of the therapy initiated (NCT00867113)
Timeframe: Baseline up to 60 months

Interventionpercentage of patients (Number)
12 months18 months24 months36 months48 months60 months
Imatinib97.797.796.595.195.190.1

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Kaplan-Meier Estimates for Overall Survival (OS) up to 60 Months

Overall survival was defined as the time from the date of the first dose of study drug to the date of death. Subjects who were alive at the time of discontinuation/completion of the study were censored at the end of study date or end of treatment visit date if the subject refused to be followed post treatment. Full analysis set. (NCT00867113)
Timeframe: Baseline up to appoximately 60 months

Interventionpercentage of participants (Number)
12 months18 months24 months36 months48 months60 months
Imatinib100.00100.0098.098.098.093.8

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Number of Patients With Adverse Events

Information about all adverse events, whether volunteered by the subject, discovered by investigator questioning, or detected through physical examination, laboratory test or other means, will be collected and recorded. (NCT00867334)
Timeframe: From consent up until 4 weeks after patient has stopped study participation

InterventionParticipants (Count of Participants)
Treatment With Increasing Doses of Imatinib5
Standard of Care Therapy With Panitumumab0

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Number of Participants With Stabilization or Reduction in Tumor Size

Results reported as number of patients with stabilization or reduction in tumor size. Tumor response is defined by the Response Evaluation Criteria in Solid Tumors (RECIST) solid tumor response criteria, evaluated by CT. (NCT00867334)
Timeframe: 8 weeks after baseline

InterventionParticipants (Count of Participants)
Treatment With Increasing Doses of Imatinib3
Standard of Care Therapy With Panitumumab0

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Level of Methylation

the percentage of methylated DNA (NCT00882206)
Timeframe: Day 0

Interventionpercentage of DNA (Mean)
Decitabine / Vorinostat84.98

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Level of Methylation

the percentage of methylated DNA (NCT00882206)
Timeframe: Day 33

Interventionpercentage of DNA (Mean)
Decitabine / Vorinostat86.1

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Level of Methylation

the percentage of methylated DNA (NCT00882206)
Timeframe: Day 5

Interventionpercentage of DNA (Mean)
Decitabine / Vorinostat79.82

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Response to Treatment

Response includes both complete remission (defined as <5% leukemic blasts in the bone marrow) and partial remission (defined as a greater than 35% reduction in the bone marrow leukemia blast percentage at day 33) (NCT00882206)
Timeframe: Day 33

Interventionparticipants (Number)
Decitabine / Vorinostat6

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Number of Patients With Survival at 48 Weeks

(NCT00891527)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
Avastin and/or Gleevec42

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Number of Patients With Disease Progression at 48 Weeks

"Patients will be classified as having disease progression if at least 2 pulmonary veins have significantly worsened at 48 weeks. This determination is based on the study defined Pulmonary Vein Status Scale, which categorizes pulmonary veins on a scale from 1- None: No narrowing of the luminal contour, to 7- Distal atretic: Complete obliteration of the luminal contour extending >5mm within the vessel segment." (NCT00891527)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
Avastin and/or Gleevec5

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Number of Patients With Disease Stabilization at 48 Weeks

(NCT00891527)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
Avastin and/or Gleevec15

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Clinical Worsening Comparing Imatinib Versus Placebo for Adjudicated Cases

Clinical worsening per participant was measured by the onset of any adjudicated event (all cause mortality; overnight hospitalization for worsening of Pulmonary Arterial Hypertension (PAH); worsening of WHO functional class by one level; 15% decline in Six Minute Walk Distance (6MWD) measured on two consecutive occasions) at 24 weeks treatment, comparing imatinib to placebo groups. A cox regression analysis model was used. (NCT00902174)
Timeframe: 24 weeks

Interventionpercentage of participants (Number)
Imatinib35.9
Placebo32.7

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Plasma Concentration of QTI571 200 mg and Its Metabolite (GCP74588) Pre-dose and Between 0 Hour to 3 Hour Post-dose Per Participant

"Blood samples were taken from each subject participating in the study (placebo group and active treatment group) once predose and once between 0 hour to 3 hour post dose at day 1 (baseline), day 14, day 28 and day 168.~The parent compound QTI571 and its active metabolite, GCP74588, were measured in plasma by validated liquid chromatography-mass spectrometry (HPLC-MS/MS) assay." (NCT00902174)
Timeframe: predose and between 0 hour to 3 hour post dose at day 1, day 14, day 28 and day 168

,
Interventionng/mL (Mean)
Day 1 - predose (n=77 imat; n=77 GCP)Day 1 - 0-3h post-dose (n=77 imat; n=77 GCP)Day 14 - predose (n=18 imat; n=18 GCP)Day 14 - 0-3h post-dose (n=19 imat; n=19 GCP)Day 28 - predose (n=20 imat; n=20 GCP)Day 28 - 0-3h post-dose (n=19 imat; n=19 GCP)Day 168 predose (n=24 imat; n=24 GCP)Day 168- 0-3h post-dose (n=23 imat; n=23 GCP)
GCP74588061.8178.8233.8228.6323.9126.6166.1
Imatinib 200 mg0471.9579.61005.7658.81438.6398.6710.8

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Change From Baseline in Systolic Arterial Blood Pressure

Change from baseline in systolic arterial blood pressure (mmHg) was measured via right heart catheterization according to the local hospital procedures. The systolic arterial blood was assessed when the participant was in a stable hemodynamic rest state. (NCT00902174)
Timeframe: baseline and week 24

Interventionmm Hg (Least Squares Mean)
Imatinib-2.92
Placebo-1.15

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Change From Baseline in Systemic Vascular Resistance

Change from baseline in systemic vascular resistance (dynes*sec*cm^-5) was measured via right heart catheterization according to the local hospital procedures. The systemic vascular resistance was assessed when the participant was in a stable hemodynamic rest state. Reduction from baseline in mean systemic vascular resistance indicates improvement. (NCT00902174)
Timeframe: baseline and week 24

Interventiondynes*sec*cm^-5 (Least Squares Mean)
Imatinib-467.84
Placebo-88.10

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Change From Baseline in Right Atrial Pressure

Change from baseline in right atrial pressure (mmHg) was measured via right heart catheterization according to the local hospital procedures. The right atrial pressure was assessed when the participant was in a stable hemodynamic rest state. A higher right atrial pressure number indicates worsening. (NCT00902174)
Timeframe: baseline and week 24

Interventionmm Hg (Least Squares Mean)
Imatinib-1.02
Placebo0.68

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Change From Baseline in Pulmonary Vascular Resistance

Change from baseline in pulmonary vascular resistance (dynes*sec*cm^-5) was measured via right heart catheterization according to the local hospital procedures. The pulmonary vascular resistance was assessed when the participant was in a stable hemodynamic rest state. Reduction from baseline in pulmonary vascular resistance indicates improvement. (NCT00902174)
Timeframe: baseline and week 24

Interventiondynes*sec*cm^-5 (Least Squares Mean)
Imatinib-366.47
Placebo12.12

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Change From Baseline in Pulmonary Resistance Index

Change from baseline in pulmonary resistance index (dynes*sec*cm^-5/m2) was measured via right heart catheterization according to the local hospital procedures. The pulmonary resistance index was assessed when the participant was in a stable hemodynamic rest state. A reduction from baseline in pulmonary resistance index indicates improvement. (NCT00902174)
Timeframe: baseline and week 24

Interventiondynes*sec*cm^-5/m2 (Least Squares Mean)
Imatinib-221.29
Placebo21.92

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Covariance of End of Study CAMPHOR Score

The CAMPHOR test consists of 65 items and 3 scales. Two scales measure Health Related Quality of Life. 1) Symptoms: consists of 25 items measuring loss or abnormality of psychological, physiological or anatomical structure or function; further sub-divided into 3 subscales (energy, breathlessness and mood), 2) Disability: consists of 15 items measuring any restriction or lack of ability to perform an activity. 3) Quality of Life (QOL): consists of 25 items defining how individuals perceived ability and capacity to satisfy their needs. The 25-item symptom and QOL scales score from 0-25 where a higher score indicates the presence of more symptoms and poor QOL, respectively. The 15-item functioning scale scores 0-30; a higher score indicates poor functioning. (NCT00902174)
Timeframe: Week 24

,
Interventionunits on a scale (Least Squares Mean)
Symptoms scoreActivity scoreQuality of life score
Imatinib7.938.997.45
Placebo9.0310.557.13

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Change From Baseline in Mean Pulmonary Capillary Wedge Pressure

Change from baseline in mean pulmonary capillary wedge pressure (mmHg)was measured via right heart catheterization according to the local hospital procedures. The right atrial mean pulmonary capillary wedge pressure was assessed when the participant was in a stable hemodynamic rest state. (NCT00902174)
Timeframe: baseline and week 24

Interventionmm Hg (Least Squares Mean)
Imatinib0.92
Placebo-0.05

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Change From Baseline in Mean Pulmonary Arterial Pressure

Change from baseline in mean pulmonary arterial pressure (mmHg) was measured via right heart catheterization according to the local hospital procedures. The mean pulmonary arterial pressure was assessed when the participant was in a stable hemodynamic rest state. A higher mean pulmonary arterial pressure number indicates worsening. (NCT00902174)
Timeframe: baseline and week 24

Interventionmm Hg (Least Squares Mean)
Imatinib-3.54
Placebo1.63

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Change From Baseline in Heart Rate

Change from baseline in heart rate (bpm) was measured via right heart catheterization according to the local hospital procedures. The heart rate was assessed when the participant was in a stable hemodynamic rest state. (NCT00902174)
Timeframe: 24 weeks

Interventionbpm (Least Squares Mean)
Imatinib0.38
Placebo0.73

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Change From Baseline in Diastolic Arterial Blood Pressure

Change from baseline in diastolic arterial blood pressure (mmHg) was measured via right heart catheterization according to the local hospital procedures. The diastolic arterial blood pressure was assessed when the participant was in a stable hemodynamic rest state. (NCT00902174)
Timeframe: baseline and week 24

Interventionmm Hg (Least Squares Mean)
Imatinib-3.81
Placebo-1.48

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Change From Baseline in Cardiac Output

Change from baseline in cardiac output (L/min) was measured via right heart catheterization according to the local hospital procedures. The cardiac output was assessed when the participant was in a stable hemodynamic rest state. An increase from baseline (higher number) in cardiac output indicates improvement. (NCT00902174)
Timeframe: 24 weeks

InterventionLiters/minute (Least Squares Mean)
Imatinib1.17
Placebo0.29

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Change in Borg Dyspnea Score During 6-minute Walk Test

Change in Borg scale was measured at different time points at week 24. The Borg Scale consists of scale range of 0 to 10. Participants pointed to indicate their level of dyspnea before and at the end of exercise testing (where 0 indicates no breathlessness at all and 10 indicates maximum breathlessness). A reduction in this score indicates an improvement. (NCT00902174)
Timeframe: week 24

,
Interventionunits on a scale (Mean)
Resting (n= 86 imatinib; 89 placebo)End of test (n= 92 imatinib; 91 placebo)2 min after end (n= 82 imatinib; 81 placebo)End of test - Resting (n= 81 imatinib; 81 placebo)2 min after end - end of test (n= 82 ima; 81plb)
Imatinib-0.06-0.38-0.37-0.24-0.07
Placebo-0.12-0.24-0.18-0.29-0.03

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Difference in Six-minute Walk Distance Test (6MWD) Between Imatinib and Placebo at 24 Weeks

This standardized walk course was 30 meters in length. During the walk the participant was connected to a portable pulse oximeter via a finger probe. Participants were instructed to walk at a comfortable speed for as far as they could manage in 6 minutes. The total distance walked (in meters) was recorded. Results were compared between the 2 groups. (NCT00902174)
Timeframe: 24 weeks

Interventionmeters (Least Squares Mean)
Imatinib382.94
Placebo351.18

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Plasma Concentration of QTI571 400 mg and Its Metabolite (GCP74588) Pre-dose and Between 0 Hour to 3 Hour Post-dose Per Participant

"Blood samples were taken from each subject participating in the study (placebo group and active treatment group) once predose and once between 0 hour to 3 hour post dose at day 1 (baseline), day 14, day 28 and day 168.~The parent compound QTI571 and its active metabolite, GCP74588, were measured in plasma by validated liquid chromatography-mass spectrometry (HPLC-MS/MS) assay." (NCT00902174)
Timeframe: predose and between 0 hour to 3 hour post dose at day 1, day 14, day 28 and day 168

,
Interventionng/mL (Mean)
Day 1 - predose (n=12 imat; n=12 GCP)Day 1 - 0-3h post-dose (n=13 imat; n=13 GCP)Day 14 - predose (n=62 imat; n=62 GCP)Day 14 - 0-3h post-dose (n=62 imat; n=62 GCP)Day 28 - predose (n=55 imat; n=55 GCP)Day 28 - 0-3h post-dose (n=58 imat; n=58 GCP)Day 168 predose (n=36 imat; n=36 GCP)Day 168- 0-3h post-dose (n=35 imat; n=35 GCP)
GCP745880109.9155.1233.7248.2320.7241.4348.0
Imatinib 400 mg0843.2516.51172.8829.81335.3869.91616.1

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Tumor Response Rates Using Modified SWOG Criteria to the Combination of Gleevec and Gemzar in Patients With Relapsed Ovarian Cancer Who Have Failed at Least One Prior Chemotherapy Treatment.

"Best response to thearpy was assessed using modified SWOG criteria (same as for outcome masure #1). Subjects were assess as complete response, partial response, stable disease, and progressive disease after 2 cycles (6 weeks) of beginning treatment and every 6 weeks afterward until progression of disease, unacceptable toxicity, or subject withdrawl from study.~the measurement reported is the number of patients who met the criteria for partial response." (NCT00928642)
Timeframe: Subjects treated until progression of disease or unacceptable toxicity. no maximum dose was specified

Interventionparticipants (Number)
Oral Imatinib Plus IV Gemcitabine0

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To Estimate the Clinical Response Rate(Partial and Complete Response as Defined Under the SWOG Criterial)

"Using SWOG criteria for response of measurable disease, subject best response was assessed. First assessment was 6 weeks after starting treatment. Subjequent evaluations were every 6 weeks in patients who remained on study.~Repsonse rate was the sum of Complete Repsonse and Partial Response." (NCT00928642)
Timeframe: until disease progression or unacceptable toxicity

Interventionparticipants (Number)
Treatment0

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To Determine the Distribution of the Overall Survival

All subjects were followed after treatment was complete to assess overall survival. (NCT00928642)
Timeframe: Until death

Interventionmonths (Median)
Treatment9

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The Cystostatic, Anti-tumor Activity of the Combination of Gleevec and Gemzar Via Progression-free Survival for at Least Six Months in Patients With Recurrent or Persistent Epithelial Ovarian or Primary Peritoneal Carcinoma.

Progression free survival at six months was assessed for all research subjects. Progression defined by SWOG criteria: Invest New Drugs. 1992 Nov;10(4):239-53. Progression is defined as > 50% increase in the sume of measured cross sectional area of areasa of measurable disease, measured from the lowest measured amount of disease. Progression is also defined as new areas of measurabe disease. (NCT00928642)
Timeframe: Time to progression was measured from enrollment in study until documented disease progression over a period not greater than 2 years.

Interventionparticipants (Number)
Oral Imatinib Plus Gemcitabine0

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To Determine the Safety and Tolerability Via Frequency and Severity of Adverse Effect of Combination Gleevec and Gemzar in This Cohort of Patients as Assessed Byt Common Toxicity Criteria

Toxicity was assess prior to each cycle of therapy (every 3 weeks) and graded based on NCI common toxicity criteria (NCT00928642)
Timeframe: Until disease progression or unacceptable toxicity

Interventionparticipants (Number)
Grade 3 toxicityGrade 4 toxicityRed Blood Cell Transfusion
Oral Imatinib Puls IV Gemcitabine311

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Overall Response Rate (ORR)

Overall Response Rate: Morphologic Complete Remission (CR) + Morphologic Complete Remission with incomplete blood count recovery (CRi) for evaluable participants. CR - Bone Marrow: < 5% blasts without Auer rods with at least 20% cellularity with maturation of all cell lines, No presence of unique phenotype by flow cytometry identical to what was found in the pretreatment specimen, No persistent dysplasia; Peripheral: normal blood counts, absolute neutrophil count (ANC) > 1.0 k/μl and platelets > 100 k/μl ANC > 1.0 k/μl and platelets > 100 k/μl (Peripheral blood counts documenting recovery can be utilized within 4 weeks of the bone marrow); No evidence of extramedullary leukemia. CRi - All CR criteria are met except for residual Neutropenia <1.0 x 10^9/L platelets < 100 k/μl. (NCT00955916)
Timeframe: 8 weeks per participant

Interventionpercentage of participants (Number)
CLAG Regimen With Gleevec®37

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Median Overall Survival (OS)

Overall Survival is defined as the time from randomization until death from any cause. (NCT00955916)
Timeframe: Up to 3 years

Interventionmonths (Median)
CLAG Regimen With Gleevec®4.9

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Median Progression Free Survival (PFS)

Progression Free Survival is defined as the duration of time from start of treatment to time of progression. Leukemia related failure (progressive disease): Failure to induce bone marrow hypoplasia after 2 cycles or regrowth of leukemic blasts ≥ 20%. (NCT00955916)
Timeframe: Up to 3 years

Interventionmonths (Median)
CLAG Regimen With Gleevec®11.1

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Toxicities

Adverse events of grade 3 or higher, according to CTCAE version 3 (NCT01011075)
Timeframe: 12 months

InterventionNumber of events (Number)
Imatinib Mesylate and Paclitaxel34

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Progression Free Survival

Number of months post treatment without measurable progression according to RECIST criteria (version 1.0) (NCT01011075)
Timeframe: 12 months

InterventionMonths (Median)
Imatinib Mesylate and Paclitaxel3.6

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Overall Survival

Overall survival as measured by the Kaplan-Meier method (NCT01011075)
Timeframe: 12 Months

InterventionMonths (Median)
Imatinib Mesylate and Paclitaxel7.3

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Response Rate

Response rates according to RECIST criteria (version 1.0) expressed as percentage of evaluable patients. (NCT01011075)
Timeframe: 6 months

InterventionPercentage of Participants (Number)
Imatinib Mesylate and Paclitaxel32

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Progression Free Survival

Progression-free survival (PFS) is defined as the duration of time from start of treatment to time of progression. It will be determined for both RECIST (Response Evaluation Criteria in Solid Tumors) and CHOI criteria. (NCT01089595)
Timeframe: 6 months until death or for 5 years

Interventionweeks (Mean)
Nilotinib13
Nilotinib + Imatinib16

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Best Overall Response Using Response Evaluation Criteria in Solid Tumors, Choi Criteria, and Positron Emission Tomography Imaging

(NCT01089595)
Timeframe: Every 8 weeks for up to 5 years

,
InterventionParticipants (Count of Participants)
Stable DiseasePartial ResponseComplete Response
Nilotinib200
Nilotinib + Imatinib010

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Airway Wall Area

Change in airway wall area as assessed by computerized tomography (CT) (NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% of area (Mean)
Imatinib Mesylate0.0002
Placebo0.0002

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Airway Wall Thickness

Change in airway wall thickness as assessed by computerized tomography (CT) (NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% of airway (Mean)
Imatinib Mesylate-0.0040
Placebo-0.0027

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Asthma Quality of Life Questionnaire (AQLQ)

Change in patient-reported Asthma Quality of Life Questionnaire (AQLQ) score The asthma quality of life questionnaire (AQLQ) is a 32-item scale with a range from 1-7 with a higher value denoting improvement. The minimal important difference is 0.5. (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionunits on a scale (Mean)
Imatinib Mesylate0.55
Placebo0.25

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Asthma Symptom Utility Index (ASUI)

Change in patient reported ASUI score The asthma symptom utility index (ASUI) is a 10-item weighted scale with a range from 0.2 to 1 with a higher value indicating improvement. The minimal important difference is 0.09. (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionunits on a scale (Mean)
Imatinib Mesylate0.07
Placebo0.05

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BAL Eosinophil %

Change in BAL eosinophil percentage (NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% eosinophils (Mean)
Imatinib Mesylate2.55
Placebo-2.63

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Endobronchial Biopsy Smooth Muscle Tryptase-positive Mast Cells

Change in the biopsy smooth muscle tryptase-positive mast cells from baseline at 6 months (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionmast cells per mm2 (Mean)
Imatinib Mesylate-102.7
Placebo-79.2

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Endobronchial Biopsy Total Tryptase-positive Mast Cells

Change in endobronchial biopsy total tryptase-positive mast cells from baseline at 6 months (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionmast cells per mm2 (Mean)
Imatinib Mesylate-54.2
Placebo-32.3

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Evening Peak Flow

Change in patient-reported evening peak flow measurement (L/s) (NCT01097694)
Timeframe: 6 months after start of treatment

InterventionL/second (Mean)
Imatinib Mesylate8.3
Placebo-8.2

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FEV1 in Liters

Change in FEV1 in treatment group compared to placebo group (NCT01097694)
Timeframe: 6 months after start of treatment

InterventionL (Mean)
Imatinib Mesylate0.046
Placebo0

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Bronchoalveolar Lavage (BAL) PGD2

Change in bronchoalveolar lavage (BAL) PGD2 levels from baseline at 6 months (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionpg/mL (Mean)
Imatinib Mesylate12.2
Placebo-4.2

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Urinary Leukotriene E4

Change in urinary leukotriene E4 levels from baseline (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionng/mg Creatinine (Mean)
Imatinib Mesylate0.07
Placebo0.01

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Serum Total Tryptase

Change in serum total tryptase after 24 weeks of imatinib vs placebo treatment (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionng/ml (Mean)
Imatinib Mesylate-2.02
Placebo-0.56

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Number of Asthma Exacerbations

Number of asthma exacerbations experienced from randomization to study completion. (NCT01097694)
Timeframe: Up to 24 weeks

Interventionevents (Number)
Imatinib Mesylate16
Placebo20

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Morning Peak Flow Measurement

Change in patient-reported morning peak flow measurement (L/s) (NCT01097694)
Timeframe: 6 months after start of treatment

InterventionL/second (Mean)
Imatinib Mesylate7.3
Placebo-6.4

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Fractional Exhaled Nitric Oxide (FeNO)

Change in Fractional Exhaled Nitric Oxide Measurement (ppb) (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionparts per billion (Mean)
Imatinib Mesylate7.89
Placebo-5.92

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Asthma Control Questionnaire (ACQ)

Change in patient-reported ACQ score The six-item Asthma Control Questionnaire (ACQ-6) is a scale from 0 to 6 with a lower value denoting an improvement in asthma control. The minimal important difference is 0.5. (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionunits on a scale (Mean)
Imatinib Mesylate-0.62
Placebo-0.49

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Bronchoalveolar Lavage (BAL) Fluid Tryptase Level

Change in BAL fluid tryptase levels after 24 weeks of imatinib vs. placebo (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionng/mL (Mean)
Imatinib Mesylate-0.74
Placebo0.43

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Blood Eosinophils

Change in blood eosinophil count (NCT01097694)
Timeframe: 6 months after start of treatment

Interventioneosinophils per microliter (Mean)
Imatinib Mesylate-10.2
Placebo-2.6

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Bronchoalveolar Lavage Histamine

Change in bronchoalveolar lavage histamine levels from baseline (NCT01097694)
Timeframe: 6 months after start of treatment

InterventionnM (Mean)
Imatinib Mesylate2.1
Placebo-1.1

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Change in Maximum Post-Bronchodilator (BD) Forced Expiratory Volume in One Second (FEV1) %

(NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% of predicted (Mean)
Imatinib Mesylate0.01
Placebo-0.08

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Change in Mean Methacholine Responsiveness as Assessed by the Provocation Concentration Causing a 20% Fall in Forced Expiratory Volume in One Second (FEV1) (PC20) at Month 3 and 6 Versus Baseline

"Our primary outcome was change in airway hyperresponsiveness, as assessed by PC20, from baseline to 3 and/or 6 months of therapy in imatinib treated participants as compared with controls. Change in PC20 was assessed using log2-transformed ratios of PC20 at month 3 and /or month 6 vs PC20 at baseline. Our null hypothesis was that the mean of this ratio will be 0 after log2-transformed. We used a linear mixed-effects model for a repeated-measures analysis to compare the primary outcome between the two groups.~PC20 is determined by the provocation concentration of methacholine causing a 20% fall in forced expiratory volume in one second (FEV1)." (NCT01097694)
Timeframe: Over 6 months from beginning of treatment

InterventionLog2 Ratio (Mean)
Imatinib Mesylate1.73
Placebo1.07

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FEV1%

Change in FEV1% of predicted (NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% of predicted (Mean)
Imatinib Mesylate2.3
Placebo0.78

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BAL Neutrophil %

Change in BAL neutrophil percentage from baseline (NCT01097694)
Timeframe: 6 months after start of treatment

Intervention% neutrophils (Mean)
Imatinib Mesylate-0.8
Placebo-0.4

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Bronchoalveolar Lavage Cysteinyl Leukotrienes

Change in bronchoalveolar lavage cysteinyl leukotrienes levels from baseline (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionpg/mL (Mean)
Imatinib Mesylate3.0
Placebo6.5

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Urinary Prostaglandin D2

Change in urinary Prostaglandin D2 levels from baseline (NCT01097694)
Timeframe: 6 months after start of treatment

Interventionng/mg Creatinine (Mean)
Imatinib Mesylate-0.30
Placebo0.39

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Number of Participants With Adverse Events, Serious Adverse Events and Deaths

Adverse event monitoring was conducted throughout the study. (NCT01117987)
Timeframe: 204 weeks

,
InterventionParticipants (Number)
Adverse events (non-serious and serious)Serious adverse eventsDeaths
Core Imatinib62406
Core Placebo765310

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Percentage of Participants With Incidence of Clinical Worsening Events

Clinical worsening events included death, overnight hospitalization for worsening of PAH, worsening of World Health Organization (WHO) functional class by at least one level (drop in WHO ), 15% decrease in the 6MWD as compared to baseline confirmed by two 6MWTs at two consecutive study visits (6MWD reduction), and drop in WHO & 6MWD reduction. Some participants have fulfilled more than one criterion. Therefore, the sum of individual components may be higher than the total number of participants with clinical worsening. (NCT01117987)
Timeframe: 204 weeks

,
InterventionPercentage of participants (Number)
Total participants with clinical worseningDeath (all deaths)Hospitalization for worsening of PAHDrop in WHO6MWD reductionDrop in WHO and 6MWD reduction
Core Imatinib50.07.633.324.212.11.5
Core Placebo46.212.828.219.219.23.8

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Change From Core Study Baseline in Six-Minute Walk Distance (6MWD)

A six minute walk test (6MWT) was performed in accordance with the guidleines of the American Thoracic Society (2002). (NCT01117987)
Timeframe: core study baseline, extension baseline, 12 weeks, 24 weeks, 48 weeks, 72 weeks, 96 weeks, 120 weeks, 144 weeks, 156 weeks, 204 weeks

,
Interventionmeters (Mean)
Extension baseline (n=61,77)Week 12 (n=58,57)Week 24 (n=54,53)Week 48 (n=47,42)Week 72 (n=40,39)Week 96 (n=38,35)Week 120 (n=32,29)Week 144 (n=27,21)Week 156 (n=21,18)Week 204 (n=4,3)
Core Imatinib42.9848.7544.7145.8149.5466.6483.1967.7072.6096.88
Core Placebo4.9116.2519.3429.1856.4641.0337.4339.4530.174.50

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Progression Free Survival

To compare PFS assessed by investigators (NCT01151852)
Timeframe: up to 12 weeks

InterventionMonths (Median)
Imatinib1.8
Placebo1.7

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Progression-free Survival

To compare the progression free survival (PFS) assessed by the blinded independent central review following resumption of dosing (re-challenge) with Imatinib plus best supportive care versus placebo plus best supportive care in patients with unresectable or metastatic GIST following failure of at least prior imatinib and sunitinib therapies (NCT01151852)
Timeframe: up tp12 weeks

InterventionMonths (Median)
Imatinib1.8
Placebo0.9

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Response Rate

"Tumour responses were initially determined by the local investigators in accordance with RECIST 1.0.Treatment decisions were based on local onsite radiological review. All imaging data were subsequently collected, anonymised, and reviewed centrally in a double-blind manner by two external academic radiology reviewers.~Response assessment was determined in a masked central review by use of RECIST1.1." (NCT01151852)
Timeframe: Up to 12weeks

Interventionpercentage of participants (Number)
Imatinib0
Placebo0

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Safety and Tolerability of Imatinib

percentage of patients who experienced toxicity from study treatment to evaluate the safety and tolerability of imatinib re-challenge in this patient population (NCT01151852)
Timeframe: Up to 3years

Interventionpercentage of participants (Number)
Imatinib100
Placebo98

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Overall Survival(OS) and Time to Progression(TTP)

To compare the overall survival (OS) and time to progression (TTP) in both arms of the study (NCT01151852)
Timeframe: Up to 3years

,
InterventionMonths (Median)
Overall survivalTime to progression
Imatinib8.21.8
Placebo7.50.9

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Disease Control Rate

"Inclusion of complete response, partial response or stable disease~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR; Progressive disease (PD), >20% increase in the sum of the longest diameter of target lesions; Stable Disease (SD), Insufficient change to qualify for PR or PD." (NCT01151852)
Timeframe: up to 12 weeks

Interventionpercentage of participants (Number)
Imatinib32
Placebo5

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Kaplan-Meier Estimates of Progression-free Survival (PFS) on Treatment

"Progression-free survival was defined as the time from the date of randomization to the date of event defined as the first disease progression to AP/BC or the date of death from any cause, whichever is earlier. This variable was analyzed in 2 ways:~On-treatment: included progressions to AP/BC or deaths occurring only on-treatment in the study as events. The time was censored at the date of last on-treatment assessment (hematology, extramedullary disease or cytogenetic evaluation) in the study before the cut-off date of the analysis for patients without event.~On-study: included progressions to AP/BC or deaths occurring in the study or during the follow-up period after discontinuation of study treatment as events. The time was censored at the last assessment date in the study for patients who were still being treated and at the date of last contact for patients who discontinued treatment." (NCT01275196)
Timeframe: End of study (up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Kaplan-Meier Estimates of Time to First CCYR

Time to first CCyR (months) = (date of first CCyR - date of randomization + 1) / 30.4375. (NCT01275196)
Timeframe: End of study (up to 40 months)

Interventionmonths (Median)
Imatinib6.1
Nilotinib5.6

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Kaplan-Meier Estimates of Time to First MMR

Time to first MMR (months) = (date of first MMR or censoring - date of randomization + 1) / 30.4375. (NCT01275196)
Timeframe: End of study (up to 40 months)

Interventionmonths (Median)
Imatinib21.7
Nilotinib8.1

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Kaplan-Meier Estimates of Time to Progression to Accelerated Phase/Blast Crisis (AP/BC) on Treatment

"Time to progression to AP/BC was defined as the time from the date of randomization to the date of event defined as the first disease progression to AP/BC or the date of CML-related death, whichever is earlier. This variable was analyzed in 2 ways:~On-treatment: included progressions to AP/BC or CML-related deaths occurring on treatment in the study as events. The time was censored at the date of last on-treatment assessment (hematology, extramedullary disease, or cytogenetic evaluation) in the study for patients without event.~On-study: included progressions to AP/BC or CML-related deaths occurring in the study or during the follow-up period after discontinuation of treatment as events. The time was censored at the last assessment date in the study for patients who were still being treated and at the date of last contact for patients who discontinued treatment" (NCT01275196)
Timeframe: End of study (up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Summary Statistics of Trough Imatinib and Major Metabolite CGP74588 of Imatinib and Nilotinib PK Concentration by Time Point

Pharmacokinetic Analysis Set (NCT01275196)
Timeframe: 12 Months

,,
Interventionng/mL (Mean)
Day 8 (Cycle 1)Day 28 (Cycle 1)Day 84 (Cycle 3)Day 168 (Cycle 6)Day 336 (Cycle 12)Average trough PK
CGP74588255.4288.9235.7243.2238.7258.7
Imatinib1235.31291.31137.81078.21111.11188.7
Nilotinib1036.8970.41172.41154.81370.51137.4

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Modified ELN2009 Criteria

"Patients satisfying criteria for several modified ELN 2009 categories are presented once under the worst category (Optimal> Suboptimal > Treatment failure). Patients in the Discontinued category are those who discontinued before the time point considered without satisfying any of the ELN 2009 criteria. Patients in the Missing category are those ongoing in the trial at the time point considered but with only missing or non evaluable data for ELN 2009 criteria." (NCT01275196)
Timeframe: End of Study (up to 40 months)

,
InterventionPercentage of Participants (Number)
Optimal ResponseSuboptimal ResponseTreatment FailureDiscontinued
Imatinib39.841.416.52.3
Nilotinib55.224.614.95.2

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MMR Rate at Each Time Point

Major molecular response (MMR) was defined as a value of ≤ 0.1% of BCR-ABL ratio on the IS. The minimum number of control genes for a sample to be valid was 3000. For statistical comparison purpose, MMR was considered as a binary variable with patients achieving MMR grouped as 'responders' and patients not achieving MMR, patients with missing PCR evaluations or patients with atypical transcripts at baseline grouped as 'non-responders'. These time points including the 12 month data were calculated based on the final analysis after the end of the study. (NCT01275196)
Timeframe: Months 3,6,9,12,15, 18, 21, 24, 36

,
InterventionPercentage of Participants (Number)
3 Months6 Months9 Months12 Months15 Months18 Months21 Months24 Months36 Months
Imatinib3.018.021.127.836.140.641.449.659.4
Nilotinib13.444.847.853.059.057.561.961.968.7

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Best MMR by Each Timepoint

Best MMR rates by scheduled time point are cumulative response rates up to that time point. In this analysis, patients who had achieved MMR at or before the time point were counted as responders, no matter if they lost the response/discontinued or not. Therefore, this response rate represented the best observed response rate up to that specific time point. (NCT01275196)
Timeframe: Months 3,6,9,12,15, 18, 21, 24, 36

,
InterventionPercentage of Participants (Number)
OverallMonth 3Month 6Month 9Month 12Month 15Month 18Month 21Month 24Month 36
Imatinib66.93.018.022.630.837.642.946.652.665.4
Nilotinib73.913.445.551.556.062.764.266.467.973.9

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Durable MMR Rate at 24 Months

The rate of durable MMR at 24 months, defined as the proportion of patients who have achieved MMR at 12 months, and also maintain continuous MMR until the 24 month time point (1 month = 28 days) without intervening loss of MMR in between 12 and 24 months (NCT01275196)
Timeframe: 24 months

InterventionPerentage of Participants (Number)
Imatinib27.8
Nilotinib50.7

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Best Complete Hematologic Response (CHR)

CHR was defined as having all of the following criteria present at any assessment, which was confirmed by another assessment at least after 4 weeks: • WBC count < 10 x 10E9 /L • Platelet count < 450 x 10E9 /L • Basophils < 5% • No blasts and promyelocytes in peripheral blood • Myelocytes + metamyelocytes < 5 % in peripheral blood • No evidence of extramedullary involvement. The assessment was not considered CHR, if there were any values indicative of CML in AP or BC (i.e. by blasts in bone marrow). For confirmation of CHR, both the initial CHR as well as the confirming assessment (at least 4 weeks after the initial assessment) had to satisfy all criteria mentioned above, without any assessment in between which indicated 'No response'. (NCT01275196)
Timeframe: Months 1, 3, 4, 5, 6, 9,12, 15,18, 21, 24, 30, 36

,
InterventionPercentage of participants (Number)
OverallMonth 1Month 3Month 4Month 5Month 6Month 9Month 12Month 15Month 18Month 21Month 24Month 30Month 36
Imatinib94.766.291.093.294.094.794.794.794.794.794.794.794.794.7
Nilotinib94.873.191.893.393.393.393.394.094.094.894.894.894.894.8

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Best Complete Cytogenic Response (CCyR) Rate by Each Time Point

CCyR is defined as 0% Ph+ metaphases based on at least 20 metaphases from bone marrow cytogenetics. (NCT01275196)
Timeframe: Months 6, 12, 18, 30, 24, 36

,
InterventionPercentage of Participants (Number)
OverallMonth 6Month 12Month 18Month 30Month 24Month 36
Imatinib89.557.180.584.288.086.589.5
Nilotinib85.866.477.680.684.383.685.8

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Major Molecular Response (MMR) at 12 Months - With Imputation.

Major molecular response (MMR) was defined as a value of ≤ 0.1% of BCR-ABL ratio on the IS. The minimum number of control genes for a sample to be valid was 3000. For statistical comparison purpose, MMR was considered as a binary variable with patients achieving MMR grouped as 'responders' and patients not achieving MMR, patients with missing PCR evaluations or patients with atypical transcripts at baseline grouped as 'non-responders'. This endpoint was calculated based on the 12 month analysis. (NCT01275196)
Timeframe: 12 months

InterventionPercentage of Participants (Number)
Imatinib27.8
Nilotinib52.2

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Kaplan-Meier Estimates of Duration of First CCyR Among Patients Who Achieved CCyR

Duration of CCyR (months) = (date of CCyR loss or censoring-date of first CCyR + 1)/30.4375 (NCT01275196)
Timeframe: End of Study (up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Kaplan-Meier Estimates of Duration of First MMR Among Patients Who Achieved MMR

Duration of first MMR (months) = (date of loss of MMR or censoring-date of first MMR + 1)/30.4375. (NCT01275196)
Timeframe: End of Study (Up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Actual Dose Intensity

Total dose/time on treatment (periods of zero dose were included). (NCT01275196)
Timeframe: End of Study (up to 40 months)

Interventionmg/day (Mean)
Imatinib416.0
Nilotinib536.4

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Kaplan-Meier Estimates of Event-free Survival (EFS) on Treatment

Event-free survival was defined as the time from the date of randomization to the date of first occurrence of any of the following:-Death due to any cause, - Progression to AP or BC, Loss of partial cytogenetic response (PCyR), - Loss of CCyR, - Loss of CHR (NCT01275196)
Timeframe: End of Study (up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Kaplan-Meier Estimates of Overall Survival (OS) on Treatment

Patients who discontinued study treatment early or completed the study protocol and did not enter into the extension protocol were to be followed for survival every 3 months for up to 2 calendar years from the date the last patient randomized received the first dose of study drug and every 6 months until Last Patient Last Visit. Overall survival (all deaths) was defined as the time between date of randomization and date of death due to any cause at any time during the study, including the follow-up period after discontinuation of treatment, i.e. overall survival on-study. The time was censored at the date of last assessment in the study for patients who are still being treated and at the date of last contact for patients who discontinued treatment. (NCT01275196)
Timeframe: End of Study (up to 40 months)

InterventionMonths (Median)
ImatinibNA
NilotinibNA

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Number of Participants With Adverse Events (AEs): Phase I & II

Assessed safety and tolerability of the combination administration of RAD001 and imatinib when given to patients with imatinib-refractory gastro-intestinal stromal tumors (GIST) by number of participants with adverse events. (NCT01275222)
Timeframe: 4 - 8 weeks

InterventionParticipants (Number)
Phase l: RAD001 20mg/Week13
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day13
Phase l: RAD001 5mg/Day + Glivec 600mg/Day5
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day11
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day27
Phase ll: Stratum ll (Post Second-line Therapy)47

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Best Overall Response (BOR) as Assessed by Overall Response (Complete Response (CR) & Partial Response (PR)) - Phase I & II

Assessed clinical efficacy of the combination regimen in this patient population per BOR by Overall response (CR + PR). Complete response: Disappearance of all target lesions; Partial response: ≥ 30% decrease in the sum of the longest diameter of target lesions compared to baseline (and not ≥20% increase compared to smallest sum). (NCT01275222)
Timeframe: 6 - 8 weeks

InterventionPercentage of Participants (Number)
Phase l: RAD001 20mg/Week0
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day1
Phase l: RAD001 5mg/Day + Glivec 600mg/Day0
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day0.0
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day0
Phase ll: Stratum ll (Post Second-line Therapy)1

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Trough Concentrations for RAD001 and for Imatinib - Phase II

Assessed the pharmacokinetics (PK) of the combination administration of RAD001 and imatinib in this patient population. (NCT01275222)
Timeframe: Part II Daily regimen: Baseline, Days 8, 15 and thereafter approximately every two months starting at month 3 whenever possible

Interventionng/mL (Median)
Week 2: RAD001Week 3: RAD001Baseline: ImatinibWeek 2: ImatinibWeek 3: ImatinibMonth 4: ImatinibMonth 6: Imatinib
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day24.30019.900472.00626.50572.00333.00181.00

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4-Month Progression-free Survival (PFS) Rate - Phase II

Assessed clinical efficacy of the combination regimen in this patient population per Progression-free survival (PFS). Progression-free survival (PFS) was the time from date of start of treatment to the date of first documented progression or death due to any cause. Per protocol (PP) population includes patients with no known overall lesion response during 4 months +/- 2 weeks, or who later had response of CR/PR/stable disease (SD). PP population excludes patients with no known response during 4 months + / -2 weeks and no subsequent CR/PR/SD. (NCT01275222)
Timeframe: about 4 months

InterventionPercentage of participants (Number)
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day17.4
Phase ll: Stratum ll (Post Second-line Therapy)37.1

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Trough Concentrations for RAD001 and for Imatinib - Phase II

Assessed the pharmacokinetics (PK) of the combination administration of RAD001 and imatinib in this patient population. (NCT01275222)
Timeframe: Part II Daily regimen: Baseline, Days 8, 15 and thereafter approximately every two months starting at month 3 whenever possible

Interventionng/mL (Median)
Week 2: RAD001Week 3: RAD001Week 9: RAD001Month 4: RAD001Baseline: ImatinibWeek 2: ImatinibWeek 3: ImatinibWeek 9: ImatinibMonth 4: ImatinibMonth 6: ImatinibMonth 8: ImatinibMonth 12: Imatinib
Phase ll: Stratum ll (Post Second-line Therapy)12.10012.75010.9507.840501.50540.00718.00899.0446.002040.00575.00324.00

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All Collected Deaths

On treatment deaths were collected from FPFT up to 28 days after study drug discontinuation, for a maximum duration of 35.52 months (treatment duration ranged from 0.36 to to 35.52 months for the phase I part) and a maximum duration of 21.88 months (treatment duration of 0.16 to 21.88 months for the phase II part). Deaths post treatment survival follow up were collected after the on treatment period, up to 70 months. (NCT01275222)
Timeframe: approx. 35.52 months, approx. 70 months

,,,,,
InterventionParticipants (Number)
Total DeathsDeaths on-treatment
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day83
Phase l: RAD001 2.5mg/Day + Glivec 800mg/Day32
Phase l: RAD001 20mg/Week122
Phase l: RAD001 5mg/Day + Glivec 600mg/Day30
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day93
Phase ll: Stratum ll (Post Second-line Therapy)226

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Progression-free Survival (PFS) - Phase II

"Assessed clinical efficacy of the combination regimen in this patient population per Progression-free survival (PFS). Progression-free survival (PFS) was the time from date of start of treatment to the date of first documented progression or death due to any cause. If a patient had not progressed or died, progression-free survival was censored at the time of last adequate tumor assessment.~According to the study protocol no tumor assessments were performed after discontinuation of treatment with study drug. Therefore, for all patients who discontinued treatment without a documented progression but died thereafter, death was considered as PFS event only if it occurred within the regular safety follow-up of 28 days after discontinuation. Otherwise, the PFS time was censored at the last adequate tumor assessment." (NCT01275222)
Timeframe: about 60 months

Interventionmonths (Median)
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day1.9
Phase ll: Stratum ll (Post Second-line Therapy)3.5

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Overall Survival (OS) - Phase I & II

Assessed clinical efficacy of the combination regimen in this patient population per Overall Survival (OS). Overall survival was defined as the time from date of start of treatment to date of death due to any cause. For patients still receiving study medication at the time of the analysis, survival was censored at the date of last examination. If a patient was not known to have died but was no longer continuing with study medication, survival was censored at the date of last contact. (NCT01275222)
Timeframe: about 60 months

Interventionmonths (Median)
Phase l: RAD001 20mg/Week9.4
Phase l: RAD001 5mg/Day + Glivec 600mg/Day10.9
Phase l: RAD001 2.5mg/Day + Glivec 600mg/Day18.7
Phase l: RAD001 2.5mg/Day + Glivec 800mg/DayNA
Phase ll - Stratum l (First-line Resistant/Refractory): RAD001 2.5mg/Day + Glivec 600mg/Day14.9
Phase ll: Stratum ll (Post Second-line Therapy)10.7

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Response Rate (CR + PR) Assessed by RECIST 1.1 (Phase II)

(NCT01281865)
Timeframe: At 8 weeks

,
Interventionparticipants (Number)
Progression of DiseaseStable Disease
Arm 1-Treatment (Everolimus and Imatinib Mesylate)45
Arm 2-Treatment (Everolimus and Imatinib Mesylate)10

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Percentage of CD27+ B Cells in Responders (SCR) and Non-responders

%CD27+ B cells (NCT01309997)
Timeframe: 6 months

Interventionpercentage of CD27+ B cells (Mean)
Rituximab Responders10
Rituximab Non-responders4.3
Imatinib Responders14.2
Imatinib Nonresponders17.1

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Significant Clinical Response

Assessed by decline in an affected area's skin score as measured with the Vienna Skin Scale (from 4 [worst] to 2, 3 to 1, or 2 to 0 [best]) without a concurrent increase of two or more points in another area OR by an increase in the range of motion of the shoulders, elbows or wrists by two points (in a 1-7 scale where 1 is worst and 7 is best) or of the ankles by one point (in a 1 to 4 scale where 1 is worst and 4 is best) without a concurrent worsening in another area. (NCT01309997)
Timeframe: 6 months

Interventionparticipants (Number)
Arm I (Enzyme Inhibitor)9
Arm II (Monoclonal Antibody)10

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Cumulative Incidence of Treatment Failure

Defined as discontinuation of randomized treatment due to chronic GVHD progression or treatment intolerance or no significant clinical response in sclerosis. (NCT01309997)
Timeframe: 6 months

Interventionparticipants (Number)
Arm I (Enzyme Inhibitor)24
Arm II (Monoclonal Antibody)26

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Number of Patients Achieving Improvement in Cutaneous Sclerosis

Assessed by decrease of >= 0.2 units (where 0 is best and 3.0 is worst ) in the Scleroderma Health Assessment Questionnaire (SHAQ). (NCT01309997)
Timeframe: 6 months

Interventionparticipants (Number)
Arm 1 (Enzyme Inhibitor)2
Arm II (Monocolonal Antibody)9

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Patients Who Were Able to Taper Corticosteroids

Patients who achieved a greater than or equal to 50% reduction in the daily corticosteroid dose at 6mo compared to baseline (NCT01309997)
Timeframe: 6 months

Interventionparticipants (Number)
Arm I (Enzyme Inhibitor)7
Arm II (Monoclonal Antibody)9

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Baseline Histopathologic Score in the Two Treatment Arms

"Instrument: Nash dermal fibrosis grade. Measures extent of sclerosis in skin biopsies by histologic examination. Scale ranges from grade 0-5. Nash grade 5 is most severe fibrosis (0 is better outcome, 5 is worse outcome). No subscales are used in Nash grade. Please see table 1 in the reference for grading of dermal fibrosis.~Nash RA, McSweeney PA, Crofford LJ, Abidi M, Chen CS, Godwin JD, et al. High-dose immunosuppressive therapy and autologous hematopoietic cell transplantation for severe systemic sclerosis: long-term follow-up of the US multicenter pilot study. Blood 2007;110:1388-96." (NCT01309997)
Timeframe: Enrollment

Interventionunits on a scale (Median)
Arm 1 (Enzyme Inhibitor)2
Arm II (Monoclonal Antibody)2

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Patients With Any Percentage Decline in Any Grade of Sclerosis Without Increase in Percentage of Higher Grades of Sclerosis in Other Areas on the Vienna Skin Scale

Maximum of 10 body areas. Each area can be graded 0 (best) to 4 (worst). Each of those grades requires a percentage of involvement. Improvement is measured by reduction of involvement in any grade and any body area. (NCT01309997)
Timeframe: 6 months

Interventionparticipants (Number)
Arm I (Enzyme Inhibitor)14
Arm II (Monoclonal Antibody)9

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Number of Subjects Who Achieved Complete Remission of Their Disease

Complete Remission (CR): A CR requires that the following be recorded concurrently: an absolute neutrophil count (segs and bands) > 1000/μL, no circulating blasts, platelets > 100,000/μL; adequate bone marrow cellularity with trilineage hematopoiesis, and < 5% marrow leukemia blast cells. All previous extramedullary manifestations of disease must be absent. If patients continue on with treatment, there can be no evidence of recurrence of ALL for at least 4 weeks. (NCT01312818)
Timeframe: Day 30

Interventionparticipants (Number)
ALL Treated Patients0

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Number of Patients With Complete Remission at One Year

The complete remission (CR) is the total number of patients who are in CR at one year divided by the total number of patients who received at least one dose of HCVAD with liposomal vincristine. CR was defined as the presence of 1x10^9/L neutrophils, >100x10^9/L platelets in the perpherial blood, and no extramedullary disease. (NCT01319981)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Hyper-CMAD + Rituximab12
Hyper-CMAD13

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Overall Survival

Time from date of treatment start until date of death due to any cause or last Follow-up. Survival will be measured by the estimated median survival computed by Kaplan-Meier (K-M) analysis, which is the time point at which the cumulative survival drops below 50%, if present. If not present then the median Overall Survival is not reached and not available (NA) as there are an insufficient number of participants with events. In either case ranges are provided for observed survival intervals used in the K-M analysis. (NCT01319981)
Timeframe: Up to 7 years, 8 months

InterventionMonths (Median)
Hyper-CMAD + RituximabNA
Hyper-CMADNA

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Complete Response Duration

The complete remission (CR) is the total number of patients who are in CR at one year divided by the total number of patients who received at least one dose of HCVAD with liposomal vincristine. CR was defined as the presence of 1x10^9/L neutrophils, >100x10^9/L platelets in the perpherial blood, and no extramedullary disease. Response date to loss of response or last follow up. Remission duration will be measured by the estimated median remission duration computed by Kaplan-Meier (K-M) analysis, which is the time point at which the cumulative remission duration drops below 50%, if present. If not present then median remission duration is not reached and not available (NA) as there are an insufficient number of participants with events. In either case ranges are provided for observed survival intervals used in the K-M analysis.. (NCT01319981)
Timeframe: Up to 7 years, 8 months

InterventionMonths (Median)
Hyper-CMAD + RituximabNA
Hyper-CMADNA

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Geometric Mean Ratio of Dose Normalized AUCtau for Sildenafil Before and After Imatinib Administrations

"AUCtau was the area under the curve calculated to the end of the dosing interval, tau. The effect of co-administration of imatinib at two doses (200 and 400 mg) on the pharmacokinetics of sildenafil was performed on dose normalized AUCtau of sildenafil. A mixed effects linear model was fitted to the log-transformed PK parameters. This model included treatment (i.e., dose of imatinib) as a fixed effect, and participant as a random effect. Estimates for the treatment differences and associated 90% confidence intervals were obtained from the above model. These estimates and confidence intervals were then back-transformed to the original scale, giving, for each dose level of imatinib, the ratio of imatinib + co-administered sildenafil and bosentan (test) relative to the co-administered drugs alone (sildenafil + bosentan) (reference)." (NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

Interventionhr*ng/mL/mg (Geometric Mean)
Bosentan + Sildenafil (Reference)7.22
Imatinib (200 mg/Day) + Bosentan + Sildenafil (Test 1)9.82
Imatinib (400 mg/Day) + Bosentan + Sildenafil (Test 2)12.3

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Geometric Mean Ratio of Dose Normalized Cmax for Sildenafil Before and After Imatinib Administrations

"Cmax was the maximum (peak) observed plasma, blood, serum, or other body fluid drug concentration after dose administration. The effect of co-administration of imatinib at two doses (200 and 400 mg) on the pharmacokinetics of sildenafil was performed on dose normalized Cmax of sildenafil. A mixed effects linear model was fitted to the log-transformed PK parameters. This model included treatment (i.e., dose of imatinib) as a fixed effect, and participant as a random effect. Estimates for the treatment differences and associated 90% confidence intervals were obtained from the above model. These estimates and confidence intervals was then back-transformed to the original scale, giving, for each dose level of imatinib, the ratio of imatinib + co-administered sildenafil and bosentan (test) relative to the co-administered drugs alone (sildenafil + bosentan) (reference)." (NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

Interventionng/mL/mg (Geometric Mean)
Bosentan + Sildenafil (Reference)2.44
Imatinib (200 mg/Day) + Bosentan + Sildenafil (Test 1)3.14
Imatinib (400 mg/Day) + Bosentan + Sildenafil (Test 2)3.81

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Geometric Mean Ratio of Dose Normalized Maximum Plasma Concentration (Cmax) for Bosentan Before and After Imatinib Administrations

"Cmax was the maximum (peak) observed plasma, blood, serum, or other body fluid drug concentration after dose administration. The effect of co-administration of imatinib at two doses (200 and 400 mg) on the pharmacokinetics of bosentan was performed on dose normalized Cmax of bosentan. A mixed effects linear model was fitted to the log-transformed PK parameters. This model included treatment (i.e., dose of imatinib) as a fixed effect, and participant as a random effect. Estimates for the treatment differences and associated 90% confidence intervals were obtained from the above model. These estimates and confidence intervals were then back-transformed to the original scale, giving, for each dose level of imatinib, the ratio of imatinib + co-administered sildenafil and bosentan (test) relative to the co-administered drugs alone (sildenafil + bosentan) (reference)." (NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

Interventionng/mL/mg (Geometric Mean)
Bosentan + Sildenafil (Reference)21.9
Imatinib (200 mg/Day) + Bosentan + Sildenafil (Test 1)21.8
Imatinib (400 mg/Day) + Bosentan + Sildenafil (Test 2)23.4

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Dose Normalized AUCtau of Imatinib and CGP74588 (Active Metabolite of Imatinib)

(NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

,
Interventionhr*ng/mL/mg (Mean)
Imatinib AUCtau/DoseCGP74588 AUCtau/Dose
Imatinib (200 mg/Day) + Bosentan + Sildenafil90.919.3
Imatinib (400 mg/Day) + Bosentan + Sildenafil88.420.6

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Number of Participants With At Least One or More Adverse Events (AEs)

An adverse event was the appearance or worsening of any undesirable sign, symptom, or medical condition that occurred after starting the study drug even if the event was not considered to be related to study drug. Number of participants with AEs were reported by treatment period. (NCT01392469)
Timeframe: From time of first administration of study drug until end of study (up to approximately 18 months)

InterventionParticipants (Count of Participants)
Bosentan + Sildenafil10
Imatinib (200 mg/Day) + Bosentan + Sildenafil9
Imatinib (400 mg/Day) + Bosentan+ Sildenafil16

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Dose Normalized Cmax of Imatinib and CGP74588 (Active Metabolite of Imatinib)

(NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

,
Interventionng/ml/mg (Mean)
Imatinib Cmax/DoseCGP74588 Cmax/Dose
Imatinib (200 mg/Day) + Bosentan + Sildenafil7.551.37
Imatinib (400 mg/Day) + Bosentan + Sildenafil6.711.39

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Geometric Mean Ratio of Dose Normalized Area Under the Curve From Time Zero to Tau (AUCtau) for Bosentan Before and After Imatinib Administrations

"AUCtau was the area under the curve calculated to the end of the dosing interval, tau. The effect of co-administration of imatinib at two doses (200 and 400 mg) on the pharmacokinetics of bosentan was performed on dose normalized AUCtau of bosentan. A mixed effects linear model was fitted to the log-transformed PK parameters. This model included treatment (i.e., dose of imatinib) as a fixed effect, and participant as a random effect. Estimates for the treatment differences and associated 90% confidence intervals were obtained from the above model. These estimates and confidence intervals were then back-transformed to the original scale, giving, for each dose level of imatinib, the ratio of imatinib + co-administered sildenafil and bosentan (test) relative to the co-administered drugs alone (sildenafil + bosentan) (reference)." (NCT01392469)
Timeframe: Day 1: pre-dose, Day 8: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10 and 12 hours post-dose, Day 9: pre-dose, Days 22 and 36: pre-dose, 0.5, 1, 2, 3, 4, 6, 8, 10, 12 and 24 hours post-dose

Interventionhr*ng/mL/mg (Geometric Mean)
Bosentan + Sildenafil (Reference)93.3
Imatinib (200 mg/Day) + Bosentan + Sildenafil (Test 1)109
Imatinib (400 mg/Day) + Bosentan + Sildenafil (Test 2)131

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Number of Patients With Adverse Events, Serious Adverse Events and Deaths

Adverse event monitoring was conducted throughout the trial. (NCT01392495)
Timeframe: 144 weeks

,
InterventionParticipants (Number)
Adverse Events (serious and non-serious)Serious Adverse EventsDeaths
QTI571 200 mg442
QTI571 400 mg1351

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Time to Molecular Response (MR)^4.5

"Time to Molecular Response (MR)^4.5 is the time between randomization date and first date that MMR (or MR4.5) criteria are satisfied. Participants who do not achieve MMR (or MR4.5) will be censored.~MR4.5 is defined as a 4.5-log reduction in BCR-ABL transcript from the standardized baseline (0.0032% IS, either detectable disease <= 0.0032% BCR-ABL (IS) or undetectable disease in cDNA (in same volume used for BCR-ABL) with >= 32,000 ABL transcripts." (NCT01593254)
Timeframe: From randomization to study completion. Approximately 115 months

InterventionMonths (Median)
Arm 1: Imatinib (≥400 mg)67.7
Arm 2: Dasatinib (100 mg)74.5

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Overall Survival (OS)

OS is the time from randomization date to death date. Participants who have not died will be censored on the last date they are known to be alive. (NCT01593254)
Timeframe: From randomization to study completion. Approximately 115 months

InterventionMonths (Median)
Arm 1: Imatinib (≥400 mg)NA
Arm 2: Dasatinib (100 mg)NA

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Percentage of Patients Achieving Major Molecular Response (MMR) After 12 Months of CML Treatment

"Major Molecular Response, is defined as a 3-log reduction in BCR-ABL transcripts from the standardized baseline, which represents 100% on the international scale, so a 3-log reduction is fixed at 0.1% for MMR; N/A = not applicable. 95% CI is Clopper-Pearson(Exact) two-sided 95% confidence intervals.~P-value is based on Cochran-Mantel-Haenszel (CMH) test stratified by Sokal score(high, intermediate, low, and unknown) and time between 3 month molecular analysis and randomization (<=4 weeks vs >4 weeks)." (NCT01593254)
Timeframe: At 12 months after Day 1 initiation of 1st line treatment with imatinib or imatinib at any dose, after less than optimal response to first-line imatinib.

InterventionPercentage of Patients (Number)
Arm 1: Imatinib (≥400 mg)12.8
Arm 2: Dasatinib (100 mg)28.7

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Progression Free Survival (PFS)

"PFS is the time from randomization date to progression date or death date, whichever occurs first. Participants who neither progress nor die will be censored.~Progression is defined as the following, meeting the criteria for accelerated or blast crisis CML are met at any time or death from any cause during treatment.~Accelerated phase of CML:~The presence of ≥15%, but < 30% blasts in the blood or bone marrow~At least 30% blasts plus promyelocytes in the blood or bone marrow~At least 20% peripheral basophils~Thrombocytopenia (fewer than 100,000 platelets/mm3) unrelated to treatment.~Blast phase of CML~At least 30% blasts in the blood or bone marrow~Extramedullary involvement (e.g., chloromas), but not hepatosplenomegaly" (NCT01593254)
Timeframe: From randomization to study completion. Approximately 115 months

InterventionMonths (Median)
Arm 1: Imatinib (≥400 mg)NA
Arm 2: Dasatinib (100 mg)NA

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Median Time to Major Molecular Response (MMR)

"Median Time to Major Molecular Response (MMR) is the time between randomization date and first date that MMR (or MR4.5) criteria are satisfied. Participants who do not achieve MMR (or MR4.5) will be censored.~Major Molecular Response, is defined as a 3-log reduction in BCR-ABL transcripts from the standardized baseline, which represents 100% on the international scale, so a 3-log reduction is fixed at 0.1% for MMR." (NCT01593254)
Timeframe: From randomization to study completion. Approximately 115 months

InterventionMonths (Median)
Arm 1: Imatinib (≥400 mg)19.7
Arm 2: Dasatinib (100 mg)13.9

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Complete Cytogenetic Response (CCyR) Rate

The percentage of Ph+ metaphases in bone marrow (peripheral blood may not be used), with a review of a minimum of 20 metaphases. Responses are defined as follows: Complete (CCyR): 0% Ph+ metaphases. (NCT01650805)
Timeframe: 12 months after first dose

Interventionparticipants (Number)
Ponatinib5
Imatinib6

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Major Molecular Response (MMR) Rate at 12 Months

A ratio of reverse transcribed transcript of BCR-ABL to ABL ≤ 0.1% on the international scale, measured by real-time quantitative polymerase chain reaction. (NCT01650805)
Timeframe: 12 months after first dose

Interventionparticipants (Number)
Ponatinib8
Imatinib5

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<10% BCR-ABL^IS Rate

To compare the proportion of patients achieving a ratio of <10% BCR-ABL to ABL transcript levels at 3 months, as measured by the international scale (<10% BCR-ABL^IS), in patients administered ponatinib versus those administered imatinib (NCT01650805)
Timeframe: 3 months after first dose

Interventionparticipants (Number)
Ponatinib103
Imatinib77

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Percent Change From Baseline in Tumor Volume at 6 Months

Volumetric measures were performed using MRI scan analysis. Response criteria include greater than 20 percent decrease in tumor volume as responsive. Greater than 20 percent increase in tumor volume as tumor progression. Less then 20 percent increase or decrease in tumor volume is stable disease (NCT01673009)
Timeframe: baseline to 6 months

Interventionpercentage change of tumor volume (Median)
Administration of Gleevec17

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Change in HbA1c Levels Over Time

Change in HbA1c levels from Week 52 to Week 104 (NCT01781975)
Timeframe: Visit 9 (Week 52) and Visit 13 (Week 104)

,
Interventionpercentage of HbA1c level (Mean)
Week 52Week 104
Imatinib Mesylate6.336.44
Placebo6.517.03

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Number of Severe Hypoglycemic Events

Major hypoglycemic events occurring from randomization at weeks 0, 52 and 104. (NCT01781975)
Timeframe: Visit 0 (Week 0), Visit 9 (Week 52), and Visit 13 (Week 104)

Interventionevents (Number)
Imatinib Mesylate2
Placebo3

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Number of Adverse Events

Number of adverse events that were reported throughout the study. (NCT01781975)
Timeframe: Adverse Events will be assessed at Visit 0 (week 0), Visit 1 (Week 2), Visit 2 (Week 4), and every month thereafter.

Interventionevents (Number)
Imatinib Mesylate172
Placebo28

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Area Under the Stimulated C-peptide Curve (AUC) Mean Over the First 2 Hours of a 4 Hour Mixed Meal Tolerance Test at the 1 Year Visit

"The primary outcome of each participant is the area under the stimulated c-peptide curve (AUC) mean based on data collected at time 0 to 2 hours of a 4-hour mixed meal tolerance test (MMTT) conducted at the primary endpoint visit. The timed measurements are done at: 0, 15, 30, 60, 90, and 120 minutes. The term AUC mean comes from the mean value theorem in calculus. It is the value on the scale of the y-axis that is equal to the AUC divided by the range on the x-axis (in this case 120 minutes)." (NCT01781975)
Timeframe: Visit 9 (Week 52) at 0, 15, 30, 60, 90, 120 minutes post-dose

Interventionnmol/L (Mean)
Imatinib Mesylate0.834
Placebo0.775

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Area Under the Stimulated C-peptide Curve (AUC) Mean Over 4 Hours at 24 Months

Area under the MMTT-stimulated peak, 4 hour C-peptide AUC mean at week 104. The units are reported as nano-moles/Liter because this is AUC mean (the AUC is divided by the time internal so that the units return to the c-peptide units of measure). (NCT01781975)
Timeframe: Visit 13 (Week 104)

Interventionnmol/L (Mean)
Imatinib Mesylate0.472
Placebo0.389

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Change in Insulin Dose (Units/kg) Over Time

Assess insulin use in units per kilogram body weight per day at weeks 52 and 104. (NCT01781975)
Timeframe: Visit 9 (Week 52) and Visit 13 (Week 104)

,
InterventionUnits per Kg (Mean)
Week 52Week 104
Imatinib Mesylate0.3070.389
Placebo0.4130.488

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Area Under Curve (AUC) Time Frame: Predose, 0.5,1,1.5,2,3,5,8,12,24,48,72hours Post-dose

(NCT01795716)
Timeframe: predose, 0.5,1,1.5,2,3,5,8,12,24,48,72hours post-dose

Interventionmcg*hr/mL (Mean)
Mesylate Imatinib Capsule37256
Glivec37206

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Rate of BCR-ABL Undetectable

The BCR-ABL transcript rate was analysed by molecular biology by RQ-PCR at study entry, 3 months, 6 months, 9 months and 12 months. (NCT01827930)
Timeframe: 12 first months

Interventionpercentage of patients (Number)
Imatinib 600 (Randomized Trial)29.2
Imatinib 400 (Randomized Trial)12.0
Imatinib400 (Parallel Cohort)5.3

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Time to the First BCR-ABL Undetectable

"The BCR-ABL transcript rate was analysed by molecular biology by RQ-PCR at study entry, 3 months, 6 months, 9 months and 12 months.~Time to the first BCR-ABL undetectable was defined by the time from inclusion/randomization and the first CMR." (NCT01827930)
Timeframe: within 12 months following randomization

InterventionMonths (Median)
Imatinib 600 (Randomized Trial)8.7
Imatinib 400 (Randomized Trial)3.2
Imatinib400 (Parallel Cohort)8.9

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Molecular Response at 3, 6, 9 and 12 Months

"The molecular response is defined by the measurement of BCR-ABL transcript rate by quantitative RT-PCR (RQ-PCR) on peripheral venous blood according to international standards.~It is defined as:~Major Molecular Response (MMR): BRC-ABL transcript rate ≤ 0.1%~Complete Molecular Response (CMR): transcript BCR-ABL undetectable and non quantifiable." (NCT01827930)
Timeframe: 3, 6, 9 and 12 months

,,
Interventionpercentage of patient (Number)
3 months - CMR3 months : MMR6 months : CMR6 months : MMR9 months : CMR9 months : MMR12 months : CMR12 months : MMR
Imatinib 400 (Randomized Trial)8.080.08.072.04.068.04.076.0
Imatinib 600 (Randomized Trial)12.575.04.287.520.866.78.383.3
Imatinib400 (Parallel Cohort)078.9073.75.368.45.363.2

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Rate of Decline of 2-log of the BCR-ABL Transcript Rate at 3 ,6, 9 and 12 Months From Baseline - Randomised Study

"The BCR-ABL transcript rate was analysed by molecular biology by RQ-PCR at study entry, 3 months, 6 months, 9 months and 12 months.~Efficacy was also evaluated at 3, 6, 9 and 12 months in terms of decreasing the rate of BCR-ABL transcripts of 2 logarithms, relative to the initial value (inclusion). The lack of data on the transcript rate was considered as failure (no decrease)." (NCT01827930)
Timeframe: 3, 6, 9 and 12 months

,,
Interventionpercentage of patients (Number)
3 months6 months9 months12 months
Imatinib 400 (Randomized Trial)0000
Imatinib 600 (Randomized Trial)4.24.204.2
Imatinib400 (Parallel Cohort)0000

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Time to Complete Molecular Response (CMR) and Major Molecular Response (MMR)

Time to complete molecular response was defined by the time from inclusion/randomization and the first CMR. (NCT01827930)
Timeframe: From date of randomization until the date of complete molecular response (up to 12 months)

,,
Interventionmonths (Median)
CMRMMR
Imatinib 400 (Randomized Trial)3.23.2
Imatinib 600 (Randomized Trial)8.73.2
Imatinib400 (Parallel Cohort)8.93.4

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Overall Survival

Overall survival is defined by the time from de date of inclusion/randomization to the date of death (of any cause). (NCT01827930)
Timeframe: First 12 months

InterventionMonths (Median)
Imatinib 600 (Randomized Trial)NA
Imatinib 400 (Randomized Trial)NA
Imatinib400 (Parallel Cohort)NA

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Percentage of Patients Presenting a Decline of the BCR-ABL Transcript Rate at 12 Months From Baseline - Randomised Study

"The BCR-ABL transcript rate was analysed by molecular biology by RQ-PCR at study entry, 3 months, 6 months, 9 months and 12 months.~Treatment is considered effective at 12 months if:~for patients with an inclusion transcript rate less than 0.1%: the transcript rate at 12 months is less or equal to 0.001% or undetectable.~for patients with an inclusion transcript rate greater than 0.1% : the transcript rate at 12 months is less or equal to 0.1% or undetectable.~If BCR-ABL transcript level was unavailable at M12, the treatment was considered ineffective." (NCT01827930)
Timeframe: 12 months

Interventionpercentage of patients (Number)
Imatinib 600 (Randomized Trial)29.2
Imatinib 400 (Randomized Trial)32.0
Imatinib400 (Parallel Cohort)10.5

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Progression-free Survival

"Progression-free survival was defined by the time from the date of inclusion and the date of progression.~Progression was defined as :~Death,~Passage into the acceleration phase defined by one of the following criteria: % of blood or medullary blasts greater than 15% but less than 30%, blasts plus promyelocytes greater than 30% in the blood or marrow, basophils greater than 20% in the blood, thrombocytopenia less than 100x10^9/L unrelated to treatment, clonal evolution)~Passage to the blast transformation phase defined by one of the following criteria: % of blasts of blood or bone marrow greater than 30%, occurrence of extramedullary damage other than histologically proven hepato-splenic.~Increase in BCR-ABL transcripts greater than or equal to 2-log compared to the previous values (this increase must be confirmed within 3 months)." (NCT01827930)
Timeframe: First 12 months

InterventionMonths (Median)
Imatinib 600 (Randomized Trial)NA
Imatinib 400 (Randomized Trial)NA
Imatinib400 (Parallel Cohort)NA

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Phase 1 - Maximum Tolerated Dose (MTD) of STI571

To determine the maximum tolerated dose (MTD) of STI571, docetaxel, and cisplatin, when administered in combination for the treatment of patients with chemo-naïve recurrent and metastatic (stage IV) NSCLC. (NCT02127372)
Timeframe: After cycle 1, day 22

Interventionmg (Number)
Phase 1400

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Phase II - Radiographic Response

"The percentage of patients with a complete or partial response.~Responses for the Phase II portion of the trial will be by Response Evaluation Criteria In Solid Tumors (RECIST) criteria as follows:~Complete Response (CR): disappearance of all target lesions; Partial Response (PR): at least a 30% decrease in the sum of the longest diameter (LD) of target lesions, taking as reference the baseline sum LD." (NCT02127372)
Timeframe: After Cycle 6, approximately 18 weeks.

Interventionpercentage of participants (Number)
Phase 225

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Phase 1 - Maximum Tolerated Dose (MTD) of Docetaxel and Cisplatin

To determine the maximum tolerated dose (MTD) of STI571, docetaxel, and cisplatin when administered in combination for the treatment of patients with chemo-naïve recurrent and metastatic (stage IV) NSCLC. (NCT02127372)
Timeframe: After cycle 1, day 22

Interventionmg/m2 (Number)
DocetaxelCisplatin
Phase 16060

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Phase 2: 1 Year Survival

Phase II: Percentage of patients alive 1 year from the start of protocol treatment. (NCT02127372)
Timeframe: 1 year

Interventionpercentage of participants (Number)
Phase 261

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Kaplan-Meier Estimate of Probability of Retaining Complete Cytogenetic Response (CCyR) at Month 48

The Kaplan-Meier curve was generated based on the first date of CCyR until the date of the confirmed loss of CCyR or censoring, objectively documented, for responders only. Confirmed loss of CCyR was the presence of at least one Ph+ metaphase confirmed by a second assessment at least 28 days later. Treatment discontinuation due to suboptimal response/treatment failure, PD or death due to PD within 28 days of last dose were considered confirmed loss of CCyR. PD was defined as disease progression to AP or BP CML. (NCT02130557)
Timeframe: Month 48

Interventionpercentage of participants (Number)
Bosutinib97.4
Imatinib93.7

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Cumulative Incidence of Event Free Survival (EFS) Events

EFS was defined as time from randomization to death due to any cause, transformation to AP or BP at any time, confirmed loss of complete hematologic response (CHR), confirmed loss of CCyR or censoring. Loss of CHR was defined as a hematologic assessment of non-CHR (chronic phase, AP, or BP) confirmed by 2 assessments at least 4 weeks apart. Loss of CHR was defined as appearance of any of the following: WBC count that rises to >20.0*10^9/L, platelet count rises to >=600*10^9/L, appearance of palpable spleen or other extramedullary involvement proven by biopsy, appearance of 5% myelocytes in peripheral blood, appearance of blasts or promyelocytes in peripheral blood. Loss of CCyR was defined as at least 1 Ph+ metaphase from analysis of <100 metaphases confirmed by follow up cytogenetic analysis after 1 month. Cumulative incidence of EFS was defined as percentage of participants with EFS event at Month 60 and was adjusted for competing risk of treatment discontinuation without event. (NCT02130557)
Timeframe: Up to Month 60

Interventionpercentage of participants (Number)
Bosutinib6.9
Imatinib10.4

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Summary of Trough Plasma Concentration by Presence of Grade 3 or Higher Adverse Events (AEs) of Bosutinib

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. AE was assessed according to maximum severity grading based on NCI CTCAE version 4.0. Grade 1= mild; Grade 2= moderate; within normal limits, Grade 3= severe or medically significant but not immediately life-threatening; Grade 4= life-threatening or disabling; urgent intervention indicated; Grade 5= death. Trough plasma concentration of participants who had grade 3 or higher AE are presented in this outcome measure. Data of plasma concentration is reported separately for each preferred term of AE. (NCT02130557)
Timeframe: Pre-dose on Days 28, 56 and 84

Interventionng/mL (Mean)
Day 28: DiarrheaDay 28: ThrombocytopeniaDay 28: RashDay 28: VomitingDay 56: DiarrheaDay 56: ThrombocytopeniaDay 56: RashDay 56: VomitingDay 84: DiarrheaDay 84: ThrombocytopeniaDay 84: RashDay 84: Vomiting
Bosutinib87.76949.22071.15014.66368.51356.85358.92538.20076.78267.62383.96712.400

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Summary of Trough Plasma Concentration by Presence of Grade 1 or Higher Adverse Events (AEs) of Bosutinib

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. AE was assessed according to maximum severity grading based on National Cancer Institute (NCI) Common Terminology Criteria for Adverse Events (CTCAE) version 4.0. Grade 1= mild; Grade 2= moderate; within normal limits, Grade 3= severe or medically significant but not immediately life-threatening; Grade 4= life-threatening or disabling; urgent intervention indicated; Grade 5= death. Trough plasma concentration of participants who had grade 1 or higher AE are presented in this outcome measure. Data of plasma concentration is reported separately for each preferred term of AE. (NCT02130557)
Timeframe: Pre-dose on Days 28, 56 and 84

Interventionng/mL (Mean)
Day 28: DiarrheaDay 28: ThrombocytopeniaDay 28: RashDay 28: NauseaDay 28: VomitingDay 56: DiarrheaDay 56: ThrombocytopeniaDay 56: RashDay 56: NauseaDay 56: VomitingDay 84: DiarrheaDay 84: ThrombocytopeniaDay 84: RashDay 84: NauseaDay 84: Vomiting
Bosutinib69.40263.52974.77966.01171.68468.83465.32770.01661.62665.98081.26971.58589.08077.70286.949

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Summary of Trough Plasma Concentration by Complete Cytogenetic Response (CCyR) of Bosutinib

CCyR was based on the prevalence of Ph+ metaphases among cells in metaphase on a BM aspirate. CCyR was achieved when there was 0% Ph+ metaphases among cells in a BM sample when at least 20 metaphases from a BM sample were analyzed, or MMR if no BM was available. Trough plasma concentration of participants who had CCyR are presented in this outcome measure. (NCT02130557)
Timeframe: Pre-dose on Days 28, 56 and 84

Interventionnanogram per milliliter (ng/mL) (Mean)
Day 28Day 56Day 84
Bosutinib71.28273.06983.973

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Number of Participants With Treatment-Emergent Adverse Events by National Cancer Institute Common Terminology Criteria for AEs (NCI CTCAE) (Version 4.0)

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. AE was assessed according to severity grading based on NCI CTCAE version 4.0. Grade 1 =mild; Grade 2 =moderate; Grade 3 =severe or medically significant but not immediately life-threatening, hospitalization or prolongation of hospitalization indicated; Grade 4 =life-threatening or disabling, urgent intervention indicated; Grade 5 =death. Treatment-emergent events were events between first dose of study drug and up to 60 months that were absent before treatment that worsened relative to pretreatment state. If the same participant in a given treatment had more than 1 adverse event, only the maximum CTCAE was reported. (NCT02130557)
Timeframe: Baseline up to end of treatment (up to Month 60)

,
InterventionParticipants (Count of Participants)
Grade 1Grade 2Grade 3Grade 4Grade 5
Bosutinib761144503
Imatinib2486120284

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Summary of Trough Plasma Concentration by Major Molecular Response (MMR) of Bosutinib

MMR was defined as a ratio of BCR-ABL/ABL <=0.1% on the international scale (>=3 log reduction from standardized baseline in ratio of BCR-ABL to ABL transcripts) by quantitative RT-qPCR. Trough plasma concentration of participants who had MMR are presented in this outcome measure. (NCT02130557)
Timeframe: Pre-dose on Days 28, 56 and 84

Interventionng/mL (Mean)
Day 28Day 56Day 84
Bosutinib75.05078.43791.081

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Number of Participants With Laboratory Test Abnormalities Based on National Cancer Institute Common Terminology Criteria for AEs (NCI CTCAE) Version 4.03

Laboratory parameters included hematological (haemoglobin, lymphocytes [absolute], neutrophils [absolute], platelets and leukocytes) and biochemistry (albumin, alanine aminotransferase, alkaline phosphatase, aspartate aminotransferase, amylase, bilirubin, creatinine kinase, calcium, creatinine, glucose, potassium, lipase, magnesium, phosphate, sodium, urate) parameters. Abnormalities in laboratory tests were graded by NCI CTCAE version 4.03 as Grade 1= mild; Grade 2= moderate; Grade 3= severe and Grade 4= life-threatening or disabling. The number of participants with laboratory test abnormalities were reported. (NCT02130557)
Timeframe: Baseline up to end of treatment (up to Month 60)

,
InterventionParticipants (Count of Participants)
Grade 1Grade 2Grade 3Grade 4
Bosutinib66713361
Imatinib75915445

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Percentage of Participants With Major Molecular Response (MMR) Up to Month 18

MMR was defined as a ratio of BCR-ABL/ABL <=0.1% on the international scale (>=3 log reduction from standardized baseline in ratio of BCR-ABL to ABL transcripts [>=3000 ABL required]) by quantitative RT-qPCR. The percentage of participants with MMR for up to Month 18 are reported. (NCT02130557)
Timeframe: Up to Month 18

Interventionpercentage of participants (Number)
Bosutinib61.0
Imatinib52.7

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Percentage of Participants With Major Molecular Response (MMR) at Month 12

MMR was defined as a ratio of breakpoint cluster region to abelson (BCR-ABL/ABL) less than or equal to (<=) 0.1 percent (%) on the international scale (IS) (greater than or equal to [>=] 3 log reduction from standardized baseline in ratio of BCR-ABL to ABL transcripts [>=3000 ABL required]) by quantitative reverse transcriptase polymerase chain reaction (RT-qPCR). The percentage of participants with MMR at Month 12 are reported. (NCT02130557)
Timeframe: Month 12

Interventionpercentage of participants (Number)
Bosutinib47.2
Imatinib36.9

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Percentage of Participants With Complete Cytogenetic Response (CCyR) Up to Month 12

Complete Cytogenetic Response (CCyR) was based on the prevalence of Ph+ metaphases among cells in metaphase on a bone marrow (BM) aspirate. CCyR was achieved when there was 0% Ph+ metaphases among cells in a BM sample when at least 20 metaphases from a BM sample were analyzed, or MMR if no BM was available. The percentage of participants with CCyR for up to Month 12 are reported. (NCT02130557)
Timeframe: Up to Month 12

Interventionpercentage of participants (Number)
Bosutinib77.2
Imatinib66.4

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Overall Survival (OS) Rate

OS was defined as the time (in months) from randomization to the occurrence of death due to any cause or censoring. Kaplan-meier analysis was used for determination of OS. Percentage of participants who were alive were estimated in this outcome measure. (NCT02130557)
Timeframe: Up to Month 60

Interventionpercentage of participants (Number)
Bosutinib94.9
Imatinib94.0

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Number of Participants With Vital Signs Abnormalities

Criteria for vital signs abnormalities: systolic blood pressure <80 millimeter of mercury (mmHg), >210 mmHg; diastolic blood pressure <40 mmHg, >130 mmHg; heart rate <40 beats per minute (bpm), >150 bpm; temperature <32 degree celsius, >40 degree celsius; weight >=10% increase from baseline, >=10% decrease from baseline. The number of participants with any vital sign abnormalities during On-treatment period are reported. On-Treatment was defined as values collected after the date of the first dose of test article until the last date of test article +28 days. (NCT02130557)
Timeframe: Baseline up to end of treatment (up to Month 60)

InterventionParticipants (Count of Participants)
Bosutinib107
Imatinib109

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Number of Participants With Clinically Significant Electrocardiogram (ECG) Abnormalities

Criteria for ECG abnormalities included heart rate: increase of >15 bpm from baseline value and >=120 bpm, decrease of >15 bpm from baseline value and <=45 bpm; PR interval: change of >=20 msec from baseline value and >=220 milliseconds (msec); QRS interval >=120 msec; QTcB interval >500 msec, increase of >60 msec from baseline; >450 msec (Men) or >470 msec (Women). QT interval using Fridericia's correction (QTcF) >500 msec, increase of >60 msec from baseline, >450 msec (Men) or >470 msec (Women). The number of participants with ECG abnormalities during On-treatment period are reported. On-Treatment was defined as values collected after the date of the first dose of test article up until the last date of test article +28 days. (NCT02130557)
Timeframe: Baseline up to end of treatment (up to Month 60)

InterventionParticipants (Count of Participants)
Bosutinib16
Imatinib13

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Number of Participants With Adverse Events (AEs) Leading to Study Drug Discontinuation

An AE was any untoward medical occurrence in a participant who received study drug without regard to possibility of causal relationship. (NCT02130557)
Timeframe: Baseline up to end of treatment (up to Month 60)

InterventionParticipants (Count of Participants)
Bosutinib68
Imatinib38

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Kaplan-Meier Estimate of Probability of Retaining Major Molecular Response (MMR) at Month 48

The Kaplan-Meier curve was generated based on the first date of MMR until the date of the confirmed loss of MMR or censoring, objectively documented, for responders only. Confirmed loss of MMR was BCR-ABL/ABL IS ratio >0.1% in association with a >=5-fold increase in BCR-ABL/ABL IS ratio from the lowest value achieved up to that time-point confirmed by a second assessment at least 28 days later. Treatment discontinuation due to suboptimal response/treatment failure, progressive disease (PD) or death due to PD within 28 days of last dose were considered confirmed loss of MMR. PD was defined as disease progression to accelerated phase (AP) or blast phase (BP) CML. (NCT02130557)
Timeframe: Month 48

Interventionpercentage of participants (Number)
Bosutinib92.2
Imatinib92.0

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Phase Ib Study: Number of Participants With Dose-Limiting Toxicities

The phase Ib will be pursued in standard 3+3 format, based on toxicities encountered during the first cycle of therapy. (NCT02257541)
Timeframe: 1 year

InterventionParticipants (Count of Participants)
Phase 1b, Dose Level -13
Phase 1b, Dose Level 18
Phase 1b, Dose Level 21
Phase 1b, Dose Level -23

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Phase Ib Portion: Response Rate (RR)

"(CR+PR, RECIST 1.1) and by CHOI criteria~PHASE 1b PARTICIPANTS ONLY~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR" (NCT02257541)
Timeframe: 32 weeks

,,,
InterventionParticipants (Count of Participants)
Partial Response/PRStable Disease/SDProgressive Disease/PDNot reported due to withdrawn from study
Phase 1b, Dose Level -11200
Phase 1b, Dose Level -20030
Phase 1b, Dose Level 10332
Phase 1b, Dose Level 20010

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Phase Ib Study: Response Rate (RR)

"defined by RECIST 1.1 criteria and by CHOI criteria,and by EORTC criteria~PHASE 1b PARTICIPANTS ONLY~Per Response Evaluation Criteria In Solid Tumors Criteria (RECIST v1.0) for target lesions and assessed by MRI: Complete Response (CR), Disappearance of all target lesions; Partial Response (PR), >=30% decrease in the sum of the longest diameter of target lesions; Overall Response (OR) = CR + PR" (NCT02257541)
Timeframe: 32 weeks

,,,
InterventionParticipants (Count of Participants)
Progressive Disease/PDStable Disease/SDNot reported due to withdrawn from study
Phase 1b, Dose Level -1120
Phase 1b, Dose Level -2300
Phase 1b, Dose Level 1242
Phase 1b, Dose Level 2010

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Number of Patients With Chronic Myeloid Leukemia (CML) Who Develop Molecular Recurrence After Discontinuing TKIs.

The number of patients who develop molecular recurrence after discontinuing TKIs. This will be reported as the number of new occurrences from the end of the prior time frame. (NCT02269267)
Timeframe: 1, 2, 3, 4, 5, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 27, 30, 33, 36 months

InterventionParticipants (Count of Participants)
Less or equal to one monthOne month to two monthsTwo months to three monthsThree months to four monthsFour months to five monthsFive months to six monthsSix months to eight monthsEight months to 10 monthsTen months to 12 months12 months to 14 months14 months to 16 months16 months to 18 months18 months to 20 months20 months to 22 months22 months to 24 months24 months to 27 months27 months to 30 months30 months to 33 months33 months to 36 months36 months
Discontinuation of TKI Medication0412117523422100112002

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Number of Participants With Adverse Events (AEs) and Serious Adverse Events (SAEs)

Clinically significant changes in laboratory values and vital signs were reported as AEs or SAEs, as appropriate. Only descriptive analysis. (NCT02272777)
Timeframe: From first dose of study treatment to 30 days after last dose of study treatment, up to 31 months

,
InterventionParticipants (Count of Participants)
Adverse Events (AEs)Serious Adverse Events (SAEs)Fatal SAEsAEs leading to drug discontinuationAEs leading to dose adjustment/interruption
Imatinib8210017
Nilotinib8430117

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Percent of Baseline Loa Loa Microfilariae

Percent of baseline Loa loa microfilariae as determined by concentrated peripheral blood smear. Daily measurements will be taken the first week, followed by measurements at day 14 and day 21 (NCT02644525)
Timeframe: Days 1-7, 14, 21

,,,
Interventionpercentage of baseline microfilariae (Geometric Mean)
Day 1Day 2Day 3Day 4Day 5Day 6Day 7Day 14Day 21
Imatinib 200mg114.596.8102.8108.595.5107.078.983.786.5
Imatinib 400mg104.798.084.059.776.962.3136.081.8107.6
Imatinib 600mg102.297.884.888.189.184.183.394.497.4
Placebo88.788.184.673.379.980.476.9100.666.8

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Event-free Survival

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

InterventionPercentage of Participants (Number)
Treatment (Chemotherapy)32

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

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

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

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Number of Participants With Adverse Events

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

InterventionParticipants (Count of Participants)
Treatment (Chemotherapy)44

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Number of Participants With Morphological Complete Response Rate

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

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

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Overall Survival

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

InterventionPercentage of Participants (Number)
Treatment (Chemotherapy)70

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Rate of Participants With Clinically Relevant Improvement of the Modified Lee cGvHD Symptom Scale Score

"To assess improvement of symptoms based on the total symptom score (TSS); a responder was defined as having achieved a clinically relevant reduction from Baseline of the TSS. The scale consists of 30 items in 7 subscales (skin, eye, mouth, lung, nutrition, energy, and psychological). Participants reported their level of symptom bother over the previous month on a 5-point likert scale: not at all, slightly, moderately, quite a bit, or extremely. Subscale scores and the summary score range from 0 to 100, with a higher score indicating worse symptoms." (NCT03112603)
Timeframe: Baseline; Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Interventionpercentage of participants (Number)
Ruxolitinib24.2
Best Available Therapy11.0

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Vz/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"Vz/F was defined as the apparent oral dose volume of distribution of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

InterventionLiters (Geometric Mean)
Day 1Day 15
Ruxolitinib54.050.9

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Tmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"tmax was defined as the time to reach the maximum plasma concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Interventionhours (Median)
Day 1Day 15
Ruxolitinib0.8331.00

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t1/2 of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"t1/2 was defined as the apparent terminal phase disposition half-life of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Interventionhours (Geometric Mean)
Day 1Day 15
Ruxolitinib2.402.32

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Percentage of Participants With a ≥ 50% Reduction in Daily Corticosteroid Dose

All corticosteroid dosages prescribed to the participant and all dose changes during the study were to be recorded for assessment of participants with a ≥ 50% reduction in daily corticosteroid dose. (NCT03112603)
Timeframe: from Day 15 up to Day 182

,
Interventionpercentage of participants (Number)
Day 15 to ≤ Day 28Day 29 to ≤ Day 42Day 43 to ≤ Day 56Day 57 to ≤ Day 70Day 71 to ≤ Day 84Day 85 to ≤ Day 98Day 99 to ≤ Day 112Day 113 to ≤ Day 126Day 127 to ≤ Day 140Day 141 to ≤ Day 154Day 155 to ≤ Day 168Day 169 to ≤ Day 182
Best Available Therapy13.233.141.147.951.454.060.466.268.368.371.688.8
Ruxolitinib12.735.048.458.762.369.571.273.272.870.074.681.9

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Percentage of Participants Successfully Tapered Off of All Corticosteroids

All corticosteroid dosages prescribed to the participant and all dose changes during the study were to be recorded for assessment of participants who successfully tapered off of all corticosteroids. Participants who completely tapered off corticosteroids refer to those who permanently discontinued steroids as per the dose administration panel and who did not restart steroids in the same interval. Participants who were tapered off and continued follow-up were also counted as being tapered off with 0 dose in subsequent intervals until they discontinued from the main treatment period or restarted steroid treatment. (NCT03112603)
Timeframe: up to Day 179

,
Interventionpercentage of participants (Number)
Day 1 to ≤ Day 28Day 29 to ≤ Day 56Day 57 to ≤ Day 84Day 85 to ≤ Day 112Day 113 to ≤ Day 140Day 141 to ≤ Day 168Day 169 to ≤ Day 179
Best Available Therapy2.65.48.510.312.416.815.9
Ruxolitinib2.59.614.016.319.724.224.1

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Cumulative Incidence of Non-relapse Mortality (NRM)

Defined as the cumulative incidence rate from competing risk analysis for NRM from the date of randomization to the date of death not preceded by underlying disease relapse/recurrence. (NCT03112603)
Timeframe: Months 3, 6, 12, 18, 24, 30, and 36

,
Interventionpercentage of participants (Number)
Month 3Month 6Month 12Month 18Month 24Month 30Month 36
Best Available Therapy4.446.4315.1216.4819.2219.2222.0
Ruxolitinib5.459.1315.3015.9317.8317.8317.83

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Cumulative Incidence of Malignancy Relapse/Recurrence (MR)

Defined as the cumulative incidence rate from competing risk analysis of MR from the date of randomization to hematologic malignancy relapse/recurrence. (NCT03112603)
Timeframe: Months 3, 6, 12, 18, 24, 30, and 36

,
Interventionpercentage of participants (Number)
0 to < 3 months3 to < 6 months6 to < 12 months12 to < 18 months18 to < 24 months24 to <30 months30 to <36 months
Best Available Therapy1.312.656.086.086.086.787.50
Ruxolitinib1.923.225.187.828.488.488.48

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Cmax of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"Cmax was defined as the maximum observed plasma concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Interventionnanograms per milliliter (ng/mL) (Geometric Mean)
Day 1Day 15
Ruxolitinib167215

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CL/F of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"CL/F was defined as the oral dose clearance of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

InterventionLiters/hour (Geometric Mean)
Day 1Day 15
Ruxolitinib15.615.2

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Change From Baseline in Functional Assessment of Cancer Therapy - Bone Marrow Transplantation (FACT-BMT)

"Change from Baseline was calculated as the post-Baseline value minus the Baseline value. The FACT-BMT is a 50-item self-report questionnaire that measures the effect of a therapy on domains including physical, functional, social/family, and emotional well-being, together with additional concerns relevant for bone marrow transplantation participants. The questions were based on a 5-point Likert scale, where 0 corresponds to not at all and 4 corresponds to very much. The higher the final score, the better the quality of life. The FACT-BMT total score ranges from 0 to 148." (NCT03112603)
Timeframe: Baseline; up to Cycle 39 Day 1 (each cycle was comprised of 4 weeks)

,
Interventionscores on a scale (Mean)
Cycle 2 Day 1Cycle 3 Day 1Cycle 4 Day 1Cycle 5 Day 1Cycle 6 Day 1Cycle 7 Day 1Cycle 9 Day 1Cycle 12 Day 1Cycle 15 Day 1Cycle 18 Day 1Cycle 21 Day 1Cycle 24 Day 1Cycle 27 Day 1Cycle 30 Day 1Cycle 33 Day 1Cycle 36 Day 1Cycle 39 Day 1
Best Available Therapy-0.22-1.82-1.05-0.232.410.851.203.747.588.193.687.845.105.755.674.776.64
Ruxolitinib2.320.621.981.252.914.145.327.265.074.105.245.906.237.535.178.728.65

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Change From Baseline in EQ-5D-5L

The EQ-5D-5L is a descriptive classification consisting of five dimensions of health: mobility, self-care, usual activities, anxiety/depression, and pain/discomfort. The five-level version (no problems, slight problems, moderate problems, severe problems, and extreme problems) uses a 5-point Likert scale, with 1 being no problems and 5 being extreme problems. (NCT03112603)
Timeframe: Baseline; up to Cycle 39 Day 1 (each cycle was comprised of 4 weeks)

,
Interventionscores on a scale (Mean)
Cycle 2 Day 1Cycle 3 Day 1Cycle 4 Day 1Cycle 5 Day 1Cycle 6 Day 1Cycle 7 Day 1Cycle 9 Day 1Cycle 12 Day 1Cycle 15 Day 1Cycle 18 Day 1Cycle 21 Day 1Cycle 24 Day 1Cycle 27 Day 1Cycle 30 Day 1Cycle 33 Day 1Cycle 36 Day 1Cycle 39 Day 1
Best Available Therapy-0.01-0.04-0.01-0.030.01-0.00-0.020.020.030.02-0.000.010.030.010.050.040.01
Ruxolitinib0.030.030.040.020.050.070.070.070.070.070.080.070.060.050.000.060.06

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AUClast of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"AUClast was defined as the area under the concentration-time curve up to the last measurable concentration of ruxolitinib. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Interventionng*hour/mL (Geometric Mean)
Day 1Day 15
Ruxolitinib636945

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AUCinf of Ruxolitinib After Single (Cycle 1 Day 1) and Multiple (Cycle 1 Day 15) Doses

"AUCinf was defined as the area under the concentration-time curve from time 0 to infinity. Early enrolling participants (approximately the first 8 adult and first 4 adolescent participants) randomized to ruxolitinib arm followed an extensive PK sampling schedule. Subsequent participants randomized to ruxolitinib, any randomized participants receiving ruxolitinib after Cycle 6, and any randomized participants receiving BAT that cross over to ruxolitinib followed the sparse PK sampling schedule." (NCT03112603)
Timeframe: Extensive Sampling Schedule: Cycle 1 Days 1 and 15: predose; 0.5, 1, 1.5, 4, 6, and 9 hours post-dose. Sparse Sampling Schedule: Cycle 1 Days 1 and 15: predose; 1.5 hours post-dose

Interventionng*hour/mL (Geometric Mean)
Day 1
Ruxolitinib642

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Utilization of Medical Resources

The percentage of participants with at least one submission to healthcare encounter was assessed. (NCT03112603)
Timeframe: from Baseline to LPLV (approximately 5 years)

Interventionpercentage of participants (Number)
Ruxolitinib57.0
Best Available Therapy65.8

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Rate of FFS at Study Completion

Composite time to event endpoint incorporating the following FFS events: (i) relapse or recurrence of underlying disease or death due to underlying disease, (ii) nonrelapse mortality, or (iii) addition or initiation of another systemic therapy for cGvHD. (NCT03112603)
Timeframe: From Baseline to Last Participant Last Visit (LPLV) (approximately 5 years)

Interventionmonths (Median)
Ruxolitinib38.4
Best Available Therapy5.7

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Rate of Failure-free Survival (FFS)

Composite time to event endpoint incorporating the following FFS events: (i) relapse or recurrence of underlying disease or death due to underlying disease, (ii) nonrelapse mortality, or (iii) addition or initiation of another systemic therapy for cGvHD. (NCT03112603)
Timeframe: Baseline to when the last participant reached Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Interventionmonths (Median)
RuxolitinibNA
Best Available Therapy5.7

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Overall Survival (OS)

Overall survival was defined as the time from the date of randomization to the date of death due to any cause. (NCT03112603)
Timeframe: from the date of randomization to the date of death due to any cause up to LPLV (approximately 5 years)

Interventionmonths (Median)
RuxolitinibNA
Best Available TherapyNA

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ORR at the End of Cycle 3

ORR was defined as the percentage of participants in each arm demonstrating a CR or PR based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response. Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: Cycle 4 Day 1 (each cycle was comprised of 4 weeks)

Interventionpercentage of participants (Number)
Ruxolitinib54.5
Best Available Therapy31.1

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Number of Participants With Any Treatment-emergent Adverse Event (TEAE)

Adverse events were defined as the appearance of (or worsening of any pre-existing) undesirable signs, symptoms, or medical conditions that occurred after the participant's signed informed consent was obtained. Abnormal laboratory values or test results occurring after informed consent constituted adverse events only if they induced clinical signs or symptoms, were considered clinically significant, required therapy (e.g., hematologic abnormality that required transfusion or hematological stem cell support), or required changes in study medication(s). TEAEs were defined as those AEs that started or worsened during the on-treatment period (either randomized or cross-over period). (NCT03112603)
Timeframe: from Baseline to LPLV (approximately 5 years)

InterventionParticipants (Count of Participants)
Ruxolitinib165
Best Available Therapy148
Ruxolitinib Cross-Over Period70

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Efficacy of Ruxolitinib Versus Investigator's Choice Best Available Therapy (BAT) in Participants With Moderate or Severe Steroid Refractory Chronic Graft Versus Host Disease (SR-cGvHD) Assessed by Overall Response Rate (ORR) at the Cycle 7 Day 1 Visit

ORR was defined as the percentage of participants in each arm demonstrating a complete response (CR) or partial response (PR) based on chronic GvHD (cGvHD) disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response. Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Interventionpercentage of participants (Number)
Ruxolitinib49.7
Best Available Therapy25.6

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Duration of Response Through Study Completion

DOR was defined as the time from first response until cGvHD progression, death, or the date of change/addition of systemic therapies for cGvHD and as assessed for responders only. Response was based on cGvHD disease assessments (National Institutes of Health consensus criteria). Duration of response was evaluated in participants who achieved a CR or PR at or before Cycle 7 Day 1. The analysis included a larger number of participants than the number of participants who achieved CR or PR at Cycle 7 Day 1 (82 ruxolitinib and 42 BAT) because the analysis took into account not only those participants who achieved CR or PR at Cycle 7 Day 1, but also participants who achieved CR or PR before Cycle 7 Day 1 but who may have lost their response at Cycle 7 Day 1. For this reason, the number of participants in this analysis does not align with the best overall response (BOR) at Cycle 7 Day 1. This analysis was based on the cutoff date upon study completion (December 2022). (NCT03112603)
Timeframe: from first response to LPLV (approximately 5 years)

InterventionMonths (Median)
RuxolitinibNA
Best Available Therapy6.4

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BOR During Cross-over Treatment With Ruxolitinib

BOR was defined as the percentage of participants who achieved an overall response (CR+PR) based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response at any time point (up to Cycle 7 Day 1 or the start of additional systemic therapy for cGvHD). Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. (NCT03112603)
Timeframe: from Crossover Cycle 1 Day 1 to any time point up to and including Crossover Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Interventionpercentage of participants (Number)
Ruxolitinib Cross-Over Period81.4

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Best Overall Response (BOR) at Cycle 7 Day 1

BOR was defined as the percentage of participants who achieved an overall response (CR+PR) based on cGvHD disease assessments (National Institutes of Health Consensus Criteria) without the requirement of additional systemic therapies for an earlier progression, mixed response, or non-response at any time point (up to Cycle 7 Day 1 or the start of additional systemic therapy for cGvHD). Scoring of response was relative to the organ score at the time of randomization. CR: complete resolution of all signs and symptoms of cGVHD in all evaluable organs without the initiation or addition of new systemic therapy. PR: improvement in at least one organ (e.g., improvement of 1 or more points on a 4- to 7-point scale, or an improvement of 2 or more points on a 10- to 12-point scale) without progression in other organs or sites, initiation, or addition of new systemic therapies. This analysis was based on the primary cutoff date (May 2020). (NCT03112603)
Timeframe: up to Cycle 7 Day 1 (each cycle was comprised of 4 weeks)

Interventionpercentage of participants (Number)
Ruxolitinib76.4
Best Available Therapy60.4

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Serum VEGF-D

Change in the square root of the intrasubject plasma VEGF-D (NCT03131999)
Timeframe: Before and 1 month after initiation of monotherapy imatinib mesylate or placebo

InterventionLog transformed VEGF-D change pg/dL (Mean)
Imatinib Mesylate 400mg Capsule0.05
Placebo Capsule0.07

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Adverse Events

Adverse event and Serious Adverse Event numbers using the CTCAE Version 4.03 definitions (NCT03131999)
Timeframe: 3 months

,
Interventionnumber of events (Number)
Adverse EventsSerious Adverse Events
Imatinib Mesylate 400mg Capsule100
Placebo Capsule120

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Number of Participants With Minimal Residual Disease (MRD)-Negative Complete Remission (CR) at The End of Induction Phase

MRD-negative CR was achieved when a participant met the criteria for both MRD negativity and CR. MRD-negativity: ≤0.01 % breakpoint cluster region-Abelson (BCR-ABL1/ABL1), or undetectable BCR-ABL1 transcripts in complementary deoxyribonucleic acid (cDNA) with ≥ 10,000 ABL1 transcripts. CR: meeting all the following for at least 4 weeks (that is no recurrence):1. No circulating blasts and less than (<) 5% blasts in the bone marrow (BM). 2. Normal maturation of all cellular components in the BM. 3. No extramedullary disease (central nervous system [CNS] involvement, lymphadenopathy, splenomegaly, skin/gum infiltration, testicular mass). 4. Absolute neutrophil count (ANC) > 1000 per microliter (/mcL) (or >1.0*10^9/L). 5. Platelets >100,000/mcL (or >100*10^9/L). (NCT03589326)
Timeframe: From Cycle 1 through Cycle 3 (approximately 3 months) (Cycle length = 28 days)

InterventionParticipants (Count of Participants)
Cohort A: Ponatinib 30 mg53
Cohort B: Imatinib 600 mg13

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White Blood Cell Count

The normal range for white blood cell counts is between 4,000 and 11,000 cells per microliter. White blood cell counts increase during infections, autoimmune diseases and some types of cancer. Low white blood cell counts occur with immune system diseases and certain types of cancer. (NCT03891901)
Timeframe: Days 1, 7, 14, 21, 28, 42

,,
Interventioncells/µL (Mean)
Day 1Day 7Day 14Day 21Day 28Day 42
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid555853915841487541415841
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid630059005150365016005800
Imatinib (100 mg)590055005400475048005300

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Number of Myelomonocytic Cells in the Blood

Immunologic effects of the study treatment are assessed by counting myelomonocytic cells in blood samples. An increase in myelomonocytic cells is used to determine the appropriate therapeutic dose of imatinib. (NCT03891901)
Timeframe: Days 1, 7, 14, 21, 28, 42

,,
Interventioncells per microliter (µL) (Mean)
Day 1Day 7Day 14Day 21Day 28Day 42
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid319732413418302123563629
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid434036803195256011404425
Imatinib (100 mg)339030753195278524803255

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Maximum Concentration (Cmax) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter Cmax is the highest concentration of imatinib in blood following dosing. (NCT03891901)
Timeframe: Day 14, Day 28

,
Interventionmicrograms per milliliter (mcg/mL) (Median)
After 14 days of imatinibAfter 14 days of imatinib plus rifabutin and isoniazid
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0.410.71
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0.690.69

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Maximum Concentration (Cmax) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter Cmax is the highest concentration of imatinib in blood following dosing. (NCT03891901)
Timeframe: Day 14, Day 28

Interventionmicrograms per milliliter (mcg/mL) (Median)
After 14 days of imatinib
Imatinib (100 mg)0.51

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Half-life (T1/2) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter T1/2 is the time when imatinib in blood is half of the maximum concentration. (NCT03891901)
Timeframe: Day 14, Day 28

,
Interventionhours (Median)
After 14 days of imatinibAfter 14 days of imatinib plus rifabutin and isoniazid
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid11.329.91
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid15.017.83

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Half-life (T1/2) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter T1/2 is the time when imatinib in blood is half of the maximum concentration. (NCT03891901)
Timeframe: Day 14, Day 28

Interventionhours (Median)
After 14 days of imatinib
Imatinib (100 mg)11.00

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Elimination Rate Constant (Ke) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The elimination rate constant is the rate that imatinib is removed from the body. (NCT03891901)
Timeframe: Day 14, Day 28

,
Intervention1/hour (Median)
After 14 days of imatinibAfter 14 days of imatinib plus rifabutin and isoniazid
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0.060.07
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0.050.09

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Elimination Rate Constant (Ke) of Rifabutin

Blood samples for pharmacokinetic (PK) analyses of rifabutin were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The elimination rate constant is the rate that the drug is removed from the body. (NCT03891901)
Timeframe: Day 28

Intervention1/hour (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0.07
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0.09

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Frequency of Grade 3 or 4 Adverse Events (AEs)

"The number of grade 3 or 4 adverse events occurring among study participants is presented here. Adverse events are graded using the FDA Guidance Document, Toxicity Grading Scale for Healthy Adult and Adolescent Volunteers Enrolled in Preventive Vaccine Clinical Trials Guidance for Industry, September 2007, or other guidance, as applicable." (NCT03891901)
Timeframe: Measured through Day 50

InterventionGrade 3 or 4 adverse events (Number)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid4
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid6
Imatinib (100 mg)0

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Frequency of Serious Adverse Events (SAEs)

"The number of serious adverse events occurring among study participants is presented here. Adverse events are graded using the FDA Guidance Document, Toxicity Grading Scale for Healthy Adult and Adolescent Volunteers Enrolled in Preventive Vaccine Clinical Trials Guidance for Industry, September 2007, or other guidance, as applicable." (NCT03891901)
Timeframe: Measured through Day 50

Interventionserious adverse events (Number)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0
Imatinib (100 mg)0

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Half-life (T1/2) of Isoniazid

Blood samples for pharmacokinetic (PK) analyses of isoniazid were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter T1/2 is the time when the drug in blood is half of the maximum concentration. (NCT03891901)
Timeframe: Day 28

Interventionhours (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid1.59
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid2.44

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Half-life (T1/2) of Rifabutin

Blood samples for pharmacokinetic (PK) analyses of rifabutin were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter T1/2 is the time when the drug in blood is half of the maximum concentration. (NCT03891901)
Timeframe: Day 28

Interventionhours (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid9.65
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid8.14

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Maximum Concentration (Cmax) of Rifabutin

Blood samples for pharmacokinetic (PK) analyses of rifabutin were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter Cmax is the highest concentration of the drug in blood following dosing. (NCT03891901)
Timeframe: Day 28

Interventionmcg/mL (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0.37
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0.53

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Area Under the Curve (AUC) for Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter AUC is the overall exposure to imatinib. (NCT03891901)
Timeframe: Day 14, Day 28

Interventionhour*mcg/mL (Median)
After 14 days of imatinib
Imatinib (100 mg)5.80

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Maximum Concentration (Cmax) of Isoniazid

Blood samples for pharmacokinetic (PK) analyses of isoniazid were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter Cmax is the highest concentration of the drug in blood following dosing. (NCT03891901)
Timeframe: Day 28

Interventionmcg/mL (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid3.14
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid3.66

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Area Under the Curve (AUC) for Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter AUC is the overall exposure to imatinib. (NCT03891901)
Timeframe: Day 14, Day 28

,
Interventionhour*mcg/mL (Median)
After 14 days of imatinibAfter 14 days of imatinib plus rifabutin and isoniazid
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid4.767.52
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid9.467.49

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Elimination Rate Constant (Ke) of Imatinib

Blood samples for pharmacokinetic (PK) analyses of imatinib were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib alone (all study arms) and after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The elimination rate constant is the rate that imatinib is removed from the body. (NCT03891901)
Timeframe: Day 14, Day 28

Intervention1/hour (Median)
After 14 days of imatinib
Imatinib (100 mg)0.06

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Area Under the Curve (AUC) for Isoniazid

Blood samples for pharmacokinetic (PK) analyses of isoniazid were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter AUC is the overall exposure to the drug. (NCT03891901)
Timeframe: Day 28

Interventionhour*mcg/mL (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid9.79
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid16.11

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Area Under the Curve (AUC) for Rifabutin

Blood samples for pharmacokinetic (PK) analyses of rifabutin were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The PK parameter AUC is the overall exposure to the drug. (NCT03891901)
Timeframe: Day 28

Interventionhour*mcg/mL (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid3.68
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid5.11

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Elimination Rate Constant (Ke) of Isoniazid

Blood samples for pharmacokinetic (PK) analyses of isoniazid were collected at 6 time points over approximately 24 hours. Samples collection occurred at hour 0 (pre-dose), and 0.5 hours, 2 hours, 4.0 hours, 8.0 hours, and 24 hours post-dose. PK samples were taken after 14 days of imatinib with rifabutin and isoniazid (Cohorts 1a and 1b). The elimination rate constant is the rate that the drug is removed from the body. (NCT03891901)
Timeframe: Day 28

Intervention1/hour (Median)
Cohort 1a: Imatinib (50 mg) + Rifabutin + Isoniazid0.44
Cohort 1b: Imatinib (100 mg) + Rifabutin + Isoniazid0.28

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Overall Survival Rate: Type of Second Line TKI

Overall survival rate in this study was defined as percentage of participants alive during analysis period of 01-January-2011 till 30-June-2020. 5 years overall survival rate was demonstrated with Kaplan-Meier curve. (NCT05286528)
Timeframe: 5 years, during analysis period from 01-January-2011 till 30-June-2020 (retrieved data assessed in this observational study for approximately 1.2 years)

InterventionPercentage of participants (Number)
Participants With CML71.5

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Overall Survival Rate: Type of First Line TKI

Overall survival rate in this study was defined as percentage of participants alive during analysis period of 01-January-2011 till 30-June-2020. 5 years overall survival rate was demonstrated with Kaplan-Meier curve. (NCT05286528)
Timeframe: 5 years, during analysis period from 01-January-2011 till 30-June-2020 (retrieved data assessed in this observational study for approximately 1.2 years)

InterventionPercentage of participants (Number)
Participants With CML77.1

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Overall Survival Rate: All Participants

Overall survival rate in this study was defined as percentage of participants alive during analysis period of 01-January-2011 till 30-June-2020. 5 years overall survival rate was demonstrated with Kaplan-Meier curve. (NCT05286528)
Timeframe: 5 years, during analysis period from 01-January-2011 till 30-June-2020 (retrieved data assessed in this observational study for approximately 1.2 years)

InterventionPercentage of participants (Number)
Participants With CML77.1

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SubstanceRelationship StrengthStudiesTrialsClassesRoles
phosphoserine
Phosphoserine: The phosphoric acid ester of serine.		2.9940non-proteinogenic alpha-amino acid;
O-phosphoamino acid;
serine derivative		human metabolite
gamma-aminobutyric acid
gamma-Aminobutyric Acid: The most common inhibitory neurotransmitter in the central nervous system.. gamma-aminobutyric acid : A gamma-amino acid that is butanoic acid with the amino substituent located at C-4.		2.4520amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid		human metabolite;
neurotransmitter;
Saccharomyces cerevisiae metabolite;
signalling molecule
acetic acid
Acetic Acid: Product of the oxidation of ethanol and of the destructive distillation of wood. It is used locally, occasionally internally, as a counterirritant and also as a reagent. (Stedman, 26th ed). acetic acid : A simple monocarboxylic acid containing two carbons.		2.5420monocarboxylic acidantimicrobial food preservative;
Daphnia magna metabolite;
food acidity regulator;
protic solvent
acetamide
acetimidic acid : A carboximidic acid that is acetic acid in which the carbonyl oxygen is replaced by an imino group.		2.0510acetamides;
carboximidic acid;
monocarboxylic acid amide;
N-acylammonia
adenine
[no description available]		7.051316-aminopurines;
purine nucleobase		Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
allantoin
[no description available]		2.0510imidazolidine-2,4-dione;
ureas		Escherichia coli metabolite;
human metabolite;
Saccharomyces cerevisiae metabolite;
vulnerary
ammonium hydroxide
azane : Saturated acyclic nitrogen hydrides having the general formula NnHn+2.		4.6111azane;
gas molecular entity;
mononuclear parent hydride		EC 3.5.1.4 (amidase) inhibitor;
metabolite;
mouse metabolite;
neurotoxin;
NMR chemical shift reference compound;
nucleophilic reagent;
refrigerant
quinacrine
Quinacrine: An acridine derivative formerly widely used as an antimalarial but superseded by chloroquine in recent years. It has also been used as an anthelmintic and in the treatment of giardiasis and malignant effusions. It is used in cell biological experiments as an inhibitor of phospholipase A2.. quinacrine : A member of the class of acridines that is acridine substituted by a chloro group at position 6, a methoxy group at position 2 and a [5-(diethylamino)pentan-2-yl]nitrilo group at position 9.		2.0510acridines;
aromatic ether;
organochlorine compound;
tertiary amino compound		antimalarial;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor
benzene
[no description available]		2.5220aromatic annulene;
benzenes;
volatile organic compound		carcinogenic agent;
environmental contaminant;
non-polar solvent
betaine
glycine betaine : The amino acid betaine derived from glycine.		2.0510amino-acid betaine;
glycine derivative		fundamental metabolite
carbamates
[no description available]		2.7730amino-acid anion
carbon monoxide
Carbon Monoxide: Carbon monoxide (CO). A poisonous colorless, odorless, tasteless gas. It combines with hemoglobin to form carboxyhemoglobin, which has no oxygen carrying capacity. The resultant oxygen deprivation causes headache, dizziness, decreased pulse and respiratory rates, unconsciousness, and death. (From Merck Index, 11th ed). carbon monoxide : A one-carbon compound in which the carbon is joined only to a single oxygen. It is a colourless, odourless, tasteless, toxic gas.		3.5920carbon oxide;
gas molecular entity;
one-carbon compound		biomarker;
EC 1.9.3.1 (cytochrome c oxidase) inhibitor;
human metabolite;
ligand;
metabolite;
mitochondrial respiratory-chain inhibitor;
mouse metabolite;
neurotoxin;
neurotransmitter;
P450 inhibitor;
probe;
signalling molecule;
vasodilator agent
carnitine
[no description available]		5.5251amino-acid betainehuman metabolite;
mouse metabolite
methane
Methane: The simplest saturated hydrocarbon. It is a colorless, flammable gas, slightly soluble in water. It is one of the chief constituents of natural gas and is formed in the decomposition of organic matter. (Grant & Hackh's Chemical Dictionary, 5th ed). methane : A one-carbon compound in which the carbon is attached by single bonds to four hydrogen atoms. It is a colourless, odourless, non-toxic but flammable gas (b.p. -161degreeC).		5.4131alkane;
gas molecular entity;
mononuclear parent hydride;
one-carbon compound		bacterial metabolite;
fossil fuel;
greenhouse gas
choline
[no description available]		3.5520cholinesallergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
neurotransmitter;
nutrient;
plant metabolite;
Saccharomyces cerevisiae metabolite
citric acid, anhydrous
Citric Acid: A key intermediate in metabolism. It is an acid compound found in citrus fruits. The salts of citric acid (citrates) can be used as anticoagulants due to their calcium chelating ability.. citric acid : A tricarboxylic acid that is propane-1,2,3-tricarboxylic acid bearing a hydroxy substituent at position 2. It is an important metabolite in the pathway of all aerobic organisms.		4.9721tricarboxylic acidantimicrobial agent;
chelator;
food acidity regulator;
fundamental metabolite
hydrochloric acid
Hydrochloric Acid: A strong corrosive acid that is commonly used as a laboratory reagent. It is formed by dissolving hydrogen chloride in water. GASTRIC ACID is the hydrochloric acid component of GASTRIC JUICE.. hydrogen chloride : A mononuclear parent hydride consisting of covalently bonded hydrogen and chlorine atoms.		2.4110chlorine molecular entity;
gas molecular entity;
hydrogen halide;
mononuclear parent hydride		mouse metabolite
salicylic acid
Scalp: The outer covering of the calvaria. It is composed of several layers: SKIN; subcutaneous connective tissue; the occipitofrontal muscle which includes the tendinous galea aponeurotica; loose connective tissue; and the pericranium (the PERIOSTEUM of the SKULL).		3.5680monohydroxybenzoic acidalgal metabolite;
antifungal agent;
antiinfective agent;
EC 1.11.1.11 (L-ascorbate peroxidase) inhibitor;
keratolytic drug;
plant hormone;
plant metabolite
phloroglucinol
Phloroglucinol: A trinitrobenzene derivative with antispasmodic properties that is used primarily as a laboratory reagent.. phloroglucinol : A benzenetriol with hydroxy groups at position 1, 3 and 5.		2.2110benzenetriol;
phenolic donor		algal metabolite
gallic acid
gallate : A trihydroxybenzoate that is the conjugate base of gallic acid.		2.5220trihydroxybenzoic acidantineoplastic agent;
antioxidant;
apoptosis inducer;
astringent;
cyclooxygenase 2 inhibitor;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
geroprotector;
human xenobiotic metabolite;
plant metabolite
bupropion
Bupropion: A propiophenone-derived antidepressant and antismoking agent that inhibits the uptake of DOPAMINE.. bupropion : An aromatic ketone that is propiophenone carrying a tert-butylamino group at position 2 and a chloro substituent at position 3 on the phenyl ring.		2.4520aromatic ketone;
monochlorobenzenes;
secondary amino compound		antidepressant;
environmental contaminant;
xenobiotic
aminocaproic acid
Aminocaproic Acid: An antifibrinolytic agent that acts by inhibiting plasminogen activators which have fibrinolytic properties.. 6-aminohexanoic acid : An epsilon-amino acid comprising hexanoic acid carrying an amino substituent at position C-6. Used to control postoperative bleeding, and to treat overdose effects of the thrombolytic agents streptokinase and tissue plasminogen activator.		2.4920amino acid zwitterion;
epsilon-amino acid;
omega-amino fatty acid		antifibrinolytic drug;
hematologic agent;
metabolite
creatine
[no description available]		2.4920glycine derivative;
guanidines;
zwitterion		geroprotector;
human metabolite;
mouse metabolite;
neuroprotective agent;
nutraceutical
cytosine
[no description available]		7.0551aminopyrimidine;
pyrimidine nucleobase;
pyrimidone		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
lactic acid
Lactic Acid: A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed). 2-hydroxypropanoic acid : A 2-hydroxy monocarboxylic acid that is propanoic acid in which one of the alpha-hydrogens is replaced by a hydroxy group.		3.971202-hydroxy monocarboxylic acidalgal metabolite;
Daphnia magna metabolite
dimethylamine
[no description available]		2.0510methylamines;
secondary aliphatic amine		metabolite
dimethyl sulfoxide
Dimethyl Sulfoxide: A highly polar organic liquid, that is used widely as a chemical solvent. Because of its ability to penetrate biological membranes, it is used as a vehicle for topical application of pharmaceuticals. It is also used to protect tissue during CRYOPRESERVATION. Dimethyl sulfoxide shows a range of pharmacological activity including analgesia and anti-inflammation.. dimethyl sulfoxide : A 2-carbon sulfoxide in which the sulfur atom has two methyl substituents.		2.7330sulfoxide;
volatile organic compound		alkylating agent;
antidote;
Escherichia coli metabolite;
geroprotector;
MRI contrast agent;
non-narcotic analgesic;
polar aprotic solvent;
radical scavenger
formaldehyde
paraform: polymerized formaldehyde; RN given refers to parent cpd; used in root canal therapy		2.4920aldehyde;
one-carbon compound		allergen;
carcinogenic agent;
disinfectant;
EC 3.5.1.4 (amidase) inhibitor;
environmental contaminant;
Escherichia coli metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
glycine
[no description available]		3.0640alpha-amino acid;
amino acid zwitterion;
proteinogenic amino acid;
serine family amino acid		EC 2.1.2.1 (glycine hydroxymethyltransferase) inhibitor;
fundamental metabolite;
hepatoprotective agent;
micronutrient;
neurotransmitter;
NMDA receptor agonist;
nutraceutical
glycerol
Moon: The natural satellite of the planet Earth. It includes the lunar cycles or phases, the lunar month, lunar landscapes, geography, and soil.		5.3131alditol;
triol		algal metabolite;
detergent;
Escherichia coli metabolite;
geroprotector;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
solvent
histamine
[no description available]		6.4141aralkylamino compound;
imidazoles		human metabolite;
mouse metabolite;
neurotransmitter
hydrogen
Hydrogen: The first chemical element in the periodic table with atomic symbol H, and atomic number 1. Protium (atomic weight 1) is by far the most common hydrogen isotope. Hydrogen also exists as the stable isotope DEUTERIUM (atomic weight 2) and the radioactive isotope TRITIUM (atomic weight 3). Hydrogen forms into a diatomic molecule at room temperature and appears as a highly flammable colorless and odorless gas.. dihydrogen : An elemental molecule consisting of two hydrogens joined by a single bond.		5.4641elemental hydrogen;
elemental molecule;
gas molecular entity		antioxidant;
electron donor;
food packaging gas;
fuel;
human metabolite
hydroquinone
[no description available]		2.0510benzenediol;
hydroquinones		antioxidant;
carcinogenic agent;
cofactor;
Escherichia coli metabolite;
human xenobiotic metabolite;
mouse metabolite;
skin lightening agent
methanol
Methanol: A colorless, flammable liquid used in the manufacture of FORMALDEHYDE and ACETIC ACID, in chemical synthesis, antifreeze, and as a solvent. Ingestion of methanol is toxic and may cause blindness.. primary alcohol : A primary alcohol is a compound in which a hydroxy group, -OH, is attached to a saturated carbon atom which has either three hydrogen atoms attached to it or only one other carbon atom and two hydrogen atoms attached to it.. methanol : The primary alcohol that is the simplest aliphatic alcohol, comprising a methyl and an alcohol group.		4.3340alkyl alcohol;
one-carbon compound;
primary alcohol;
volatile organic compound		amphiprotic solvent;
Escherichia coli metabolite;
fuel;
human metabolite;
mouse metabolite;
Mycoplasma genitalium metabolite
inositol
Inositol: An isomer of glucose that has traditionally been considered to be a B vitamin although it has an uncertain status as a vitamin and a deficiency syndrome has not been identified in man. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1379) Inositol phospholipids are important in signal transduction.. inositol : Any cyclohexane-1,2,3,4,5,6-hexol.. 1D-chiro-inositol : Belonging to the inositol family of compounds, D-chiro-inositol (DCI) is an isomer of glucose. It is an important secondary messenger in insulin signal transduction.. muco-inositol : An inositol that is cyclohexane-1,2,3,4,5,6-hexol having a (1R,2R,3r,4R,5S,6r)-configuration.		2.4520cyclitol;
hexol
nickel
Nickel: A trace element with the atomic symbol Ni, atomic number 28, and atomic weight 58.69. It is a cofactor of the enzyme UREASE.. nickel ion : A nickel atom having a net electric charge.. nickel atom : Chemical element (nickel group element atom) with atomic number 28.		2.1310metal allergen;
nickel group element atom		epitope;
micronutrient
niacinamide
nicotinamide : A pyridinecarboxamide that is pyridine in which the hydrogen at position 3 is replaced by a carboxamide group.		15.11024pyridine alkaloid;
pyridinecarboxamide;
vitamin B3		anti-inflammatory agent;
antioxidant;
cofactor;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
Escherichia coli metabolite;
geroprotector;
human urinary metabolite;
metabolite;
mouse metabolite;
neuroprotective agent;
Saccharomyces cerevisiae metabolite;
Sir2 inhibitor
niacin
Niacin: A water-soluble vitamin of the B complex occurring in various animal and plant tissues. It is required by the body for the formation of coenzymes NAD and NADP. It has PELLAGRA-curative, vasodilating, and antilipemic properties.. vitamin B3 : Any member of a group of vitamers that belong to the chemical structural class called pyridines that exhibit biological activity against vitamin B3 deficiency. Vitamin B3 deficiency causes a condition known as pellagra whose symptoms include depression, dermatitis and diarrhea. The vitamers include nicotinic acid and nicotinamide (and their ionized and salt forms).. nicotinic acid : A pyridinemonocarboxylic acid that is pyridine in which the hydrogen at position 3 is replaced by a carboxy group.		2.0510pyridine alkaloid;
pyridinemonocarboxylic acid;
vitamin B3		antidote;
antilipemic drug;
EC 3.5.1.19 (nicotinamidase) inhibitor;
Escherichia coli metabolite;
human urinary metabolite;
metabolite;
mouse metabolite;
plant metabolite;
vasodilator agent
nitrates
Nitrates: Inorganic or organic salts and esters of nitric acid. These compounds contain the NO3- radical.		4.6111monovalent inorganic anion;
nitrogen oxoanion;
reactive nitrogen species
nitrites
Nitrites: Salts of nitrous acid or compounds containing the group NO2-. The inorganic nitrites of the type MNO2 (where M=metal) are all insoluble, except the alkali nitrites. The organic nitrites may be isomeric, but not identical with the corresponding nitro compounds. (Grant & Hackh's Chemical Dictionary, 5th ed)		4.6111monovalent inorganic anion;
nitrogen oxoanion;
reactive nitrogen species		human metabolite
orotic acid
Orotic Acid: An intermediate product in PYRIMIDINE synthesis which plays a role in chemical conversions between DIHYDROFOLATE and TETRAHYDROFOLATE.. orotic acid : A pyrimidinemonocarboxylic acid that is uracil bearing a carboxy substituent at position C-6.		2.4720pyrimidinemonocarboxylic acidEscherichia coli metabolite;
metabolite;
mouse metabolite
4-aminobenzoic acid
4-Aminobenzoic Acid: An aminobenzoic acid isomer that combines with pteridine and GLUTAMIC ACID to form FOLIC ACID. The fact that 4-aminobenzoic acid absorbs light throughout the UVB range has also resulted in its use as an ingredient in SUNSCREENS.. 4-ammoniobenzoate : A zwitterion obtained by transfer of a proton from the carboxy to the amino group of 4-aminobenzoic acid.. 4-aminobenzoic acid : An aminobenzoic acid in which the amino group is para to the carboxy group.		2.0510aminobenzoic acid;
aromatic amino-acid zwitterion		allergen;
Escherichia coli metabolite;
plant metabolite
phenol
[no description available]		3.8730phenolsantiseptic drug;
disinfectant;
human xenobiotic metabolite;
mouse metabolite
phenylacetic acid
phenylacetic acid : A monocarboxylic acid that is toluene in which one of the hydrogens of the methyl group has been replaced by a carboxy group.		2.0510benzenes;
monocarboxylic acid;
phenylacetic acids		allergen;
Aspergillus metabolite;
auxin;
EC 6.4.1.1 (pyruvate carboxylase) inhibitor;
Escherichia coli metabolite;
human metabolite;
plant growth retardant;
plant metabolite;
Saccharomyces cerevisiae metabolite;
toxin
phosphorylcholine
Phosphorylcholine: Calcium and magnesium salts used therapeutically in hepatobiliary dysfunction.. phosphocholine : The phosphate of choline; and the parent compound of the phosphocholine family.		5.7431phosphocholinesallergen;
epitope;
hapten;
human metabolite;
mouse metabolite
propylene glycol
Propylene Glycol: A clear, colorless, viscous organic solvent and diluent used in pharmaceutical preparations.. propane-1,2-diol : The simplest member of the class of propane-1,2-diols, consisting of propane in which a hydrogen at position 1 and a hydrogen at position 2 are substituted by hydroxy groups. A colourless, viscous, hygroscopic, low-melting (-59degreeC) and high-boiling (188degreeC) liquid with low toxicity, it is used as a solvent, emulsifying agent, and antifreeze.		4.6111glycol;
propane-1,2-diols		allergen;
human xenobiotic metabolite;
mouse metabolite;
protic solvent
pteridines
[no description available]		2.7930azaarene;
mancude organic heterobicyclic parent;
ortho-fused heteroarene;
pteridines
pyrazinamide
pyrazinecarboxamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of pyrazinoic acid (pyrazine-2-carboxylic acid) with ammonia. A prodrug for pyrazinoic acid, pyrazinecarboxamide is used as part of multidrug regimens for the treatment of tuberculosis.		2.0510monocarboxylic acid amide;
N-acylammonia;
pyrazines		antitubercular agent;
prodrug
pyridoxal phosphate
Pyridoxal Phosphate: This is the active form of VITAMIN B 6 serving as a coenzyme for synthesis of amino acids, neurotransmitters (serotonin, norepinephrine), sphingolipids, aminolevulinic acid. During transamination of amino acids, pyridoxal phosphate is transiently converted into pyridoxamine phosphate (PYRIDOXAMINE).. pyridoxal 5'-phosphate : The monophosphate ester obtained by condensation of phosphoric acid with the primary hydroxy group of pyridoxal.		2.0510methylpyridines;
monohydroxypyridine;
pyridinecarbaldehyde;
vitamin B6 phosphate		coenzyme;
cofactor;
EC 2.7.7.7 (DNA-directed DNA polymerase) inhibitor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyridoxine
4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source. vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).		2.4820hydroxymethylpyridine;
methylpyridines;
monohydroxypyridine;
vitamin B6		cofactor;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyruvic acid
Pyruvic Acid: An intermediate compound in the metabolism of carbohydrates, proteins, and fats. In thiamine deficiency, its oxidation is retarded and it accumulates in the tissues, especially in nervous structures. (From Stedman, 26th ed). pyruvic acid : A 2-oxo monocarboxylic acid that is the 2-keto derivative of propionic acid. It is a metabolite obtained during glycolysis.		2.6102-oxo monocarboxylic acidcofactor;
fundamental metabolite
sarcosine
cocobetaine: N-alkyl-betaine; cause of shampoo dermatitis		2.5220N-alkylglycine zwitterion;
N-alkylglycine;
N-methyl-amino acid;
N-methylglycines		Escherichia coli metabolite;
glycine receptor agonist;
glycine transporter 1 inhibitor;
human metabolite;
mouse metabolite
selenious acid
Selenious Acid: A selenium compound with the molecular formula H2SO3. It used as a source of SELENIUM, especially for patients that develop selenium deficiency following prolonged PARENTERAL NUTRITION.		2.1110selenium oxoacid
sulfur dioxide
Sulfur Dioxide: A highly toxic, colorless, nonflammable gas. It is used as a pharmaceutical aid and antioxidant. It is also an environmental air pollutant.		4.6111sulfur oxideEscherichia coli metabolite;
food bleaching agent;
refrigerant
thiamine
thiamine(1+) : A primary alcohol that is 1,3-thiazol-3-ium substituted by (4-amino-2-methylpyrimidin-5-yl)methyl, methyl and 2-hydroxyethyl groups at positions 3, 4 and 5, respectively.		2.0510primary alcohol;
vitamin B1		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
toluene
methylbenzene : Any alkylbenzene that is benzene substituted with one or more methyl groups.		2.4110methylbenzene;
toluenes;
volatile organic compound		cholinergic antagonist;
fuel additive;
neurotoxin;
non-polar solvent
uracil
2,4-dihydroxypyrimidine: a urinary biomarker for bipolar disorder		2.0510pyrimidine nucleobase;
pyrimidone		allergen;
Daphnia magna metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
prodrug;
Saccharomyces cerevisiae metabolite
uric acid
Uric Acid: An oxidation product, via XANTHINE OXIDASE, of oxypurines such as XANTHINE and HYPOXANTHINE. It is the final oxidation product of purine catabolism in humans and primates, whereas in most other mammals URATE OXIDASE further oxidizes it to ALLANTOIN.. uric acid : An oxopurine that is the final oxidation product of purine metabolism.. 6-hydroxy-1H-purine-2,8(7H,9H)-dione : A tautomer of uric acid having oxo groups at C-2 and C-8 and a hydroxy group at C-6.. 7,9-dihydro-1H-purine-2,6,8(3H)-trione : An oxopurine in which the purine ring is substituted by oxo groups at positions 2, 6, and 8.		9.1140uric acidEscherichia coli metabolite;
human metabolite;
mouse metabolite
urea
pseudourea: clinical use; structure. isourea : A carboximidic acid that is the imidic acid tautomer of urea, H2NC(=NH)OH, and its hydrocarbyl derivatives.		9.15173isourea;
monocarboxylic acid amide;
one-carbon compound		Daphnia magna metabolite;
Escherichia coli metabolite;
fertilizer;
flour treatment agent;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
catechin
[no description available]		2.0510hydroxyflavan
menthol
Menthol: A monoterpene cyclohexanol produced from mint oils.		2.0510p-menthane monoterpenoid;
secondary alcohol		volatile oil component
1-anilino-8-naphthalenesulfonate
1-anilino-8-naphthalenesulfonate: RN given refers to parent cpd. 8-anilinonaphthalene-1-sulfonic acid : A naphthalenesulfonic acid that is naphthalene-1-sulfonic acid substituted by a phenylamino group at position 8.		2.0510aminonaphthalene;
naphthalenesulfonic acid		fluorescent probe
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine: A dopaminergic neurotoxic compound which produces irreversible clinical, chemical, and pathological alterations that mimic those found in Parkinson disease.. 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine : A tetrahydropyridine that is 1,2,3,6-tetrahydropyridine substituted by a methyl group at position 1 and a phenyl group at position 4.		2.1310methylpyridines;
phenylpyridine;
tetrahydropyridine		neurotoxin
pd 173074
[no description available]		3.3160aromatic amine;
biaryl;
dimethoxybenzene;
pyridopyrimidine;
tertiary amino compound;
ureas		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
fibroblast growth factor receptor antagonist
1h-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one
1H-(1,2,4)oxadiazolo(4,3-a)quinoxalin-1-one: structure given in first source; inhibits guanylyl cyclase. 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one : A member of the class of oxadiazoloquinoxalines that is 1H-[1,2,4]oxadiazolo[4,3-a]quinoxaline substituted at position 1 by an oxo group.		2.0810oxadiazoloquinoxalineEC 4.6.1.2 (guanylate cyclase) inhibitor
hoe 33342
BXI-72: structure in first source		2.0410bibenzimidazole;
N-methylpiperazine		fluorochrome
pyrithione
pyrithione: split from cephalosporin molecule; some metal complexes of this have fumarate reductase inhibitory activity and may be useful against trypanosomes; RN given refers to parent cpd; structure. pyrithione : A pyridinethione that is pyridine-2(1H)-thione in which the hydrogen attached to the nitrogen is replaced by a hydroxy group. It is a Zn(2+) ionophore; the zinc salt is used as an antifungal and antibacterial agent.		2.1310monohydroxypyridine;
pyridinethione		ionophore
amitrole
Amitrole: A non-selective post-emergence, translocated herbicide. According to the Seventh Annual Report on Carcinogens (PB95-109781, 1994) this substance may reasonably be anticipated to be a carcinogen. (From Merck Index, 12th ed) It is an irreversible inhibitor of CATALASE, and thus impairs activity of peroxisomes.. amitrole : A member of the class of triazoles that is 1H-1,2,4-triazole substituted by an amino group at position 3. Used to control annual grasses and aquatic weeds (but not on food crops because it causes cancer in laboratory animals). Its use within the EU was banned from September 2017 on the grounds of potential groundwater contamination and risks to aquatic life; there have also been concerns about its endocrine-disrupting properties.		2.0410aromatic amine;
triazoles		carotenoid biosynthesis inhibitor;
EC 1.11.1.6 (catalase) inhibitor;
herbicide
4,5,6,7-tetrabromo-2-azabenzimidazole
4,5,6,7-tetrabromobenzotriazole: a CK2 kinase inhibitor		2.0310
phenytoin
[no description available]		2.7730imidazolidine-2,4-dioneanticonvulsant;
drug allergen;
sodium channel blocker;
teratogenic agent
N-(2-aminoethyl)-5-chloro-1-naphthalenesulfonamide
[no description available]		2.0310naphthalenes;
sulfonic acid derivative
acebutolol
Acebutolol: A cardioselective beta-1 adrenergic antagonist with little effect on the bronchial receptors. The drug has stabilizing and quinidine-like effects on cardiac rhythm, as well as weak inherent sympathomimetic action.. acebutolol : An ether that is the 2-acetyl-4-(butanoylamino)phenyl ether of the primary hydroxy group of 3-(propan-2-ylamino)propane-1,2-diol.		4.7821aromatic amide;
ethanolamines;
ether;
monocarboxylic acid amide;
propanolamine;
secondary amino compound		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympathomimetic agent
acetaminophen
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.		8.1650acetamides;
phenols		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
cyclooxygenase 3 inhibitor;
environmental contaminant;
ferroptosis inducer;
geroprotector;
hepatotoxic agent;
human blood serum metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
acetazolamide
Acetazolamide: One of the CARBONIC ANHYDRASE INHIBITORS that is sometimes effective against absence seizures. It is sometimes useful also as an adjunct in the treatment of tonic-clonic, myoclonic, and atonic seizures, particularly in women whose seizures occur or are exacerbated at specific times in the menstrual cycle. However, its usefulness is transient often because of rapid development of tolerance. Its antiepileptic effect may be due to its inhibitory effect on brain carbonic anhydrase, which leads to an increased transneuronal chloride gradient, increased chloride current, and increased inhibition. (From Smith and Reynard, Textbook of Pharmacology, 1991, p337)		2.4820monocarboxylic acid amide;
sulfonamide;
thiadiazoles		anticonvulsant;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
acetohexamide
Acetohexamide: A sulfonylurea hypoglycemic agent that is metabolized in the liver to 1-hydrohexamide.. acetohexamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is replaced by a p-acetylphenylsulfonyl group, while a hydrogen attached to the other nitrogen is replaced by a cyclohexyl group.		2.0510acetophenones;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
acetohydroxamic acid
acetohydroxamic acid: urease inhibitor. oxime : Compounds of structure R2C=NOH derived from condensation of aldehydes or ketones with hydroxylamine. Oximes from aldehydes may be called aldoximes; those from ketones may be called ketoximes.. N-hydroxyacetimidic acid : A carbohydroximic acid consisting of acetimidic acid having a hydroxy group attached to the imide nitrogen.. acetohydroxamic acid : A member of the class of acetohydroxamic acids that is acetamide in which one of the amino hydrogens has been replaced by a hydroxy group.		2.0510acetohydroxamic acids;
carbohydroximic acid		algal metabolite;
EC 3.5.1.5 (urease) inhibitor
tyrphostin ag 1024
tyrphostin AG 1024: modulates radiosensitivity in human breast cancer cells; also an IGF1 receptor inhibitor		2.0210alkylbenzene
ag 1295
[no description available]		2.0310quinoxaline derivativegeroprotector
ag-1296
6,7-dimethoxy-3-phenylquinoxaline: ATP-competitive inhibitor of receptor kinase		2.7430quinoxaline derivative
tyrphostin a23
tyrphostin A23: inhibits EGF-stimulated thymidine incorporation as well as EGF-stimulated receptor autophosphorylation & tyrosine phosphorylation & cell proliferation; structure given in first source		2.0310catechols
tyrphostin ag957
tyrphostin AG957: tyrosine kinase blocker; structure given in first source		2.4220aromatic amine
albendazole
[no description available]		2.830aryl sulfide;
benzimidazoles;
benzimidazolylcarbamate fungicide;
carbamate ester		anthelminthic drug;
microtubule-destabilising agent;
tubulin modulator
albuterol
Albuterol: A short-acting beta-2 adrenergic agonist that is primarily used as a bronchodilator agent to treat ASTHMA. Albuterol is prepared as a racemic mixture of R(-) and S(+) stereoisomers. The stereospecific preparation of R(-) isomer of albuterol is referred to as levalbuterol.. albuterol : A member of the class of phenylethanolamines that is 4-(2-amino-1-hydroxyethyl)-2-(hydroxymethyl)phenol having a tert-butyl group attached to the nirogen atom. It acts as a beta-adrenergic agonist used in the treatment of asthma and chronic obstructive pulmonary disease (COPD).		2.0510phenols;
phenylethanolamines;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
environmental contaminant;
xenobiotic
alfuzosin
alfuzosin: structure given in first source		2.4620monocarboxylic acid amide;
quinazolines;
tetrahydrofuranol		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
alprazolam
Alprazolam: A triazolobenzodiazepine compound with antianxiety and sedative-hypnotic actions, that is efficacious in the treatment of PANIC DISORDERS, with or without AGORAPHOBIA, and in generalized ANXIETY DISORDERS. (From AMA Drug Evaluations Annual, 1994, p238). alprazolam : A member of the class of triazolobenzodiazepines that is 4H-[1,2,4]triazolo[4,3-a][1,4]benzodiazepine carrying methyl, phenyl and chloro substituents at positions 1, 6 and 8 respectively. Alprazolam is only found in individuals that have taken this drug.		2.2110organochlorine compound;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA agonist;
muscle relaxant;
sedative;
xenobiotic
amantadine
amant: an antiviral compound consisting of an adamantane derivative chemically linked to a water-solube polyanioic matrix; structure in first source		3.940adamantanes;
primary aliphatic amine		analgesic;
antiparkinson drug;
antiviral drug;
dopaminergic agent;
NMDA receptor antagonist;
non-narcotic analgesic
ambroxol
Ambroxol: A metabolite of BROMHEXINE that stimulates mucociliary action and clears the air passages in the respiratory tract. It is usually administered as the hydrochloride.		2.0510aromatic amine
amifostine anhydrous
Amifostine: A phosphorothioate proposed as a radiation-protective agent. It causes splenic vasodilation and may block autonomic ganglia.. amifostine : An organic thiophosphate that is the S-phospho derivative of 2-[(3-aminopropyl)amino]ethanethiol. A prodrug for the free thiol, WR-1065, which is used as a cytoprotectant in cancer chemotherapy and radiotherapy.		2.7130diamine;
organic thiophosphate		antioxidant;
prodrug;
radiation protective agent
aminoglutethimide
Aminoglutethimide: An aromatase inhibitor that is used in the treatment of advanced BREAST CANCER.. aminoglutethimide : A dicarboximide that is a six-membered cyclic compound having ethyl and 4-aminophenyl substituents at the 3-position.		2.0510dicarboximide;
piperidones;
substituted aniline		adrenergic agent;
anticonvulsant;
antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
pimagedine
pimagedine: diamine oxidase & nitric oxide synthase inhibitor; an advanced glycosylation end product inhibitor; used in the treatment of diabetic complications; structure. aminoguanidine : A one-carbon compound whose unique structure renders it capable of acting as a derivative of hydrazine, guanidine or formamide.		2.0510guanidines;
one-carbon compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
EC 1.4.3.4 (monoamine oxidase) inhibitor
p-aminohippuric acid
p-Aminohippuric Acid: The glycine amide of 4-aminobenzoic acid. Its sodium salt is used as a diagnostic aid to measure effective renal plasma flow (ERPF) and excretory capacity.. p-aminohippurate : A hippurate that is the conjugate base of p-aminohippuric acid, arising from deprotonation of the carboxy group.. p-aminohippuric acid : An N-acylglycine that is the 4-amino derivative of hippuric acid; used as a diagnostic agent in the measurement of renal plasma flow.		2.0410N-acylglycineDaphnia magna metabolite
theophylline
[no description available]		2.0510dimethylxanthineadenosine receptor antagonist;
anti-asthmatic drug;
anti-inflammatory agent;
bronchodilator agent;
drug metabolite;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
fungal metabolite;
human blood serum metabolite;
immunomodulator;
muscle relaxant;
vasodilator agent
amiodarone
Amiodarone: An antianginal and class III antiarrhythmic drug. It increases the duration of ventricular and atrial muscle action by inhibiting POTASSIUM CHANNELS and VOLTAGE-GATED SODIUM CHANNELS. There is a resulting decrease in heart rate and in vascular resistance.. amiodarone : A member of the class of 1-benzofurans that is 1-benzofuran substituted by a butyl group at position 2 and a 4-[2-(diethylamino)ethoxy]-3,5-diiodobenzoyl group at position 3. It is a cardiovascular drug used for the treatment of cardiac dysrhythmias.		2.45201-benzofurans;
aromatic ketone;
organoiodine compound;
tertiary amino compound		cardiovascular drug
amitriptyline
Amitriptyline: Tricyclic antidepressant with anticholinergic and sedative properties. It appears to prevent the re-uptake of norepinephrine and serotonin at nerve terminals, thus potentiating the action of these neurotransmitters. Amitriptyline also appears to antagonize cholinergic and alpha-1 adrenergic responses to bioactive amines.. amitriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(dimethylamino)propylidene group at position 5.		2.4520carbotricyclic compound;
tertiary amine		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
tropomyosin-related kinase B receptor agonist;
xenobiotic
amlodipine
Amlodipine: A long-acting dihydropyridine calcium channel blocker. It is effective in the treatment of ANGINA PECTORIS and HYPERTENSION.. amlodipine : A fully substituted dialkyl 1,4-dihydropyridine-3,5-dicarboxylate derivative, which is used for the treatment of hypertension, chronic stable angina and confirmed or suspected vasospastic angina.		2.4620dihydropyridine;
ethyl ester;
methyl ester;
monochlorobenzenes;
primary amino compound		antihypertensive agent;
calcium channel blocker;
vasodilator agent
amobarbital
Amobarbital: A barbiturate with hypnotic and sedative properties (but not antianxiety). Adverse effects are mainly a consequence of dose-related CNS depression and the risk of dependence with continued use is high. (From Martindale, The Extra Pharmacopoeia, 30th ed, p565). amobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by a 3-methylbutyl and an ethyl group at position 5. Amobarbital has been shown to exhibit sedative and hypnotic properties.		2.0510barbiturates
amsacrine
Amsacrine: An aminoacridine derivative that intercalates into DNA and is used as an antineoplastic agent.. amsacrine : A sulfonamide that is N-phenylmethanesulfonamide substituted by a methoxy group at position 3 and an acridin-9-ylamino group at position 4. It exhibits antineoplastic activity.		2.4320acridines;
aromatic ether;
sulfonamide		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
anastrozole
[no description available]		4.140nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
anethole trithione
Anethole Trithione: Choleretic used to allay dry mouth and constipation due to tranquilizers.		2.0510methoxybenzenes
anthralin
Anthralin: An anthracene derivative that disrupts MITOCHONDRIA function and structure and is used for the treatment of DERMATOSES, especially PSORIASIS. It may cause FOLLICULITIS.. anthralin : An anthracene compound derived by the substitution of -OH groups for hydrogen at C-1 and C-8, and with an oxo group at C-9.		2.0510anthracenesantipsoriatic
antipyrine
Antipyrine: An analgesic and antipyretic that has been given by mouth and as ear drops. Antipyrine is often used in testing the effects of other drugs or diseases on drug-metabolizing enzymes in the liver. (From Martindale, The Extra Pharmacopoeia, 30th ed, p29). antipyrine : A pyrazolone derivative that is 1,2-dihydropyrazol-3-one substituted with methyl groups at N-1 and C-5 and with a phenyl group at N-2.		2.0410pyrazoloneantipyretic;
cyclooxygenase 3 inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
aspirin
Aspirin: The prototypical analgesic used in the treatment of mild to moderate pain. It has anti-inflammatory and antipyretic properties and acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5). acetylsalicylate : A benzoate that is the conjugate base of acetylsalicylic acid, arising from deprotonation of the carboxy group.. acetylsalicylic acid : A member of the class of benzoic acids that is salicylic acid in which the hydrogen that is attached to the phenolic hydroxy group has been replaced by an acetoxy group. A non-steroidal anti-inflammatory drug with cyclooxygenase inhibitor activity.		4.5940benzoic acids;
phenyl acetates;
salicylates		anticoagulant;
antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
EC 1.1.1.188 (prostaglandin-F synthase) inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
plant activator;
platelet aggregation inhibitor;
prostaglandin antagonist;
teratogenic agent
astemizole
Astemizole: Antihistamine drug now withdrawn from the market in many countries because of rare but potentially fatal side effects.. astemizole : A piperidine compound having a 2-(4-methoxyphenyl)ethyl group at the 1-position and an N-[(4-fluorobenzyl)benzimidazol-2-yl]amino group at the 4-position.		2.0410benzimidazoles;
piperidines		anti-allergic agent;
anticoronaviral agent;
H1-receptor antagonist
atenolol
Atenolol: A cardioselective beta-1 adrenergic blocker possessing properties and potency similar to PROPRANOLOL, but without a negative inotropic effect.. atenolol : An ethanolamine compound having a (4-carbamoylmethylphenoxy)methyl group at the 1-position and an N-isopropyl substituent.		2.0510ethanolamines;
monocarboxylic acid amide;
propanolamine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
sympatholytic agent;
xenobiotic
azathioprine
Azathioprine: An immunosuppressive agent used in combination with cyclophosphamide and hydroxychloroquine in the treatment of rheumatoid arthritis. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance has been listed as a known carcinogen. (Merck Index, 11th ed). azathioprine : A thiopurine that is 6-mercaptopurine in which the mercapto hydrogen is replaced by a 1-methyl-4-nitroimidazol-5-yl group. It is a prodrug for mercaptopurine and is used as an immunosuppressant, prescribed for the treatment of inflammatory conditions and after organ transplantation and also for treatment of Crohn's didease and MS.		6.1180aryl sulfide;
C-nitro compound;
imidazoles;
thiopurine		antimetabolite;
antineoplastic agent;
carcinogenic agent;
DNA synthesis inhibitor;
hepatotoxic agent;
immunosuppressive agent;
prodrug
baclofen
[no description available]		2.0510amino acid zwitterion;
gamma-amino acid;
monocarboxylic acid;
monochlorobenzenes;
primary amino compound		central nervous system depressant;
GABA agonist;
muscle relaxant
barbital
5,5-diethylbarbituric acid : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by two ethyl groups. Formerly used as a hypnotic (sleeping aid).		2.0510barbituratesdrug allergen
bendazac
bendazac : A monocarboxylic acid that is glycolic acid in which the hydrogen attached to the 2-hydroxy group is replaced by a 1-benzyl-1H-indazol-3-yl group. Although it has anti-inflammatory, antinecrotic, choleretic and antilipidaemic properties and has been used for the treatment of various inflammatory skin disorders, its principal effect is to inhibit the denaturation of proteins. Its lysine salt is used in the management of cataracts.		2.0510indazoles;
monocarboxylic acid		non-steroidal anti-inflammatory drug;
radical scavenger
benzamide
benzamide : An aromatic amide that consists of benzene bearing a single carboxamido substituent. The parent of the class of benzamides.		2.4620benzamides
benzbromarone
Benzbromarone: Uricosuric that acts by increasing uric acid clearance. It is used in the treatment of gout.. benzbromarone : 1-Benzofuran substituted at C-2 and C-3 by an ethyl group and a 3,5-dibromo-4-hydroxybenzoyl group respectively. An inhibitor of CYP2C9, it is used as an anti-gout medication.		2.45201-benzofurans;
aromatic ketone		uricosuric drug
benzothiazide
benzothiazide: structure. benzthiazide : 7-Sulfamoyl-1,2,4-benzothiadiazine 1,1-dioxide in which the hydrogen at position 6 is substituted by chlorine and that at position 3 is substituted by a benzylsulfanylmethyl group. A diuretic, it is used to treat hypertension and edema.		4.6111benzothiadiazine;
sulfonamide		antihypertensive agent;
diuretic
berberine
[no description available]		8.4750alkaloid antibiotic;
berberine alkaloid;
botanical anti-fungal agent;
organic heteropentacyclic compound		antilipemic drug;
antineoplastic agent;
antioxidant;
EC 1.1.1.141 [15-hydroxyprostaglandin dehydrogenase (NAD(+))] inhibitor;
EC 1.1.1.21 (aldehyde reductase) inhibitor;
EC 1.13.11.52 (indoleamine 2,3-dioxygenase) inhibitor;
EC 1.21.3.3 (reticuline oxidase) inhibitor;
EC 2.1.1.116 [3'-hydroxy-N-methyl-(S)-coclaurine 4'-O-methyltransferase] inhibitor;
EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor;
EC 2.7.11.10 (IkappaB kinase) inhibitor;
EC 3.1.1.4 (phospholipase A2) inhibitor;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor;
EC 3.4.14.5 (dipeptidyl-peptidase IV) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
geroprotector;
hypoglycemic agent;
metabolite;
potassium channel blocker
bicalutamide
bicalutamide: approved for treatment of advanced prostate cancer. N-[4-cyano-3-(trifluoromethyl)phenyl]-3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanamide : A member of the class of (trifluoromethyl)benzenes that is 4-amino-2-(trifluoromethyl)benzonitrile in which one of the amino hydrogens is substituted by a 3-[(4-fluorophenyl)sulfonyl]-2-hydroxy-2-methylpropanoyl group.. bicalutamide : A racemate comprising of equal amounts of (R)-bicalutamide and (S)-bicalutamide. It is an oral non-steroidal antiandrogen used in the treatment of prostate cancer and hirsutism.		2.0510(trifluoromethyl)benzenes;
monocarboxylic acid amide;
monofluorobenzenes;
nitrile;
sulfone;
tertiary alcohol
bay h 4502
bifonazole : A racemate comprising equimolar amounts of R- and S-bifonazole. It is a broad spectrum antifungal drug used for the treatment of fungal skin and nail infections.. 1-[biphenyl-4-yl(phenyl)methyl]imidazole : A member of the class of imidazoles carrying an alpha-(biphenyl-4-yl)benzyl substituent at position 1.		2.0510biphenyls;
imidazoles
bisindolylmaleimide i
bisindolylmaleimide I: a bis(indolyl)maleimide		2.0310
bisindolylmaleimide iv
[no description available]		2.5120indoles;
maleimides
bisoprolol
Bisoprolol: A cardioselective beta-1 adrenergic blocker. It is effective in the management of HYPERTENSION and ANGINA PECTORIS.		2.0510secondary alcohol;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
beta-adrenergic antagonist;
sympatholytic agent
bohemine
bohemine : Purine substituted on C-2, C-6 and N-9 with (3-hydroxypropyl)amino, benzylamino and isopropyl groups respectively; a synthetic, cell-permeable, cyclin-dependent kinase (CDK) inhibitor that is structurally similar to olomoucine and roscovitine.		2.0310purinesEC 2.7.11.22 (cyclin-dependent kinase) inhibitor
bromhexine
Bromhexine: A mucolytic agent used in the treatment of respiratory disorders associated with viscid or excessive mucus. (From Martindale, The Extra Pharmacopoeia, 30th ed, p744). bromhexine : A substituted aniline that is 2,4-dibromoaniline which is substituted at position 6 by a [cyclohexyl(methyl)amino]methyl group. It is used (as the monohydrochloride salt) as a mucolytic for the treatment of respiratory disorders associated with productive cough (i.e. a cough characterised by the production of sputum).		3.1210organobromine compound;
substituted aniline;
tertiary amino compound		mucolytic
bromisovalum
Bromisovalum: A sedative and mild hypnotic with potentially toxic effects.. bromisoval : A racemate comprising equimolar amounts of (R)- and (S)-bromisoval. It was previously used for its hypnotic and sedative properties but the use of bromides is now deprecated due to the possibility of the toxic accumulation of bromine in the body.. 2-bromo-N-carbamoyl-3-methylbutanamide : An N-acylurea that is urea in which one of the hydrogens is replaced by a 2-bromo-3-methybutanoyl group.		2.0510N-acylurea;
organobromine compound
brotizolam
brotizolam: structure		2.4720organic molecular entity
bumetanide
[no description available]		2.0510amino acid;
benzoic acids;
sulfonamide		diuretic;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor
bupivacaine
Bupivacaine: A widely used local anesthetic agent.. 1-butyl-N-(2,6-dimethylphenyl)piperidine-2-carboxamide : A piperidinecarboxamide obtained by formal condensation of the carboxy group of N-butylpipecolic acid with the amino group of 2,6-dimethylaniline.. bupivacaine : A racemate composed of equimolar amounts of dextrobupivacaine and levobupivacaine. Used (in the form of its hydrochloride hydrate) as a local anaesthetic.		2.0510aromatic amide;
piperidinecarboxamide;
tertiary amino compound
buspirone
Buspirone: An anxiolytic agent and serotonin receptor agonist belonging to the azaspirodecanedione class of compounds. Its structure is unrelated to those of the BENZODIAZAPINES, but it has an efficacy comparable to DIAZEPAM.. buspirone : An azaspiro compound that is 8-azaspiro[4.5]decane-7,9-dione substituted at the nitrogen atom by a 4-(piperazin-1-yl)butyl group which in turn is substituted by a pyrimidin-2-yl group at the N(4) position.		2.0510azaspiro compound;
N-alkylpiperazine;
N-arylpiperazine;
organic heteropolycyclic compound;
piperidones;
pyrimidines		anxiolytic drug;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
sedative;
serotonergic agonist
busulfan
[no description available]		6.53190methanesulfonate esteralkylating agent;
antineoplastic agent;
carcinogenic agent;
insect sterilant;
teratogenic agent
butalbital
butalbital: management of butalbital withdrawal can be simplified by using a phenobarbital-loading protocol; RN given refers to parent cpd. butalbital : A member of the class of barbiturates that is barbituric acid in which the hydrogens at position 5 are substituted by an allyl group and an isobutyl group. Frequently combined with other medicines, such as aspirin, paracetamol and codeine, it is used for treatment of pain and headache.		2.0510barbituratesanalgesic;
sedative
caffeine
[no description available]		2.4920purine alkaloid;
trimethylxanthine		adenosine A2A receptor antagonist;
adenosine receptor antagonist;
adjuvant;
central nervous system stimulant;
diuretic;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 3.1.4.* (phosphoric diester hydrolase) inhibitor;
environmental contaminant;
food additive;
fungal metabolite;
geroprotector;
human blood serum metabolite;
mouse metabolite;
mutagen;
plant metabolite;
psychotropic drug;
ryanodine receptor agonist;
xenobiotic
verapamil
Verapamil: A calcium channel blocker that is a class IV anti-arrhythmia agent.. verapamil : A racemate comprising equimolar amounts of dexverapamil and (S)-verapamil. An L-type calcium channel blocker of the phenylalkylamine class, it is used (particularly as the hydrochloride salt) in the treatment of hypertension, angina pectoris and cardiac arrhythmia, and as a preventive medication for migraine.. 2-(3,4-dimethoxyphenyl)-5-{[2-(3,4-dimethoxyphenyl)ethyl](methyl)amino}-2-(propan-2-yl)pentanenitrile : A tertiary amino compound that is 3,4-dimethoxyphenylethylamine in which the hydrogens attached to the nitrogen are replaced by a methyl group and a 4-cyano-4-(3,4-dimethoxyphenyl)-5-methylhexyl group.		5.4651aromatic ether;
nitrile;
polyether;
tertiary amino compound
candesartan cilexetil
candesartan cilexetil: a prodrug which is metabolized to an active form candesartan to exert its biological effects		2.0510biphenyls
carbamazepine
Carbamazepine: A dibenzazepine that acts as a sodium channel blocker. It is used as an anticonvulsant for the treatment of grand mal and psychomotor or focal SEIZURES. It may also be used in the management of BIPOLAR DISORDER, and has analgesic properties.. carbamazepine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine carrying a carbamoyl substituent at the azepine nitrogen, used as an anticonvulsant.		3.0140dibenzoazepine;
ureas		analgesic;
anticonvulsant;
antimanic drug;
drug allergen;
EC 3.5.1.98 (histone deacetylase) inhibitor;
environmental contaminant;
glutamate transporter activator;
mitogen;
non-narcotic analgesic;
sodium channel blocker;
xenobiotic
carisoprodol
Carisoprodol: A centrally acting skeletal muscle relaxant whose mechanism of action is not completely understood but may be related to its sedative actions. It is used as an adjunct in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1202). carisoprodol : A carbamate ester that is the mono-N-isopropyl derivative of meprobamate (which is a significant metabolite). Carisoprodol interrupts neuronal communication within the reticular formation and spinal cord, resulting in sedation and alteration in pain perception. It is used as a muscle relaxant in the symptomatic treatment of musculoskeletal conditions associated with painful muscle spasm.		2.0510carbamate estermuscle relaxant
carmustine
Carmustine: A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed). carmustine : A member of the class of N-nitrosoureas that is 1,3-bis(2-chloroethyl)urea in which one of the nitrogens is substituted by a nitroso group.		2.4720N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
carprofen
carprofen: RN given refers to cpd without isomeric designation. carprofen : Propanoic acid in which one of the methylene hydrogens is substituted by a 6-chloro-9H-carbazol-2-yl group. A non-steroidal anti-inflammatory drug, it is no longer used in human medicine but is still used for treatment of arthritis in elderly dogs.		2.0510carbazoles;
organochlorine compound		EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug;
photosensitizing agent
carvedilol
[no description available]		2.4620carbazoles;
secondary alcohol;
secondary amino compound		alpha-adrenergic antagonist;
antihypertensive agent;
beta-adrenergic antagonist;
cardiovascular drug;
vasodilator agent
celecoxib
[no description available]		3.93120organofluorine compound;
pyrazoles;
sulfonamide;
toluenes		cyclooxygenase 2 inhibitor;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
cetirizine
Cetirizine: A potent second-generation histamine H1 antagonist that is effective in the treatment of allergic rhinitis, chronic urticaria, and pollen-induced asthma. Unlike many traditional antihistamines, it does not cause drowsiness or anticholinergic side effects.. cetirizine : A member of the class of piperazines that is piperazine in which the hydrogens attached to nitrogen are replaced by a (4-chlorophenyl)(phenyl)methyl and a 2-(carboxymethoxy)ethyl group respectively.		2.0510ether;
monocarboxylic acid;
monochlorobenzenes;
piperazines		anti-allergic agent;
environmental contaminant;
H1-receptor antagonist;
xenobiotic
chelerythrine
chelerythrine : A benzophenanthridine alkaloid isolated from the root of Zanthoxylum simulans, Chelidonium majus L., and other Papaveraceae.		2.0310benzophenanthridine alkaloid;
organic cation		antibacterial agent;
antineoplastic agent;
EC 2.7.11.13 (protein kinase C) inhibitor
chloral hydrate
[no description available]		2.0510aldehyde hydrate;
ethanediol;
organochlorine compound		general anaesthetic;
mouse metabolite;
sedative;
xenobiotic
chlorambucil
Chlorambucil: A nitrogen mustard alkylating agent used as antineoplastic for chronic lymphocytic leukemia, Hodgkin's disease, and others. Although it is less toxic than most other nitrogen mustards, it has been listed as a known carcinogen in the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (Merck Index, 11th ed). chlorambucil : A monocarboxylic acid that is butanoic acid substituted at position 4 by a 4-[bis(2-chloroethyl)amino]phenyl group. A chemotherapy drug that can be used in combination with the antibody obinutuzumab for the treatment of chronic lymphocytic leukemia.		11.6381aromatic amine;
monocarboxylic acid;
nitrogen mustard;
organochlorine compound;
tertiary amino compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
chlordiazepoxide
Chlordiazepoxide: An anxiolytic benzodiazepine derivative with anticonvulsant, sedative, and amnesic properties. It has also been used in the symptomatic treatment of alcohol withdrawal.. chlordiazepoxide : A benzodiazepine that is 3H-1,4-benzodiazepine 4-oxide substituted by a chloro group at position 7, a phenyl group at position 5 and a methylamino group at position 2.		2.4420benzodiazepine
chlormezanone
Chlormezanone: A non-benzodiazepine that is used in the management of anxiety. It has been suggested for use in the treatment of muscle spasm.. chlormezanone : A 1,3-thiazine that is 1,3-thiazinan-4-one S,S-dioxide in which a hydrogen at position 2 is substituted by a 4-chlorophenyl group and the hydrogen attached to the nitrogen is substituted by methyl. A non-benzodiazepine muscle relaxant, it was used in the management of anxiety and in the treatment of muscle spasms until being discontinued worldwide by its manufacturer in 1996, due to rare but serious cutaneous reactions.		2.05101,3-thiazine;
lactam;
monochlorobenzenes;
sulfone		antipsychotic agent;
anxiolytic drug;
muscle relaxant
chloroquine
Chloroquine: The prototypical antimalarial agent with a mechanism that is not well understood. It has also been used to treat rheumatoid arthritis, systemic lupus erythematosus, and in the systemic therapy of amebic liver abscesses.. chloroquine : An aminoquinoline that is quinoline which is substituted at position 4 by a [5-(diethylamino)pentan-2-yl]amino group at at position 7 by chlorine. It is used for the treatment of malaria, hepatic amoebiasis, lupus erythematosus, light-sensitive skin eruptions, and rheumatoid arthritis.		6.16120aminoquinoline;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
autophagy inhibitor;
dermatologic drug
chloroxylenol
chloroxylenol: topical antiseptic; RN given refers to parent cpd; structure. 4-chloro-3,5-dimethylphenol : A member of the class of phenols that is 3,5-xylenol which is substituted at position 4 by chlorine. It is bactericidal against most Gram-positive bacteria but less effective against Staphylococci and Gram-negative bacteria, and often inactive against Pseudomonas species. It is ineffective against bacterial spores.		2.0510monochlorobenzenes;
phenols		antiseptic drug;
disinfectant;
molluscicide
chlorpheniramine
Chlorpheniramine: A histamine H1 antagonist used in allergic reactions, hay fever, rhinitis, urticaria, and asthma. It has also been used in veterinary applications. One of the most widely used of the classical antihistaminics, it generally causes less drowsiness and sedation than PROMETHAZINE.. chlorphenamine : A tertiary amino compound that is propylamine which is substituted at position 3 by a pyridin-2-yl group and a p-chlorophenyl group and in which the hydrogens attached to the nitrogen are replaced by methyl groups. A histamine H1 antagonist, it is used to relieve the symptoms of hay fever, rhinitis, urticaria, and asthma.		2.4720monochlorobenzenes;
pyridines;
tertiary amino compound		anti-allergic agent;
antidepressant;
antipruritic drug;
H1-receptor antagonist;
histamine antagonist;
serotonin uptake inhibitor
chlorpromazine
Chlorpromazine: The prototypical phenothiazine antipsychotic drug. Like the other drugs in this class chlorpromazine's antipsychotic actions are thought to be due to long-term adaptation by the brain to blocking DOPAMINE RECEPTORS. Chlorpromazine has several other actions and therapeutic uses, including as an antiemetic and in the treatment of intractable hiccup.. chlorpromazine : A substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropanamine moiety.		2.4520organochlorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
phenothiazine antipsychotic drug
chlorpropamide
Chlorpropamide: A sulfonylurea hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277). chlorpropamide : An N-sulfonylurea that is urea in which a hydrogen attached to one of the nitrogens is substituted by 4-chlorobenzenesulfonyl group and a hydrogen attached to the other nitrogen is substituted by propyl group. Chlorpropamide is a hypoglycaemic agent used in the treatment of type 2 (non-insulin-dependent) diabetes mellitus not responding to dietary modification.		2.0510monochlorobenzenes;
N-sulfonylurea		hypoglycemic agent;
insulin secretagogue
chlorzoxazone
Chlorzoxazone: A centrally acting central muscle relaxant with sedative properties. It is claimed to inhibit muscle spasm by exerting an effect primarily at the level of the spinal cord and subcortical areas of the brain. (From Martindale, The Extra Pharmacopoea, 30th ed, p1202). chlorzoxazone : A member of the class of 1,3-benzoxazoles that is 1,3-benzoxazol-2-ol in which the hydrogen atom at position 5 is substituted by chlorine. A centrally acting muscle relaxant with sedative properties, it is used for the symptomatic treatment of painful muscle spasm.		2.45201,3-benzoxazoles;
heteroaryl hydroxy compound;
organochlorine compound		muscle relaxant;
sedative
cilostazol
[no description available]		2.1510lactam;
tetrazoles		anticoagulant;
bronchodilator agent;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
fibrin modulating drug;
neuroprotective agent;
platelet aggregation inhibitor;
vasodilator agent
cimetidine
Cimetidine: A histamine congener, it competitively inhibits HISTAMINE binding to HISTAMINE H2 RECEPTORS. Cimetidine has a range of pharmacological actions. It inhibits GASTRIC ACID secretion, as well as PEPSIN and GASTRIN output.. cimetidine : A member of the class of guanidines that consists of guanidine carrying a methyl substituent at position 1, a cyano group at position 2 and a 2-{[(5-methyl-1H-imidazol-4-yl)methyl]sulfanyl}ethyl group at position 3. It is a H2-receptor antagonist that inhibits the production of acid in stomach.		2.4520aliphatic sulfide;
guanidines;
imidazoles;
nitrile		adjuvant;
analgesic;
anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
cinoxacin
Cinoxacin: Synthetic antimicrobial related to OXOLINIC ACID and NALIDIXIC ACID and used in URINARY TRACT INFECTIONS.. cinoxacin : A member of the class of cinnolines that is 6,7-methylenedioxycinnolin-4(1H)-one bearing an ethyl group at position 1 and a carboxylic acid group at position 3. An analogue of oxolinic acid, it has similar antibacterial actions. It was formerly used for the treatment of urinary tract infections.		2.0510cinnolines;
oxacycle;
oxo carboxylic acid		antibacterial drug;
antiinfective agent
ciprofibrate
[no description available]		2.0510cyclopropanes;
monocarboxylic acid;
organochlorine compound		antilipemic drug
ciprofloxacin
Ciprofloxacin: A broad-spectrum antimicrobial carboxyfluoroquinoline.. ciprofloxacin : A quinolone that is quinolin-4(1H)-one bearing cyclopropyl, carboxylic acid, fluoro and piperazin-1-yl substituents at positions 1, 3, 6 and 7, respectively.		340aminoquinoline;
cyclopropanes;
fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone;
zwitterion		antibacterial drug;
antiinfective agent;
antimicrobial agent;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
environmental contaminant;
topoisomerase IV inhibitor;
xenobiotic
cisapride
Cisapride: A substituted benzamide used for its prokinetic properties. It is used in the management of gastroesophageal reflux disease, functional dyspepsia, and other disorders associated with impaired gastrointestinal motility. (Martindale The Extra Pharmacopoeia, 31st ed). cisapride : The amide resulting from formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with cis-1-[3-(4-fluorophenoxy)propyl]-3-methoxypiperidin-4-amine. It has been used (as its monohydrate or as its tartrate) for the treatment of gastro-oesophageal reflux disease and for non-ulcer dyspepsia, but its propensity to cause cardiac arrhythmias resulted in its complete withdrawal from many countries, including the U.K., and restrictions on its use elsewhere.		2.0510benzamides
citalopram
Citalopram: A furancarbonitrile that is one of the serotonin uptake inhibitors used as an antidepressant. The drug is also effective in reducing ethanol uptake in alcoholics and is used in depressed patients who also suffer from TARDIVE DYSKINESIA in preference to tricyclic antidepressants, which aggravate dyskinesia.. citalopram : A racemate comprising equimolar amounts of (R)-citalopram and its enantiomer, escitalopram. It is used as an antidepressant, although only escitalopram is active.. 1-[3-(dimethylamino)propyl]-1-(4-fluorophenyl)-1,3-dihydro-2-benzofuran-5-carbonitrile : A nitrile that is 1,3-dihydro-2-benzofuran-5-carbonitrile in which one of the hydrogens at position 1 is replaced by a p-fluorophenyl group, while the other is replaced by a 3-(dimethylamino)propyl group.		2.05102-benzofurans;
cyclic ether;
nitrile;
organofluorine compound;
tertiary amino compound
clioquinol
Clioquinol: A potentially neurotoxic 8-hydroxyquinoline derivative long used as a topical anti-infective, intestinal antiamebic, and vaginal trichomonacide. The oral preparation has been shown to cause subacute myelo-optic neuropathy and has been banned worldwide.. 5-chloro-7-iodoquinolin-8-ol : A monohydroxyquinoline that is quinolin-8-ol in which the hydrogens at positions 5 and 7 are replaced by chlorine and iodine, respectively. It has antibacterial and atifungal properties, and is used in creams for the treatment of skin infections. It has also been investigated as a chelator of copper and zinc ions for the possible treatment of Alzheimer's disease.		2.0510monohydroxyquinoline;
organochlorine compound;
organoiodine compound		antibacterial agent;
antifungal agent;
antimicrobial agent;
antineoplastic agent;
antiprotozoal drug;
chelator;
copper chelator
clobazam
Clobazam: A benzodiazepine derivative that is a long-acting GABA-A RECEPTOR agonist. It is used as an antiepileptic in the treatment of SEIZURES, including seizures associated with LENNOX-GASTAUT SYNDROME. It is also used as an anxiolytic, for the short-term treatment of acute ANXIETY.. clobazam : 7-Chloro-1H-1,5-benzodiazepine-2,4(3H,5H)-dione in which the hydrogen attached to the nitrogen at position 1 is substituted by a methyl group, whilst that attached to the other nitrogen is substituted by a phenyl group. It is used for the short-term management of acute anxiety and as an adjunct in the treatment of epilepsy in association with other antiepileptics.		2.05101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
GABA modulator
clofazimine
Clofazimine: A fat-soluble riminophenazine dye used for the treatment of leprosy. It has been used investigationally in combination with other antimycobacterial drugs to treat Mycobacterium avium infections in AIDS patients. Clofazimine also has a marked anti-inflammatory effect and is given to control the leprosy reaction, erythema nodosum leprosum. (From AMA Drug Evaluations Annual, 1993, p1619). clofazimine : 3-Isopropylimino-3,5-dihydro-phenazine in which the hydrogen at position 5 is substituted substituted by a 4-chlorophenyl group, and that at position 2 is substituted by a (4-chlorophenyl)amino group. A dark red crystalline solid, clofazimine is an antimycobacterial and is one of the main drugs used for the treatment of multi-bacillary leprosy. However, it can cause red/brown discolouration of the skin, so other treatments are often preferred in light-skinned patients.		2.0510monochlorobenzenes;
phenazines		dye;
leprostatic drug;
non-steroidal anti-inflammatory drug
clofibrate
angiokapsul: contains clofibrate & insoitolnicotinate		2.0510aromatic ether;
ethyl ester;
monochlorobenzenes		anticholesteremic drug;
antilipemic drug;
geroprotector;
PPARalpha agonist
clomiphene
[no description available]		2.0510tertiary amineestrogen antagonist;
estrogen receptor modulator
clomipramine
Clomipramine: A tricyclic antidepressant similar to IMIPRAMINE that selectively inhibits the uptake of serotonin in the brain. It is readily absorbed from the gastrointestinal tract and demethylated in the liver to form its primary active metabolite, desmethylclomipramine.. clomipramine : A dibenzoazepine that is 10,11-dihydro-5H-dibenzo[b,f]azepine which is substituted by chlorine at position 3 and in which the hydrogen attached to the nitrogen is replaced by a 3-(dimethylamino)propyl group. One of the more sedating tricyclic antidepressants, it is used as the hydrochloride salt for the treatment of depression as well as obsessive-compulsive disorder and phobias.		2.0410dibenzoazepineanticoronaviral agent;
antidepressant;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
serotonergic antagonist;
serotonergic drug;
serotonin uptake inhibitor
clonidine
Clonidine: An imidazoline sympatholytic agent that stimulates ALPHA-2 ADRENERGIC RECEPTORS and central IMIDAZOLINE RECEPTORS. It is commonly used in the management of HYPERTENSION.. clonidine (amino form) : A clonidine that is 4,5-dihydro-1H-imidazol-2-amine in which one of the amino hydrogens is replaced by a 2,6-dichlorophenyl group.		2.0510clonidine;
imidazoline
clotiazepam
clotiazepam: was heading 1975-94 (see under AZEPINES 1978-90; was Y 6047 see under AZEPINES 1975-77); Y 6047 was see CLOTIAZEPAM 1978-94; use AZEPINES to search CLOTIAZEPAM 1975-94; thienodiazepine derivative with actions similar to those of benzodiazepines		2.0510organic molecular entity
clotrimazole
[no description available]		2.7630conazole antifungal drug;
imidazole antifungal drug;
imidazoles;
monochlorobenzenes		antiinfective agent;
environmental contaminant;
xenobiotic
cyclandelate
Cyclandelate: A direct-acting SMOOTH MUSCLE relaxant used to dilate BLOOD VESSELS.. cyclandelate : The ester obtained by formal condensation of mandelic acid and 3,3,5-tricyclohexanol. It is a direct-acting smooth muscle relaxant used to dilate blood vessels.		2.0510carboxylic ester;
secondary alcohol		vasodilator agent
cyproheptadine
Cyproheptadine: A serotonin antagonist and a histamine H1 blocker used as antipruritic, appetite stimulant, antiallergic, and for the post-gastrectomy dumping syndrome, etc.. cyproheptadine : The product resulting from the formal oxidative coupling of position 5 of 5H-dibenzo[a,d]cycloheptene with position 4 of 1-methylpiperidine resulting in the formation of a double bond between the two fragments. It is a sedating antihistamine with antimuscarinic and calcium-channel blocking actions. It is used (particularly as the hydrochloride sesquihydrate) for the relief of allergic conditions including rhinitis, conjunctivitis due to inhalant allergens and foods, urticaria and angioedema, and in pruritic skin disorders. Unlike other antihistamines, it is also a seratonin receptor antagonist, making it useful in conditions such as vascular headache and anorexia.		2.0510piperidines;
tertiary amine		anti-allergic agent;
antipruritic drug;
gastrointestinal drug;
H1-receptor antagonist;
serotonergic antagonist
damnacanthal
damnacanthal: structure given in first source; isolated from the stem bark and roots of Morinda lucida; a selective inhibitor of p56(lck) tyrosine kinase activity		2.0310aldehyde;
monohydroxyanthraquinone
danthron
danthron: structure. chrysazin : A dihydroxyanthraquinone that is anthracene-9,10-dione substituted by hydroxy groups at positions 1 and 8.		2.0510dihydroxyanthraquinoneapoptosis inducer;
plant metabolite
dapi
DAPI: RN given refers to parent cpd.		3.820indolesfluorochrome
dapsone
[no description available]		2.0510substituted aniline;
sulfone		anti-inflammatory drug;
antiinfective agent;
antimalarial;
leprostatic drug
deferoxamine
Deferoxamine: Natural product isolated from Streptomyces pilosus. It forms iron complexes and is used as a chelating agent, particularly in the mesylate form.. desferrioxamine B : An acyclic desferrioxamine that is butanedioic acid in which one of the carboxy groups undergoes formal condensation with the primary amino group of N-(5-aminopentyl)-N-hydroxyacetamide and the second carboxy group undergoes formal condensation with the hydroxyamino group of N(1)-(5-aminopentyl)-N(1)-hydroxy-N(4)-[5-(hydroxyamino)pentyl]butanediamide. It is a siderophore native to Streptomyces pilosus biosynthesised by the DesABCD enzyme cluster as a high affinity Fe(III) chelator.		2.0510acyclic desferrioxaminebacterial metabolite;
ferroptosis inhibitor;
iron chelator;
siderophore
desipramine
Desipramine: A tricyclic dibenzazepine compound that potentiates neurotransmission. Desipramine selectively blocks reuptake of norepinephrine from the neural synapse, and also appears to impair serotonin transport. This compound also possesses minor anticholinergic activity, through its affinity to muscarinic receptors.. desipramine : A dibenzoazepine consisting of 10,11-dihydro-5H-dibenzo[b,f]azepine substituted on nitrogen with a 3-(methylamino)propyl group.		2.0410dibenzoazepine;
secondary amino compound		adrenergic uptake inhibitor;
alpha-adrenergic antagonist;
antidepressant;
cholinergic antagonist;
drug allergen;
EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
serotonin uptake inhibitor
amphetamine
Amphetamine: A powerful central nervous system stimulant and sympathomimetic. Amphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulation of release of monamines, and inhibiting monoamine oxidase. Amphetamine is also a drug of abuse and a psychotomimetic. The l- and the d,l-forms are included here. The l-form has less central nervous system activity but stronger cardiovascular effects. The d-form is DEXTROAMPHETAMINE.. 1-phenylpropan-2-amine : A primary amine that is isopropylamine in which a hydrogen attached to one of the methyl groups has been replaced by a phenyl group.. amphetamine : A racemate comprising equimolar amounts of (R)-amphetamine (also known as levamphetamine or levoamphetamine) and (S)-amphetamine (also known as dexamfetamine or dextroamphetamine.		2.0510primary amine
eflornithine
Eflornithine: An inhibitor of ORNITHINE DECARBOXYLASE, the rate limiting enzyme of the polyamine biosynthetic pathway.. eflornithine : A fluoroamino acid that is ornithine substituted by a difluoromethyl group at position 2.		4.2230alpha-amino acid;
fluoroamino acid		trypanocidal drug
r 59022
R 59022: diacylglycerol kinase inhibitor; structure given in first source; platelet activator factor antagonist		2.0310diarylmethane
diazepam
Diazepam: A benzodiazepine with anticonvulsant, anxiolytic, sedative, muscle relaxant, and amnesic properties and a long duration of action. Its actions are mediated by enhancement of GAMMA-AMINOBUTYRIC ACID activity.. diazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a methyl group at position 1 and a phenyl group at position 5.		2.05101,4-benzodiazepinone;
organochlorine compound		anticonvulsant;
anxiolytic drug;
environmental contaminant;
sedative;
xenobiotic
diazoxide
Diazoxide: A benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group.. diazoxide : A benzothiadiazine that is the S,S-dioxide of 2H-1,2,4-benzothiadiazine which is substituted at position 3 by a methyl group and at position 7 by chlorine. A peripheral vasodilator, it increases the concentration of glucose in the plasma and inhibits the secretion of insulin by the beta- cells of the pancreas. It is used orally in the management of intractable hypoglycaemia and intravenously in the management of hypertensive emergencies.		2.0510benzothiadiazine;
organochlorine compound;
sulfone		antihypertensive agent;
beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
diuretic;
K-ATP channel agonist;
sodium channel blocker;
sympathomimetic agent;
vasodilator agent
diclofenac
Diclofenac: A non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt.. diclofenac : A monocarboxylic acid consisting of phenylacetic acid having a (2,6-dichlorophenyl)amino group at the 2-position.		3.4670amino acid;
aromatic amine;
dichlorobenzene;
monocarboxylic acid;
secondary amino compound		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
ddt
1,1-bis(p-chlorophenyl)-2,2,2-trichloroethane: structure in first source		2.0510benzenoid aromatic compound;
chlorophenylethane;
monochlorobenzenes;
organochlorine insecticide		bridged diphenyl acaricide;
carcinogenic agent;
endocrine disruptor;
persistent organic pollutant
diflunisal
Diflunisal: A salicylate derivative and anti-inflammatory analgesic with actions and side effects similar to those of ASPIRIN.. diflunisal : An organofluorine compound comprising salicylic acid having a 2,4-difluorophenyl group at the 5-position.		2.0510monohydroxybenzoic acid;
organofluorine compound		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
diphenhydramine
Diphenhydramine: A histamine H1 antagonist used as an antiemetic, antitussive, for dermatoses and pruritus, for hypersensitivity reactions, as a hypnotic, an antiparkinson, and as an ingredient in common cold preparations. It has some undesired antimuscarinic and sedative effects.. diphenhydramine : An ether that is the benzhydryl ether of 2-(dimethylamino)ethanol. It is a H1-receptor antagonist used as a antipruritic and antitussive drug.. antitussive : An agent that suppresses cough. Antitussives have a central or a peripheral action on the cough reflex, or a combination of both. Compare with expectorants, which are considered to increase the volume of secretions in the respiratory tract, so facilitating their removal by ciliary action and coughing, and mucolytics, which decrease the viscosity of mucus, facilitating its removal by ciliary action and expectoration.		2.4920ether;
tertiary amino compound		anti-allergic agent;
antidyskinesia agent;
antiemetic;
antiparkinson drug;
antipruritic drug;
antitussive;
H1-receptor antagonist;
local anaesthetic;
muscarinic antagonist;
oneirogen;
sedative
dipyridamole
Dipyridamole: A phosphodiesterase inhibitor that blocks uptake and metabolism of adenosine by erythrocytes and vascular endothelial cells. Dipyridamole also potentiates the antiaggregating action of prostacyclin. (From AMA Drug Evaluations Annual, 1994, p752). dipyridamole : A pyrimidopyrimidine that is 2,2',2'',2'''-(pyrimido[5,4-d]pyrimidine-2,6-diyldinitrilo)tetraethanol substituted by piperidin-1-yl groups at positions 4 and 8 respectively. A vasodilator agent, it inhibits the formation of blood clots.		2.4520piperidines;
pyrimidopyrimidine;
tertiary amino compound;
tetrol		adenosine phosphodiesterase inhibitor;
EC 3.5.4.4 (adenosine deaminase) inhibitor;
platelet aggregation inhibitor;
vasodilator agent
disopyramide
Disopyramide: A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties.. disopyramide : A monocarboxylic acid amide that is butanamide substituted by a diisopropylamino group at position 4, a phenyl group at position 2 and a pyridin-2-yl group at position 2. It is used as a anti-arrhythmia drug.		2.0510monocarboxylic acid amide;
pyridines;
tertiary amino compound		anti-arrhythmia drug
disulfiram
[no description available]		2.8130organic disulfide;
organosulfur acaricide		angiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor;
EC 3.1.1.1 (carboxylesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
ferroptosis inducer;
fungicide;
NF-kappaB inhibitor
valproic acid
Valproic Acid: A fatty acid with anticonvulsant and anti-manic properties that is used in the treatment of EPILEPSY and BIPOLAR DISORDER. The mechanisms of its therapeutic actions are not well understood. It may act by increasing GAMMA-AMINOBUTYRIC ACID levels in the brain or by altering the properties of VOLTAGE-GATED SODIUM CHANNELS.. valproic acid : A branched-chain saturated fatty acid that comprises of a propyl substituent on a pentanoic acid stem.		10.55120branched-chain fatty acid;
branched-chain saturated fatty acid		anticonvulsant;
antimanic drug;
EC 3.5.1.98 (histone deacetylase) inhibitor;
GABA agent;
neuroprotective agent;
psychotropic drug;
teratogenic agent
n(6),n(6)-dimethyladenine
N(6),N(6)-dimethyladenine : A tertiary amine that is adenine substituted at N-6 by geminal methyl groups.		2.0310tertiary amine
doxazosin
Doxazosin: A prazosin-related compound that is a selective alpha-1-adrenergic blocker.. doxazosin : A member of the class of quinazolines that is quinazoline substituted by an amino group at position 4, methoxy groups at positions 6 and 7 and a piperazin-1-yl group at position 2 which in turn is substituted by a 2,3-dihydro-1,4-benzodioxin-2-ylcarbonyl group at position 4. An antihypertensive agent, it is used in the treatment of high blood pressure.		2.1710aromatic amine;
benzodioxine;
monocarboxylic acid amide;
N-acylpiperazine;
N-arylpiperazine;
quinazolines		alpha-adrenergic antagonist;
antihyperplasia drug;
antihypertensive agent;
antineoplastic agent;
vasodilator agent
doxepin
Doxepin: A dibenzoxepin tricyclic compound. It displays a range of pharmacological actions including maintaining adrenergic innervation. Its mechanism of action is not fully understood, but it appears to block reuptake of monoaminergic neurotransmitters into presynaptic terminals. It also possesses anticholinergic activity and modulates antagonism of histamine H(1)- and H(2)-receptors.. doxepin : A dibenzooxepine that is 6,11-dihydrodibenzo[b,e]oxepine substituted by a 3-(dimethylamino)propylidene group at position 11. It is used as an antidepressant drug.		2.0510dibenzooxepine;
tertiary amino compound		antidepressant
droperidol
Droperidol: A butyrophenone with general properties similar to those of HALOPERIDOL. It is used in conjunction with an opioid analgesic such as FENTANYL to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon. It is also used as a premedicant, as an antiemetic, and for the control of agitation in acute psychoses. (From Martindale, The Extra Pharmacopoeia, 29th ed, p593). droperidol : An organofluorine compound that is haloperidol in which the hydroxy group has been eliminated with the introduction of a double bond in the piperidine ring, and the 4-chlorophenyl group has been replaced by a benzimidazol-2-on-1-yl group. It is used in the management of chemotherapy-induced nausea and vomiting, and in conjunction with an opioid analgesic such as fentanyl to maintain the patient in a calm state of neuroleptanalgesia with indifference to surroundings but still able to cooperate with the surgeon.		2.0510aromatic ketone;
benzimidazoles;
organofluorine compound		anaesthesia adjuvant;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic
ebselen
ebselen : A benzoselenazole that is 1,2-benzoselenazol-3-one carrying an additional phenyl substituent at position 2. Acts as a mimic of glutathione peroxidase.		2.110benzoselenazoleanti-inflammatory drug;
antibacterial agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
EC 3.1.3.25 (inositol-phosphate phosphatase) inhibitor;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
EC 3.5.4.1 (cytosine deaminase) inhibitor;
EC 5.1.3.2 (UDP-glucose 4-epimerase) inhibitor;
enzyme mimic;
ferroptosis inhibitor;
genotoxin;
hepatoprotective agent;
neuroprotective agent;
radical scavenger
econazole
Econazole: An imidazole derivative that is commonly used as a topical antifungal agent.. econazole : A racemate composed of equimolar amounts of (R)- and (S)-econazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections.. 1-{2-(4-chlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl}imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 4-chlorobenzyl group.		2.0510dichlorobenzene;
ether;
imidazoles;
monochlorobenzenes
ellipticine
ellipticine : A organic heterotetracyclic compound that is pyrido[4,3-b]carbazole carrying two methyl substituents at positions 5 and 11.		2.0310indole alkaloid;
organic heterotetracyclic compound;
organonitrogen heterocyclic compound;
polycyclic heteroarene		antineoplastic agent;
plant metabolite
emodin
Emodin: Purgative anthraquinone found in several plants, especially RHAMNUS PURSHIANA. It was formerly used as a laxative, but is now used mainly as a tool in toxicity studies.. emodin : A trihydroxyanthraquinone that is 9,10-anthraquinone which is substituted by hydroxy groups at positions 1, 3, and 8 and by a methyl group at position 6. It is present in the roots and barks of numerous plants (particularly rhubarb and buckthorn), moulds, and lichens. It is an active ingredient of various Chinese herbs.		3.0640trihydroxyanthraquinoneantineoplastic agent;
laxative;
plant metabolite;
tyrosine kinase inhibitor
enflurane
Enflurane: An extremely stable inhalation anesthetic that allows rapid adjustments of anesthesia depth with little change in pulse or respiratory rate.. enflurane : An ether in which the oxygen atom is connected to 2-chloro-1,1,2-trifluoroethyl and difluoromethyl groups.		2.0510ether;
organochlorine compound;
organofluorine compound		anaesthetic
enoxacin
Enoxacin: A broad-spectrum 6-fluoronaphthyridinone antibacterial agent that is structurally related to NALIDIXIC ACID.. enoxacin : A 1,8-naphthyridine derivative that is 1,4-dihydro-1,8-naphthyridine with an ethyl group at the 1 position, a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a piperazin-1-yl group at the 7 position. An antibacterial, it is used in the treatment of urinary-tract infections and gonorrhoea.		2.05101,8-naphthyridine derivative;
amino acid;
fluoroquinolone antibiotic;
monocarboxylic acid;
N-arylpiperazine;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor
erythrosine
Fluoresceins: A family of spiro(isobenzofuran-1(3H),9'-(9H)xanthen)-3-one derivatives. These are used as dyes, as indicators for various metals, and as fluorescent labels in immunoassays.		3.5220
estazolam
Estazolam: A benzodiazepine with anticonvulsant, hypnotic, and muscle relaxant properties. It has been shown in some cases to be more potent than DIAZEPAM or NITRAZEPAM.. estazolam : A triazolo[4,3-a][1,4]benzodiazepine having a phenyl group at position 6 and a chloro substituent at position 8. A short-acting benzodiazepine with general properties similar to diazepam, it is given by mouth as a hypnotic in the short-term management of insomnia.		2.0510triazoles;
triazolobenzodiazepine		anticonvulsant;
anxiolytic drug;
GABA modulator
ethacrynic acid
Ethacrynic Acid: A compound that inhibits symport of sodium, potassium, and chloride primarily in the ascending limb of Henle, but also in the proximal and distal tubules. This pharmacological action results in excretion of these ions, increased urinary output, and reduction in extracellular fluid. This compound has been classified as a loop or high ceiling diuretic.. etacrynic acid : An aromatic ether that is phenoxyacetic acid in which the phenyl ring is substituted by chlorines at positions 2 and 3, and by a 2-methylidenebutanoyl group at position 4. It is a loop diuretic used to treat high blood pressure resulting from diseases such as congestive heart failure, liver failure, and kidney failure. It is also a glutathione S-transferase (EC 2.5.1.18) inhibitor.		2.0510aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid		EC 2.5.1.18 (glutathione transferase) inhibitor;
ion transport inhibitor;
loop diuretic
ethenzamide
ethenzamide: structure		2.0110organic molecular entity
ethoxzolamide
Ethoxzolamide: A carbonic anhydrase inhibitor used as diuretic and in glaucoma. It may cause hypokalemia.. ethoxzolamide : A sulfonamide that is 1,3-benzothiazole-2-sulfonamide which is substituted by an ethoxy group at position 6. A carbonic anhydrase inhibitor, it has been used in the treatment of glaucoma, and as a diuretic.		2.0510aromatic ether;
benzothiazoles;
sulfonamide		antiglaucoma drug;
diuretic;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
ethylenediamine
ethylenediamine: RN given refers to parent cpd; edamine is the recommended contraction for the ethylenediamine radical. ethylenediamine : An alkane-alpha,omega-diamine in which the alkane is ethane.		2.1710alkane-alpha,omega-diamineGABA agonist
etidronate
Etidronic Acid: A diphosphonate which affects calcium metabolism. It inhibits ectopic calcification and slows down bone resorption and bone turnover.. etidronic acid : A 1,1-bis(phosphonic acid) that is (ethane-1,1-diyl)bis(phosphonic acid) having a hydroxy substituent at the 1-position. It inhibits the formation, growth, and dissolution of hydroxyapatite crystals by chemisorption to calcium phosphate surfaces.		2.01101,1-bis(phosphonic acid)antineoplastic agent;
bone density conservation agent;
chelator
etodolac
Etodolac: A non-steroidal anti-inflammatory agent and cyclooxygenase-2 (COX-2) inhibitor with potent analgesic and anti-arthritic properties. It has been shown to be effective in the treatment of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; ANKYLOSING SPONDYLITIS; and in the alleviation of postoperative pain (PAIN, POSTOPERATIVE).. etodolac : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is substituted by a 1,8-diethyl-1,3,4,9-tetrahydropyrano[3,4-b]indol-1-yl moiety. A preferential inhibitor of cyclo-oxygenase 2 and non-steroidal anti-inflammatory, it is used for the treatment of rheumatoid arthritis and osteoarthritis, and for the alleviation of postoperative pain. Administered as the racemate, only the (S)-enantiomer is active.		2.0510monocarboxylic acid;
organic heterotricyclic compound		antipyretic;
cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
brl 42810
[no description available]		2.05102-aminopurines;
acetate ester		antiviral drug;
prodrug
felbamate
Felbamate: A PEGylated phenylcarbamate derivative that acts as an antagonist of NMDA RECEPTORS. It is used as an anticonvulsant, primarily for the treatment of SEIZURES in severe refractory EPILEPSY.. felbamate : The bis(carbamate ester) of 2-phenylpropane-1,3-diol. An anticonvulsant, it is used in the treatment of epilepsy.		2.0510carbamate esteranticonvulsant;
neuroprotective agent
felodipine
Felodipine: A dihydropyridine calcium antagonist with positive inotropic effects. It lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels.. felodipine : The mixed (methyl, ethyl) diester of 4-(2,3-dichlorophenyl)-2,6-dimethyl-1,4-dihydropyridine-3,5-dicarboxylic acid. A calcium-channel blocker, it lowers blood pressure by reducing peripheral vascular resistance through a highly selective action on smooth muscle in arteriolar resistance vessels. It is used in the management of hypertension and angina pectoris.		2.7830dichlorobenzene;
dihydropyridine;
ethyl ester;
methyl ester		anti-arrhythmia drug;
antihypertensive agent;
calcium channel blocker;
vasodilator agent
fendiline
Fendiline: Coronary vasodilator; inhibits calcium function in muscle cells in excitation-contraction coupling; proposed as antiarrhythmic and antianginal agents.		2.0410diarylmethane
fenofibrate
Pharmavit: a polyvitamin product, comprising vitamins A, D2, B1, B2, B6, C, E, nicotinamide, & calcium pantothene; may be a promising agent for application to human populations exposed to carcinogenic and genetic hazards of ionizing radiation; RN from CHEMLINE		2.4520aromatic ether;
chlorobenzophenone;
isopropyl ester;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
fentanyl
Fentanyl: A potent narcotic analgesic, abuse of which leads to habituation or addiction. It is primarily a mu-opioid agonist. Fentanyl is also used as an adjunct to general anesthetics, and as an anesthetic for induction and maintenance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1078). fentanyl : A monocarboxylic acid amide resulting from the formal condensation of the aryl amino group of N-phenyl-1-(2-phenylethyl)piperidin-4-amine with propanoic acid.		2.7930anilide;
monocarboxylic acid amide;
piperidines		adjuvant;
anaesthesia adjuvant;
anaesthetic;
intravenous anaesthetic;
mu-opioid receptor agonist;
opioid analgesic
fexofenadine
fexofenadine: a second generation antihistamine; metabolite of the antihistaminic drug terfenadine; structure in first source; RN refers to HCl. fexofenadine : A piperidine-based anti-histamine compound.		2.0410piperidines;
tertiary amine		anti-allergic agent;
H1-receptor antagonist
flecainide
Flecainide: A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial ARRHYTHMIAS and TACHYCARDIAS.. flecainide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2,5-bis(2,2,2-trifluoroethoxy)benzoic acid with the primary amino group of piperidin-2-ylmethylamine. An antiarrhythmic agent used (in the form of its acetate salt) to prevent and treat tachyarrhythmia (abnormal fast rhythm of the heart).		2.0510aromatic ether;
monocarboxylic acid amide;
organofluorine compound;
piperidines		anti-arrhythmia drug
fluconazole
Fluconazole: Triazole antifungal agent that is used to treat oropharyngeal CANDIDIASIS and cryptococcal MENINGITIS in AIDS.. fluconazole : A member of the class of triazoles that is propan-2-ol substituted at position 1 and 3 by 1H-1,2,4-triazol-1-yl groups and at position 2 by a 2,4-difluorophenyl group. It is an antifungal drug used for the treatment of mucosal candidiasis and for systemic infections including systemic candidiasis, coccidioidomycosis, and cryptococcosis.		2.0510conazole antifungal drug;
difluorobenzene;
tertiary alcohol;
triazole antifungal drug		environmental contaminant;
P450 inhibitor;
xenobiotic
flucytosine
Flucytosine: A fluorinated cytosine analog that is used as an antifungal agent.. flucytosine : An organofluorine compound that is cytosine that is substituted at position 5 by a fluorine. A prodrug for the antifungal 5-fluorouracil, it is used for the treatment of systemic fungal infections.		2.0510aminopyrimidine;
nucleoside analogue;
organofluorine compound;
pyrimidine antifungal drug;
pyrimidone		prodrug
flufenamic acid
Flufenamic Acid: An anthranilic acid derivative with analgesic, anti-inflammatory, and antipyretic properties. It is used in musculoskeletal and joint disorders and administered by mouth and topically. (From Martindale, The Extra Pharmacopoeia, 30th ed, p16). flufenamic acid : An aromatic amino acid consisting of anthranilic acid carrying an N-(trifluoromethyl)phenyl substituent. An analgesic and anti-inflammatory, it is used in rheumatic disorders.		2.0510aromatic amino acid;
organofluorine compound		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
flumazenil
Flumazenil: A potent benzodiazepine receptor antagonist. Since it reverses the sedative and other actions of benzodiazepines, it has been suggested as an antidote to benzodiazepine overdoses.. flumazenil : An organic heterotricyclic compound that is 5,6-dihydro-4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted at positions 3, 5, 6, and 8 by ethoxycarbonyl, methyl, oxo, and fluoro groups, respectively. It is used as an antidote to benzodiazepine overdose.		2.4620ethyl ester;
imidazobenzodiazepine;
organofluorine compound		antidote to benzodiazepine poisoning;
GABA antagonist
flunitrazepam
Flunitrazepam: A benzodiazepine with pharmacologic actions similar to those of DIAZEPAM that can cause ANTEROGRADE AMNESIA. Some reports indicate that it is used as a date rape drug and suggest that it may precipitate violent behavior. The United States Government has banned the importation of this drug.. flunitrazepam : A 1,4-benzodiazepinone that is nitrazepam substituted by a methyl group at position 1 and by a fluoro group at position 2'. It is a potent hypnotic, sedative, and amnestic drug used to treat chronic insomnia.		2.05101,4-benzodiazepinone;
C-nitro compound;
monofluorobenzenes		anxiolytic drug;
GABAA receptor agonist;
sedative
fluorescite
fluorescein (acid form) : A xanthene dye that is highly fluorescent and commonly used as a fluorescent tracer.		2.0410benzoic acids;
cyclic ketone;
hydroxy monocarboxylic acid;
organic heterotricyclic compound;
phenols;
xanthene dye		fluorescent dye;
radioopaque medium
fluorouracil
Fluorouracil: A pyrimidine analog that is an antineoplastic antimetabolite. It interferes with DNA synthesis by blocking the THYMIDYLATE SYNTHETASE conversion of deoxyuridylic acid to thymidylic acid.. 5-fluorouracil : A nucleobase analogue that is uracil in which the hydrogen at position 5 is replaced by fluorine. It is an antineoplastic agent which acts as an antimetabolite - following conversion to the active deoxynucleotide, it inhibits DNA synthesis (by blocking the conversion of deoxyuridylic acid to thymidylic acid by the cellular enzyme thymidylate synthetase) and so slows tumour growth.		12.39357nucleobase analogue;
organofluorine compound		antimetabolite;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
radiosensitizing agent;
xenobiotic
fluoxetine
Fluoxetine: The first highly specific serotonin uptake inhibitor. It is used as an antidepressant and often has a more acceptable side-effects profile than traditional antidepressants.. fluoxetine : A racemate comprising equimolar amounts of (R)- and (S)-fluoxetine. A selective serotonin reuptake inhibitor (SSRI), it is used (generally as the hydrochloride salt) for the treatment of depression (and the depressive phase of bipolar disorder), bullimia nervosa, and obsessive-compulsive disorder.. N-methyl-3-phenyl-3-[4-(trifluoromethyl)phenoxy]propan-1-amine : An aromatic ether consisting of 4-trifluoromethylphenol in which the hydrogen of the phenolic hydroxy group is replaced by a 3-(methylamino)-1-phenylpropyl group.		3.8430(trifluoromethyl)benzenes;
aromatic ether;
secondary amino compound
flurbiprofen
Flurbiprofen: An anti-inflammatory analgesic and antipyretic of the phenylalkynoic acid series. It has been shown to reduce bone resorption in periodontal disease by inhibiting CARBONIC ANHYDRASE.. flurbiprofen : A monocarboxylic acid that is a 2-fluoro-[1,1'-biphenyl-4-yl] moiety linked to C-2 of propionic acid. A non-steroidal anti-inflammatory, analgesic and antipyretic, it is used as a pre-operative anti-miotic as well as orally for arthritis or dental pain.		2.4520fluorobiphenyl;
monocarboxylic acid		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
flutamide
Flutamide: An antiandrogen with about the same potency as cyproterone in rodent and canine species.		2.4520(trifluoromethyl)benzenes;
monocarboxylic acid amide		androgen antagonist;
antineoplastic agent
fomepizole
Fomepizole: A pyrazole and competitive inhibitor of ALCOHOL DEHYDROGENASE that is used for the treatment of poisoning by ETHYLENE GLYCOL or METHANOL.. fomepizole : A member of the class of pyrazoles that is 1H-pyrazole substituted by a methyl group at position 4.		2.0510pyrazolesantidote;
EC 1.1.1.1 (alcohol dehydrogenase) inhibitor;
protective agent
furosemide
Furosemide: A benzoic-sulfonamide-furan. It is a diuretic with fast onset and short duration that is used for EDEMA and chronic RENAL INSUFFICIENCY.. furosemide : A chlorobenzoic acid that is 4-chlorobenzoic acid substituted by a (furan-2-ylmethyl)amino and a sulfamoyl group at position 2 and 5 respectively. It is a diuretic used in the treatment of congestive heart failure.		4.0740chlorobenzoic acid;
furans;
sulfonamide		environmental contaminant;
loop diuretic;
xenobiotic
gabexate
Gabexate: A serine proteinase inhibitor used therapeutically in the treatment of pancreatitis, disseminated intravascular coagulation (DIC), and as a regional anticoagulant for hemodialysis. The drug inhibits the hydrolytic effects of thrombin, plasmin, and kallikrein, but not of chymotrypsin and aprotinin.		3.2110benzoate ester
gemfibrozil
[no description available]		3.8621aromatic etherantilipemic drug
glafenine
Glafenine: An anthranilic acid derivative with analgesic properties used for the relief of all types of pain.. glafenine : A carboxylic ester that is 2,3-dihydroxypropyl anthranilate in which the amino group is substituted by a 7-chloroquinolin-4-yl group. A non-steroidal anti-inflammatory drug, glafenine and its hydrochloride salt were used for the relief of all types of pain, but high incidence of anaphylactic reactions resulted in their withdrawal from the market.		2.0510aminoquinoline;
carboxylic ester;
glycol;
organochlorine compound;
secondary amino compound		inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
gliclazide
Gliclazide: An oral sulfonylurea hypoglycemic agent which stimulates insulin secretion.		2.4520N-sulfonylureahypoglycemic agent;
insulin secretagogue;
radical scavenger
glimepiride
glimepiride: structure given in first source		2.0410sulfonamide
glipizide
Glipizide: An oral hypoglycemic agent which is rapidly absorbed and completely metabolized.. glipizide : An N-sulfonylurea that is glyburide in which the (5-chloro-2-methoxybenzoyl group is replaced by a (5-methylpyrazin-2-yl)carbonyl group. An oral hypoglycemic agent, it is used in the treatment of type 2 diabetes mellitus.		2.0410aromatic amide;
monocarboxylic acid amide;
N-sulfonylurea;
pyrazines		EC 2.7.1.33 (pantothenate kinase) inhibitor;
hypoglycemic agent;
insulin secretagogue
glutethimide
Glutethimide: A hypnotic and sedative. Its use has been largely superseded by other drugs.		2.0510piperidines
glyburide
Glyburide: An antidiabetic sulfonylurea derivative with actions like those of chlorpropamide. glyburide : An N-sulfonylurea that is acetohexamide in which the acetyl group is replaced by a 2-(5-chloro-2-methoxybenzamido)ethyl group.		2.7430monochlorobenzenes;
N-sulfonylurea		anti-arrhythmia drug;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 3.6.3.49 (channel-conductance-controlling ATPase) inhibitor;
hypoglycemic agent
go 6976
[no description available]		2.0310indolocarbazole;
organic heterohexacyclic compound		EC 2.7.11.13 (protein kinase C) inhibitor
gossypol
Gossypol: A dimeric sesquiterpene found in cottonseed (GOSSYPIUM). The (-) isomer is active as a male contraceptive (CONTRACEPTIVE AGENTS, MALE) whereas toxic symptoms are associated with the (+) isomer.		2.7730
guaiazulene
guaiazulene: structure		2.0510sesquiterpene
1-(5-isoquinolinesulfonyl)-2-methylpiperazine
1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine: A specific protein kinase C inhibitor, which inhibits superoxide release from human neutrophils (PMN) stimulated with phorbol myristate acetate or synthetic diacylglycerol.. 1-(5-isoquinolinesulfonyl)-2-methylpiperazine : A member of the class of N-sulfonylpiperazines that is 2-methylpiperazine substituted at position 1 by a 5-isoquinolinesulfonyl group.		4.1140isoquinolines;
N-sulfonylpiperazine		EC 2.7.11.13 (protein kinase C) inhibitor
ha 1004
N-(2-guanidinoethyl)-5-isoquinolinesulfonamide: structure given in first source		2.0310isoquinolines
fasudil
fasudil: intracellular calcium antagonist; structure in first source. fasudil : An isoquinoline substituted by a (1,4-diazepan-1-yl)sulfonyl group at position 5. It is a Rho-kinase inhibitor and its hydrochloride hydrate form is approved for the treatment of cerebral vasospasm and cerebral ischemia.		4.5870isoquinolines;
N-sulfonyldiazepane		antihypertensive agent;
calcium channel blocker;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
geroprotector;
neuroprotective agent;
nootropic agent;
vasodilator agent
haloperidol
Haloperidol: A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279). haloperidol : A compound composed of a central piperidine structure with hydroxy and p-chlorophenyl substituents at position 4 and an N-linked p-fluorobutyrophenone moiety.		2.7330aromatic ketone;
hydroxypiperidine;
monochlorobenzenes;
organofluorine compound;
tertiary alcohol		antidyskinesia agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic;
serotonergic antagonist
halothane
[no description available]		2.0510haloalkane;
organobromine compound;
organochlorine compound;
organofluorine compound		inhalation anaesthetic
hexachlorophene
Hexachlorophene: A chlorinated bisphenol antiseptic with a bacteriostatic action against Gram-positive organisms, but much less effective against Gram-negative organisms. It is mainly used in soaps and creams and is an ingredient of various preparations used for skin disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797). hexachlorophene : An organochlorine compound that is diphenylmethane in which each of the phenyl groups is substituted by chlorines at positions 2, 3, and 5, and by a hydroxy group at position 6. An antiseptic that is effective against Gram-positive organisms, it is used in soaps and creams for the treatment of various skin disorders. It is also used in agriculture as an acaricide and fungicide, but is not approved for such use within the European Union.		2.0510bridged diphenyl fungicide;
polyphenol;
trichlorobenzene		acaricide;
antibacterial agent;
antifungal agrochemical;
antiseptic drug
miltefosine
miltefosine: hexadecyl phosphocholine derivative of cisplatin; did not substantially activate HIV long terminal repeat; less toxic than cisplatin. miltefosine : A phospholipid that is the hexadecyl monoester of phosphocholine.		2.0510phosphocholines;
phospholipid		anti-inflammatory agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antiprotozoal drug;
apoptosis inducer;
immunomodulator;
protein kinase inhibitor
hexestrol
[no description available]		2.0510stilbenoid
hexetidine
Hexetidine: A bactericidal and fungicidal antiseptic. It is used as a 0.1% mouthwash for local infections and oral hygiene. (From Martindale, The Extra Pharmacopoeia, 30th ed, p797)		2.0510organic heteromonocyclic compound;
organonitrogen heterocyclic compound
hexobarbital
Hexobarbital: A barbiturate that is effective as a hypnotic and sedative.. hexobarbital : A member of the class of barbiturates taht is barbituric acid substituted at N-1 by methyl and at C-5 by methyl and cyclohex-1-enyl groups.		2.0510barbiturates
hydralazine
Hydralazine: A direct-acting vasodilator that is used as an antihypertensive agent.. hydralazine : The 1-hydrazino derivative of phthalazine; a direct-acting vasodilator that is used as an antihypertensive agent.		2.4720azaarene;
hydrazines;
ortho-fused heteroarene;
phthalazines		antihypertensive agent;
vasodilator agent
hydrochlorothiazide
Hydrochlorothiazide: A thiazide diuretic often considered the prototypical member of this class. It reduces the reabsorption of electrolytes from the renal tubules. This results in increased excretion of water and electrolytes, including sodium, potassium, chloride, and magnesium. It is used in the treatment of several disorders including edema, hypertension, diabetes insipidus, and hypoparathyroidism.. hydrochlorothiazide : A benzothiadiazine that is 3,4-dihydro-2H-1,2,4-benzothiadiazine 1,1-dioxide substituted by a chloro group at position 6 and a sulfonamide at 7. It is diuretic used for the treatment of hypertension and congestive heart failure.		2.4520benzothiadiazine;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
hydroxychloroquine
Hydroxychloroquine: A chemotherapeutic agent that acts against erythrocytic forms of malarial parasites. Hydroxychloroquine appears to concentrate in food vacuoles of affected protozoa. It inhibits plasmodial heme polymerase. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p970). hydroxychloroquine : An aminoquinoline that is chloroquine in which one of the N-ethyl groups is hydroxylated at position 2. An antimalarial with properties similar to chloroquine that acts against erythrocytic forms of malarial parasites, it is mainly used as the sulfate salt for the treatment of lupus erythematosus, rheumatoid arthritis, and light-sensitive skin eruptions.		9.3892aminoquinoline;
organochlorine compound;
primary alcohol;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antimalarial;
antirheumatic drug;
dermatologic drug
hydroxyurea
[no description available]		16.6112616one-carbon compound;
ureas		antimetabolite;
antimitotic;
antineoplastic agent;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
genotoxin;
immunomodulator;
radical scavenger;
teratogenic agent
hydroxyzine
Hydroxyzine: A histamine H1 receptor antagonist that is effective in the treatment of chronic urticaria, dermatitis, and histamine-mediated pruritus. Unlike its major metabolite CETIRIZINE, it does cause drowsiness. It is also effective as an antiemetic, for relief of anxiety and tension, and as a sedative.. hydroxyzine : A N-alkylpiperazine that is piperzine in which the nitrogens atoms are substituted by 2-(2-hydroxyethoxy)ethyl and (4-chlorophenyl)(phenyl)methyl groups respectively.		2.0510hydroxyether;
monochlorobenzenes;
N-alkylpiperazine		anticoronaviral agent;
antipruritic drug;
anxiolytic drug;
dermatologic drug;
H1-receptor antagonist
ibuprofen
Midol: combination of cinnamedrine, phenacetin, aspirin & caffeine		2.7530monocarboxylic acidantipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
geroprotector;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
radical scavenger;
xenobiotic
phenelzine
Phenelzine: One of the MONOAMINE OXIDASE INHIBITORS used to treat DEPRESSION; PHOBIC DISORDERS; and PANIC.		2.0510primary amine
lidocaine
Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.		2.0510benzenes;
monocarboxylic acid amide;
tertiary amino compound		anti-arrhythmia drug;
drug allergen;
environmental contaminant;
local anaesthetic;
xenobiotic
alverine
alverine : A tertiary amine having one ethyl and two 3-phenylprop-1-yl groups attached to the nitrogen. An antispasmodic that acts directly on intestinal and uterine smooth muscle, it is used (particularly as the citrate salt) in the treatment of irritable bowel syndrome.		2.0510tertiary amineantispasmodic drug
idebenone
[no description available]		2.05101,4-benzoquinones;
primary alcohol		antioxidant;
ferroptosis inhibitor
ifenprodil
ifenprodil: NMDA receptor antagonist		2.1510piperidines
ifosfamide
[no description available]		6.6100ifosfamidesalkylating agent;
antineoplastic agent;
environmental contaminant;
immunosuppressive agent;
xenobiotic
imipramine
Imipramine: The prototypical tricyclic antidepressant. It has been used in major depression, dysthymia, bipolar depression, attention-deficit disorders, agoraphobia, and panic disorders. It has less sedative effect than some other members of this therapeutic group.. imipramine : A dibenzoazepine that is 5H-dibenzo[b,f]azepine substituted by a 3-(dimethylamino)propyl group at the nitrogen atom.		2.4420dibenzoazepineadrenergic uptake inhibitor;
antidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
amrinone
Amrinone: A positive inotropic cardiotonic (CARDIOTONIC AGENTS) with vasodilator properties, phosphodiesterase 3 inhibitory activity, and the ability to stimulate calcium ion influx into the cardiac cell.. amrinone : A 3,4'-bipyridine substituted at positions 5 and 6 by an amino group and a keto function respectively. A pyridine phosphodiesterase 3 inhibitor, it is a drug that may improve the prognosis in patients with congestive heart failure.		2.0510bipyridinesEC 3.1.4.* (phosphoric diester hydrolase) inhibitor
indapamide
Indapamide: A benzamide-sulfonamide-indole derived DIURETIC that functions by inhibiting SODIUM CHLORIDE SYMPORTERS.. indapamide : A sulfonamide formed by condensation of the carboxylic group of 4-chloro-3-sulfamoylbenzoic acid with the amino group of 2-methyl-2,3-dihydro-1H-indol-1-amine.		2.0510indoles;
organochlorine compound;
sulfonamide		antihypertensive agent;
diuretic
indirubin-3'-monoxime
indirubin-3'-monoxime: has antiangiogenic activity. indirubin-3'-monoxime : A member of the class of biindoles that is indirubin in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.		2.0310
indole-3-carbinol
indole-3-carbinol: occurs in edible cruciferous vegetables. indole-3-methanol : An indolyl alcohol carrying a hydroxymethyl group at position 3. It is a constituent of the cruciferous vegetables and had anticancer activity.		2.0710indolyl alcoholantineoplastic agent;
plant metabolite
indomethacin
Indomethacin: A non-steroidal anti-inflammatory agent (NSAID) that inhibits CYCLOOXYGENASE, which is necessary for the formation of PROSTAGLANDINS and other AUTACOIDS. It also inhibits the motility of POLYMORPHONUCLEAR LEUKOCYTES.. indometacin : A member of the class of indole-3-acetic acids that is indole-3-acetic acid in which the indole ring is substituted at positions 1, 2 and 5 by p-chlorobenzoyl, methyl, and methoxy groups, respectively. A non-steroidal anti-inflammatory drug, it is used in the treatment of musculoskeletal and joint disorders including osteoarthritis, rheumatoid arthritis, gout, bursitis and tendinitis.		3.1550aromatic ether;
indole-3-acetic acids;
monochlorobenzenes;
N-acylindole		analgesic;
drug metabolite;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
gout suppressant;
non-steroidal anti-inflammatory drug;
xenobiotic metabolite;
xenobiotic
iohexol
Iohexol: An effective non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiographic procedures. Its low systemic toxicity is the combined result of low chemotoxicity and low osmolality.. iohexol : A benzenedicarboxamide compound having N-(2,3-dihydroxypropyl)carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and an N-(2,3-dihydroxypropyl)acetamido group at the 5-position.		2.4420benzenedicarboxamide;
organoiodine compound		environmental contaminant;
radioopaque medium;
xenobiotic
iodipamide
Iodipamide: A water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.. adipiodone : An organoiodine compound that is 3-amino-2,4,6-triiodobenzoic acid in which one of the amino hydrogens is substituted by a 6-(3-carboxy-2,4,6-triiodoanilino)-6-oxohexanoyl group. It is a water-soluble radiographic contrast media for cholecystography and intravenous cholangiography.		2.0510benzoic acids;
organoiodine compound;
secondary carboxamide		radioopaque medium
iproniazid
[no description available]		2.0510carbohydrazide;
pyridines
avapro
Irbesartan: A spiro compound, biphenyl and tetrazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION, and in the treatment of kidney disease.. irbesartan : A biphenylyltetrazole that is an angiotensin II receptor antagonist used mainly for the treatment of hypertension.		2.0510azaspiro compound;
biphenylyltetrazole		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
isoflurane
Isoflurane: A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.		4.9721organofluorine compoundinhalation anaesthetic
isoniazid
Hydra: A genus of freshwater polyps in the family Hydridae, order Hydroida, class HYDROZOA. They are of special interest because of their complex organization and because their adult organization corresponds roughly to the gastrula of higher animals.. hydrazide : Compounds derived from oxoacids RkE(=O)l(OH)m (l =/= 0) by replacing -OH by -NRNR2 (R groups are commonly H). (IUPAC).		2.4520carbohydrazideantitubercular agent;
drug allergen
2-propanol
2-Propanol: An isomer of 1-PROPANOL. It is a colorless liquid having disinfectant properties. It is used in the manufacture of acetone and its derivatives and as a solvent. Topically, it is used as an antiseptic.. propan-2-ol : A secondary alcohol that is propane in which one of the hydrogens attached to the central carbon is substituted by a hydroxy group.		2.0510secondary alcohol;
secondary fatty alcohol		protic solvent
isoproterenol
Isoproterenol: Isopropyl analog of EPINEPHRINE; beta-sympathomimetic that acts on the heart, bronchi, skeletal muscle, alimentary tract, etc. It is used mainly as bronchodilator and heart stimulant.. isoprenaline : A secondary amino compound that is noradrenaline in which one of the hydrogens attached to the nitrogen is replaced by an isopropyl group. A sympathomimetic acting almost exclusively on beta-adrenergic receptors, it is used (mainly as the hydrochloride salt) as a bronghodilator and heart stimulant for the management of a variety of cardiac disorders.		2.8230catechols;
secondary alcohol;
secondary amino compound		beta-adrenergic agonist;
bronchodilator agent;
cardiotonic drug;
sympathomimetic agent
isoxsuprine
Isoxsuprine: A beta-adrenergic agonist that causes direct relaxation of uterine and vascular smooth muscle. Its vasodilating actions are greater on the arteries supplying skeletal muscle than on those supplying skin. It is used in the treatment of peripheral vascular disease and in premature labor.		2.0510alkylbenzene
isradipine
Isradipine: A potent antagonist of CALCIUM CHANNELS that is highly selective for VASCULAR SMOOTH MUSCLE. It is effective in the treatment of chronic stable angina pectoris, hypertension, and congestive cardiac failure.		2.4520benzoxadiazole;
dihydropyridine;
isopropyl ester;
methyl ester
itraconazole
[no description available]		2.0510piperazines
juglone
juglone: structure. juglone : A hydroxy-1,4-naphthoquinone that is 1,4-naphthoquinone in which the hydrogen at position 5 has been replaced by a hydroxy group. A plant-derived 1,4-naphthoquinone with confirmed antibacterial and antitumor activities.		2.2110hydroxy-1,4-naphthoquinonegeroprotector;
herbicide;
reactive oxygen species generator
nsc 664704
kenpaullone: inhibits CDK1/cyclin B; structure in first source. kenpaullone : An indolobenzazepine that is paullone in which the hydrogen at position 9 is replaced by a bromo substituent. It is an ATP-competitive inhibitor of cyclin-dependent kinases (CDKs) and glycogen synthase kinase 3beta (GSK3beta).		2.0310indolobenzazepine;
lactam;
organobromine compound		cardioprotective agent;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor;
EC 2.7.11.26 (tau-protein kinase) inhibitor;
geroprotector
ketamine
Ketamine: A cyclohexanone derivative used for induction of anesthesia. Its mechanism of action is not well understood, but ketamine can block NMDA receptors (RECEPTORS, N-METHYL-D-ASPARTATE) and may interact with sigma receptors.. ketamine : A member of the class of cyclohexanones in which one of the hydrogens at position 2 is substituted by a 2-chlorophenyl group, while the other is substituted by a methylamino group.		4.9721cyclohexanones;
monochlorobenzenes;
secondary amino compound		analgesic;
environmental contaminant;
intravenous anaesthetic;
neurotoxin;
NMDA receptor antagonist;
xenobiotic
ketanserin
Ketanserin: A selective serotonin receptor antagonist with weak adrenergic receptor blocking properties. The drug is effective in lowering blood pressure in essential hypertension. It also inhibits platelet aggregation. It is well tolerated and is particularly effective in older patients.. ketanserin : A member of the class of quinazolines that is quinazoline-2,4(1H,3H)-dione which is substituted at position 3 by a 2-[4-(p-fluorobenzoyl)piperidin-1-yl]ethyl group.		2.0510aromatic ketone;
organofluorine compound;
piperidines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
cardiovascular drug;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
serotonergic antagonist
ketoconazole
1-acetyl-4-(4-{[2-(2,4-dichlorophenyl)-2-(1H-imidazol-1-ylmethyl)-1,3-dioxolan-4-yl]methoxy}phenyl)piperazine : A dioxolane that is 1,3-dioxolane which is substituted at positions 2, 2, and 4 by imidazol-1-ylmethyl, 2,4-dichlorophenyl, and [para-(4-acetylpiperazin-1-yl)phenoxy]methyl groups, respectively.		9.9681dichlorobenzene;
dioxolane;
ether;
imidazoles;
N-acylpiperazine;
N-arylpiperazine
ketoprofen
Ketoprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It is used in the treatment of rheumatoid arthritis and osteoarthritis.. ketoprofen : An oxo monocarboxylic acid that consists of propionic acid substituted by a 3-benzoylphenyl group at position 2.		3.0140benzophenones;
oxo monocarboxylic acid		antipyretic;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
ketotifen
Ketotifen: A cycloheptathiophene blocker of histamine H1 receptors and release of inflammatory mediators. It has been proposed for the treatment of asthma, rhinitis, skin allergies, and anaphylaxis.. ketotifen : An organic heterotricyclic compound that is 4,9-dihydro-10H-benzo[4,5]cyclohepta[1,2-b]thiophen-10-one which is substituted at position 4 by a 1-methylpiperidin-4-ylidene group. A blocker of histamine H1 receptors with a stabilising action on mast cells, it is used (usually as its hydrogen fumarate salt) for the treatment of asthma, where it may take several weeks to exert its full effect.		2.0610cyclic ketone;
olefinic compound;
organic heterotricyclic compound;
organosulfur heterocyclic compound;
piperidines;
tertiary amino compound		anti-asthmatic drug;
H1-receptor antagonist
khellin
Khellin: A vasodilator that also has bronchodilatory action. It has been employed in the treatment of angina pectoris, in the treatment of asthma, and in conjunction with ultraviolet light A, has been tried in the treatment of vitiligo. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1024). khellin : A furanochrome in which the basic tricyclic skeleton is substituted at positions 4 and 9 with methoxy groups and at position 7 with a methyl group. A major constituent of the plant Ammi visnaga it is a herbal folk medicine used for various illnesses, its main effect being as a vasodilator.		2.4620furanochromone;
organic heterotricyclic compound;
oxacycle		anti-asthmatic agent;
bronchodilator agent;
cardiovascular drug;
vasodilator agent
labetalol
Labetalol: A salicylamide derivative that is a non-cardioselective blocker of BETA-ADRENERGIC RECEPTORS and ALPHA-1 ADRENERGIC RECEPTORS.. labetalol : A diastereoisomeric mixture of approximately equal amounts of all four possible stereoisomers ((R,S)-labetolol, (S,R)-labetolol, (S,S)-labetalol and (R,R)-labetalol). It is an adrenergic antagonist used to treat high blood pressure.. 2-hydroxy-5-{1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl}benzamide : A member of the class of benzamides that is benzamide substituted by a hydroxy group at position 2 and by a 1-hydroxy-2-[(4-phenylbutan-2-yl)amino]ethyl group at position 5.		2.0510benzamides;
benzenes;
phenols;
primary carboxamide;
salicylamides;
secondary alcohol;
secondary amino compound
lamotrigine
[no description available]		2.05101,2,4-triazines;
dichlorobenzene;
primary arylamine		anticonvulsant;
antidepressant;
antimanic drug;
calcium channel blocker;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
excitatory amino acid antagonist;
geroprotector;
non-narcotic analgesic;
xenobiotic
lansoprazole
Lansoprazole: A 2,2,2-trifluoroethoxypyridyl derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS. Lansoprazole is a racemic mixture of (R)- and (S)-isomers.		2.7330benzimidazoles;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor
beta-lapachone
beta-lapachone: antineoplastic inhibitor of reverse transcriptase, DNA topoisomerase, and DNA polymerase. beta-lapachone : A benzochromenone that is 3,4-dihydro-2H-benzo[h]chromene-5,6-dione substituted by geminal methyl groups at position 2. Isolated from Tabebuia avellanedae, it exhibits antineoplastic and anti-inflammatory activities.		2.0510benzochromenone;
orthoquinones		anti-inflammatory agent;
antineoplastic agent;
plant metabolite
lavendustin a
lavendustin A: from Streptomyces griseolavendus; structure given in first source		2.7230aromatic amine
2-hydroxy-5-(2,5-dihydrobenzyl)aminobenzoic acid
[no description available]		2.0310aromatic amine
leflunomide
Leflunomide: An isoxazole derivative that inhibits dihydroorotate dehydrogenase, the fourth enzyme in the pyrimidine biosynthetic pathway. It is used an immunosuppressive agent in the treatment of RHEUMATOID ARTHRITIS and PSORIATIC ARTHRITIS.. leflunomide : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-methyl-1,2-oxazole-4-carboxylic acid with the anilino group of 4-(trifluoromethyl)aniline. The prodrug of teriflunomide.		4.7730(trifluoromethyl)benzenes;
isoxazoles;
monocarboxylic acid amide		antineoplastic agent;
antiparasitic agent;
EC 1.3.98.1 [dihydroorotate oxidase (fumarate)] inhibitor;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
hepatotoxic agent;
immunosuppressive agent;
non-steroidal anti-inflammatory drug;
prodrug;
pyrimidine synthesis inhibitor;
tyrosine kinase inhibitor
letrozole
[no description available]		11.0542nitrile;
triazoles		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor
lofepramine
Lofepramine: A psychotropic IMIPRAMINE derivative that acts as a tricyclic antidepressant and possesses few anticholinergic properties. It is metabolized to DESIPRAMINE.		2.0510aromatic ketone;
dibenzoazepine;
monochlorobenzenes;
tertiary amino compound		antidepressant
lomustine
[no description available]		3.8521N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
loperamide
Loperamide: One of the long-acting synthetic ANTIDIARRHEALS; it is not significantly absorbed from the gut, and has no effect on the adrenergic system or central nervous system, but may antagonize histamine and interfere with acetylcholine release locally.. loperamide : A synthetic piperidine derivative, effective against diarrhoea resulting from gastroenteritis or inflammatory bowel disease.		2.4520monocarboxylic acid amide;
monochlorobenzenes;
piperidines;
tertiary alcohol		anticoronaviral agent;
antidiarrhoeal drug;
mu-opioid receptor agonist
loratadine
Loratadine: A second-generation histamine H1 receptor antagonist used in the treatment of allergic rhinitis and urticaria. Unlike most classical antihistamines (HISTAMINE H1 ANTAGONISTS) it lacks central nervous system depressing effects such as drowsiness.. loratadine : A benzocycloheptapyridine that is 6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridine substituted by a chloro group at position 8 and a 1-(ethoxycarbonyl)piperidin-4-ylidene group at position 11. It is a H1-receptor antagonist commonly employed in the treatment of allergic disorders.		2.0410benzocycloheptapyridine;
ethyl ester;
N-acylpiperidine;
organochlorine compound;
tertiary carboxamide		anti-allergic agent;
cholinergic antagonist;
geroprotector;
H1-receptor antagonist
losartan
Losartan: An antagonist of ANGIOTENSIN TYPE 1 RECEPTOR with antihypertensive activity due to the reduced pressor effect of ANGIOTENSIN II.. losartan : A biphenylyltetrazole where a 1,1'-biphenyl group is attached at the 5-position and has an additional trisubstituted imidazol-1-ylmethyl group at the 4'-position		2.4520biphenylyltetrazole;
imidazoles		angiotensin receptor antagonist;
anti-arrhythmia drug;
antihypertensive agent;
endothelin receptor antagonist
2-(4-morpholinyl)-8-phenyl-4h-1-benzopyran-4-one
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one: specific inhibitor of phosphatidylinositol 3-kinase; structure in first source		5.62230chromones;
morpholines;
organochlorine compound		autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector
malathion
Malathion: A wide spectrum aliphatic organophosphate insecticide widely used for both domestic and commercial agricultural purposes.. malathion : A racemate comprising equimolar amounts of (R) and (S)-malathion. It is a broad spectrum organophosphate proinsecticide used to control a wide range of pests including Coleoptera, Diptera, fruit flies, mosquitos and spider mites.. diethyl 2-[(dimethoxyphosphorothioyl)thio]succinate : A diester that is diethyl succinate in which position 2 is substituted by a (dimethoxyphosphorothioyl)thio group.		2.0510diester;
ethyl ester;
organic thiophosphate
diisopropyl 1,3-dithiol-2-ylidenemalonate
diisopropyl 1,3-dithiol-2-ylidenemalonate: structure in first source		2.0510isopropyl ester
maprotiline
Maprotiline: A bridged-ring tetracyclic antidepressant that is both mechanistically and functionally similar to the tricyclic antidepressants, including side effects associated with its use.		2.0410anthracenes
mazindol
Mazindol: Tricyclic anorexigenic agent unrelated to and less toxic than AMPHETAMINE, but with some similar side effects. It inhibits uptake of catecholamines and blocks the binding of cocaine to the dopamine uptake transporter.		2.0510organic molecular entity
mebendazole
Mebendazole: A benzimidazole that acts by interfering with CARBOHYDRATE METABOLISM and inhibiting polymerization of MICROTUBULES.. mebendazole : A carbamate ester that is methyl 1H-benzimidazol-2-ylcarbamate substituted by a benzoyl group at position 5.		2.0510aromatic ketone;
benzimidazoles;
carbamate ester		antinematodal drug;
microtubule-destabilising agent;
tubulin modulator
mechlorethamine
nitrogen mustard : Compounds having two beta-haloalkyl groups bound to a nitrogen atom, as in (X-CH2-CH2)2NR.		2.0210nitrogen mustard;
organochlorine compound		alkylating agent
meclizine
Meclizine: A histamine H1 antagonist used in the treatment of motion sickness, vertigo, and nausea during pregnancy and radiation sickness.		2.0510diarylmethane
meclofenoxate
Meclofenoxate: An ester of DIMETHYLAMINOETHANOL and para-chlorophenoxyacetic acid.		2.0510monocarboxylic acid
mefenamic acid
Mefenamic Acid: A non-steroidal anti-inflammatory agent with analgesic, anti-inflammatory, and antipyretic properties. It is an inhibitor of cyclooxygenase.. mefenamic acid : An aminobenzoic acid that is anthranilic acid in which one of the hydrogens attached to the nitrogen is replaced by a 2,3-dimethylphenyl group. Although classed as a non-steroidal anti-inflammatory drug, its anti-inflammatory properties are considered to be minor. It is used to relieve mild to moderate pain, including headaches, dental pain, osteoarthritis and rheumatoid arthritis.		2.0510aminobenzoic acid;
secondary amino compound		analgesic;
antipyretic;
antirheumatic drug;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
environmental contaminant;
non-steroidal anti-inflammatory drug;
xenobiotic
memantine
[no description available]		4.6111adamantanes;
primary aliphatic amine		antidepressant;
antiparkinson drug;
dopaminergic agent;
neuroprotective agent;
NMDA receptor antagonist
vitamin k 3
Vitamin K 3: A synthetic naphthoquinone without the isoprenoid side chain and biological activity, but can be converted to active vitamin K2, menaquinone, after alkylation in vivo.		2.82301,4-naphthoquinones;
vitamin K		angiogenesis inhibitor;
antineoplastic agent;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
human urinary metabolite;
nutraceutical
meperidine
Meperidine: A narcotic analgesic that can be used for the relief of most types of moderate to severe pain, including postoperative pain and the pain of labor. Prolonged use may lead to dependence of the morphine type; withdrawal symptoms appear more rapidly than with morphine and are of shorter duration.. pethidine : A piperidinecarboxylate ester that is piperidine which is substituted by a methyl group at position 1 and by phenyl and ethoxycarbonyl groups at position 4. It is an analgesic which is used for the treatment of moderate to severe pain, including postoperative pain and labour pain.		2.0510ethyl ester;
piperidinecarboxylate ester;
tertiary amino compound		antispasmodic drug;
kappa-opioid receptor agonist;
mu-opioid receptor agonist;
opioid analgesic
mephenytoin
Mephenytoin: An anticonvulsant effective in tonic-clonic epilepsy (EPILEPSY, TONIC-CLONIC). It may cause blood dyscrasias.. mephenytoin : An imidazolidine-2,4-dione (hydantoin) in which the imidazolidine nucleus carries a methyl group at N-3 and has ethyl and phenyl substituents at C-5. An anticonvulsant, it is no longer available in the USA or the UK but is still studied largely because of its interesting hydroxylation polymorphism.		2.0510imidazolidine-2,4-dioneanticonvulsant
mepivacaine
Mepivacaine: A local anesthetic that is chemically related to BUPIVACAINE but pharmacologically related to LIDOCAINE. It is indicated for infiltration, nerve block, and epidural anesthesia. Mepivacaine is effective topically only in large doses and therefore should not be used by this route. (From AMA Drug Evaluations, 1994, p168). mepivacaine : A piperidinecarboxamide in which N-methylpipecolic acid and 2,6-dimethylaniline have combined to form the amide bond. It is used as a local amide-type anaesthetic.		2.0510piperidinecarboxamidedrug allergen;
local anaesthetic
meprobamate
Meprobamate: A carbamate with hypnotic, sedative, and some muscle relaxant properties, although in therapeutic doses reduction of anxiety rather than a direct effect may be responsible for muscle relaxation. Meprobamate has been reported to have anticonvulsant actions against petit mal seizures, but not against grand mal seizures (which may be exacerbated). It is used in the treatment of ANXIETY DISORDERS, and also for the short-term management of INSOMNIA but has largely been superseded by the BENZODIAZEPINES. (From Martindale, The Extra Pharmacopoeia, 30th ed, p603)		2.0510organic molecular entity
mesalamine
Mesalamine: An anti-inflammatory agent, structurally related to the SALICYLATES, which is active in INFLAMMATORY BOWEL DISEASE. It is considered to be the active moiety of SULPHASALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed). mesalamine : A monohydroxybenzoic acid that is salicylic acid substituted by an amino group at the 5-position.		2.4520amino acid;
aromatic amine;
monocarboxylic acid;
monohydroxybenzoic acid;
phenols		non-steroidal anti-inflammatory drug
metformin
Metformin: A biguanide hypoglycemic agent used in the treatment of non-insulin-dependent diabetes mellitus not responding to dietary modification. Metformin improves glycemic control by improving insulin sensitivity and decreasing intestinal absorption of glucose. (From Martindale, The Extra Pharmacopoeia, 30th ed, p289). metformin : A member of the class of guanidines that is biguanide the carrying two methyl substituents at position 1.		5.2380guanidinesenvironmental contaminant;
geroprotector;
hypoglycemic agent;
xenobiotic
methadone
Methadone: A synthetic opioid that is used as the hydrochloride. It is an opioid analgesic that is primarily a mu-opioid agonist. It has actions and uses similar to those of MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1082-3). methadone : A racemate comprising equimolar amounts of dextromethadone and levomethadone. It is a opioid analgesic which is used as a painkiller and as a substitute for heroin in the treatment of heroin addiction.. 6-(dimethylamino)-4,4-diphenylheptan-3-one : A ketone that is heptan-3-one substituted by a dimethylamino group at position 6 and two phenyl groups at position 4.		4.9721benzenes;
diarylmethane;
ketone;
tertiary amino compound
methazolamide
Methazolamide: A carbonic anhydrase inhibitor that is used as a diuretic and in the treatment of glaucoma.		2.4110sulfonamide;
thiadiazoles
methoxyamine
methoxyamine: analytical reagent for aldehydes and ketones; strong irritant, can probably produce methemoglobinemia; RN given refers to parent cpd; structure		2.110organooxygen compound
methoxsalen
Methoxsalen: A naturally occurring furocoumarin compound found in several species of plants, including Psoralea corylifolia. It is a photoactive substance that forms DNA ADDUCTS in the presence of ultraviolet A irradiation.. methoxsalen : A member of the class of psoralens that is 7H-furo[3,2-g]chromen-7-one in which the 9 position is substituted by a methoxy group. It is a constituent of the fruits of Ammi majus. Like other psoralens, trioxsalen causes photosensitization of the skin. It is administered topically or orally in conjunction with UV-A for phototherapy treatment of vitiligo and severe psoriasis.		2.5220aromatic ether;
psoralens		antineoplastic agent;
cross-linking reagent;
dermatologic drug;
photosensitizing agent;
plant metabolite
methoxyflurane
Methoxyflurane: An inhalation anesthetic. Currently, methoxyflurane is rarely used for surgical, obstetric, or dental anesthesia. If so employed, it should be administered with NITROUS OXIDE to achieve a relatively light level of anesthesia, and a neuromuscular blocking agent given concurrently to obtain the desired degree of muscular relaxation. (From AMA Drug Evaluations Annual, 1994, p180). methoxyflurane : An ether in which the two groups attached to the central oxygen atom are methyl and 2,2-dichloro-1,1-difluoroethyl.		2.0510ether;
organochlorine compound;
organofluorine compound		hepatotoxic agent;
inhalation anaesthetic;
nephrotoxic agent;
non-narcotic analgesic
nocodazole
[no description available]		2.0810aromatic ketone;
benzimidazoles;
carbamate ester;
thiophenes		antimitotic;
antineoplastic agent;
microtubule-destabilising agent;
tubulin modulator
methyl salicylate
methyl salicylate: used in over-the-counter liniments, ointments, lotions for relief of musculoskeletal aches and pains; has hemolytic effect on human & sheep erythrocytes; RN given refers to parent cpd; structure in Merck Index, 9th ed, #5990. methyl salicylate : A benzoate ester that is the methyl ester of salicylic acid.		5.2831benzoate ester;
methyl ester;
salicylates		flavouring agent;
insect attractant;
metabolite
methyl methanesulfonate
[no description available]		7.4820methanesulfonate esteralkylating agent;
apoptosis inducer;
carcinogenic agent;
genotoxin;
mutagen
methylphenidate
Methylphenidate: A central nervous system stimulant used most commonly in the treatment of ATTENTION DEFICIT DISORDER in children and for NARCOLEPSY. Its mechanisms appear to be similar to those of DEXTROAMPHETAMINE. The d-isomer of this drug is referred to as DEXMETHYLPHENIDATE HYDROCHLORIDE.. methylphenidate : A racemate comprising equimolar amounts of the two threo isomers of methyl phenyl(piperidin-2-yl)acetate. A central stimulant and indirect-acting sympathomimetic, is used (generally as the hydrochloride salt) in the treatment of hyperactivity disorders in children and for the treatment of narcolepsy.. methyl phenyl(piperidin-2-yl)acetate : A amino acid ester that is methyl phenylacetate in which one of the hydrogens alpha to the carbonyl group is replaced by a piperidin-2-yl group.		2.0510beta-amino acid ester;
methyl ester;
piperidines
methyprylon
methyprylon: was heading 1973-94 (see under HYPNOTICS AND SEDATIVES 1963-72); use PIPERIDONES to search METHYPRYLON 1973-94		2.0510organic molecular entity
metoclopramide
Metoclopramide: A dopamine D2 antagonist that is used as an antiemetic.. metoclopramide : A member of the class of benzamides resulting from the formal condensation of 4-amino-5-chloro-2-methoxybenzoic acid with the primary amino group of N,N-diethylethane-1,2-diamine.		2.0510benzamides;
monochlorobenzenes;
substituted aniline;
tertiary amino compound		antiemetic;
dopaminergic antagonist;
environmental contaminant;
gastrointestinal drug;
xenobiotic
metoprolol
Metoprolol: A selective adrenergic beta-1 blocking agent that is commonly used to treat ANGINA PECTORIS; HYPERTENSION; and CARDIAC ARRHYTHMIAS.. metoprolol : A propanolamine that is 1-(propan-2-ylamino)propan-2-ol substituted by a 4-(2-methoxyethyl)phenoxy group at position 1.		2.7430aromatic ether;
propanolamine;
secondary alcohol;
secondary amino compound		antihypertensive agent;
beta-adrenergic antagonist;
environmental contaminant;
geroprotector;
xenobiotic
metronidazole
Metronidazole: A nitroimidazole used to treat AMEBIASIS; VAGINITIS; TRICHOMONAS INFECTIONS; GIARDIASIS; ANAEROBIC BACTERIA; and TREPONEMAL INFECTIONS.. metronidazole : A member of the class of imidazoles substituted at C-1, -2 and -5 with 2-hydroxyethyl, nitro and methyl groups respectively. It has activity against anaerobic bacteria and protozoa, and has a radiosensitising effect on hypoxic tumour cells. It may be given by mouth in tablets, or as the benzoate in an oral suspension. The hydrochloride salt can be used in intravenous infusions. Metronidazole is a prodrug and is selective for anaerobic bacteria due to their ability to intracellularly reduce the nitro group of metronidazole to give nitroso-containing intermediates. These can covalently bind to DNA, disrupting its helical structure, inducing DNA strand breaks and inhibiting bacterial nucleic acid synthesis, ultimately resulting in bacterial cell death.		2.4620C-nitro compound;
imidazoles;
primary alcohol		antiamoebic agent;
antibacterial drug;
antimicrobial agent;
antiparasitic agent;
antitrichomonal drug;
environmental contaminant;
prodrug;
radiosensitizing agent;
xenobiotic
metyrapone
Metyrapone: An inhibitor of the enzyme STEROID 11-BETA-MONOOXYGENASE. It is used as a test of the feedback hypothalamic-pituitary mechanism in the diagnosis of CUSHING SYNDROME.. metyrapone : An aromatic ketone that is 3,3-dimethylbutan-2-one in which the methyl groups at positions 1 and 4 are replaced by pyridin-3-yl groups. A steroid 11beta-monooxygenase (EC 1.14.15.4) inhibitor, it is used in the diagnosis of adrenal insufficiency.		2.0510aromatic ketoneantimetabolite;
diagnostic agent;
EC 1.14.15.4 (steroid 11beta-monooxygenase) inhibitor
mianserin
Mianserin: A tetracyclic compound with antidepressant effects. It may cause drowsiness and hematological problems. Its mechanism of therapeutic action is not well understood, although it apparently blocks alpha-adrenergic, histamine H1, and some types of serotonin receptors.. mianserin : A dibenzoazepine (specifically 1,2,3,4,10,14b-hexahydrodibenzo[c,f]pyrazino[1,2-a]azepine) methyl-substituted on N-2. Closely related to (and now mostly superseded by) the tetracyclic antidepressant mirtazapinean, it is an atypical antidepressant used in the treatment of depression throughout Europe and elsewhere.		2.0510dibenzoazepineadrenergic uptake inhibitor;
alpha-adrenergic antagonist;
antidepressant;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
geroprotector;
H1-receptor antagonist;
histamine agonist;
sedative;
serotonergic antagonist
miconazole
Miconazole: An imidazole antifungal agent that is used topically and by intravenous infusion.. 1-[2-(2,4-dichlorobenzyloxy)-2-(2,4-dichlorophenyl)ethyl]imidazole : A member of the class of imidazoles that is 1-(2,4-dichlorophenyl)-2-(imidazol-1-yl)ethanol in which the hydroxyl hydrogen is replaced by a 2,4-dichlorobenzyl group.. miconazole : A racemate composed of equimolar amounts of (R)- and (S)-miconazole. Used (as its nitrate salt) to treat skin infections such as athlete's foot, jock itch, ringworm and other fungal skin infections. It inhibits the synthesis of ergosterol, a critical component of fungal cell membranes.		2.0510dichlorobenzene;
ether;
imidazoles
midazolam
Midazolam: A short-acting hypnotic-sedative drug with anxiolytic and amnestic properties. It is used in dentistry, cardiac surgery, endoscopic procedures, as preanesthetic medication, and as an adjunct to local anesthesia. The short duration and cardiorespiratory stability makes it useful in poor-risk, elderly, and cardiac patients. It is water-soluble at pH less than 4 and lipid-soluble at physiological pH.. midazolam : An imidazobenzodiazepine that is 4H-imidazo[1,5-a][1,4]benzodiazepine which is substituted by a methyl, 2-fluorophenyl and chloro groups at positions 1, 6 and 8, respectively.		2.5120imidazobenzodiazepine;
monofluorobenzenes;
organochlorine compound		anticonvulsant;
antineoplastic agent;
anxiolytic drug;
apoptosis inducer;
central nervous system depressant;
GABAA receptor agonist;
general anaesthetic;
muscle relaxant;
sedative
minoxidil
Minoxidil: A potent direct-acting peripheral vasodilator (VASODILATOR AGENTS) that reduces peripheral resistance and produces a fall in BLOOD PRESSURE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p371). minoxidil : A pyrimidine N-oxide that is pyrimidine-2,4-diamine 3-oxide substituted by a piperidin-1-yl group at position 6.		2.0510dialkylarylamine;
tertiary amino compound
mirtazapine
Mirtazapine: A piperazinoazepine tetracyclic compound that enhances the release of NOREPINEPHRINE and SEROTONIN through blockage of presynaptic ALPHA-2 ADRENERGIC RECEPTORS. It also blocks both 5-HT2 and 5-HT3 serotonin receptors and is a potent HISTAMINE H1 RECEPTOR antagonist. It is used for the treatment of depression, and may also be useful for the treatment of anxiety disorders.		2.0510benzazepine;
tetracyclic antidepressant		alpha-adrenergic antagonist;
anxiolytic drug;
H1-receptor antagonist;
histamine antagonist;
oneirogen;
serotonergic antagonist
mitotane
Mitotane: A derivative of the insecticide DICHLORODIPHENYLDICHLOROETHANE that specifically inhibits cells of the adrenal cortex and their production of hormones. It is used to treat adrenocortical tumors and causes CNS damage, but no bone marrow depression.		2.0510diarylmethane
mitoxantrone
Mitoxantrone: An anthracenedione-derived antineoplastic agent.. mitoxantrone : A dihydroxyanthraquinone that is 1,4-dihydroxy-9,10-anthraquinone which is substituted by 6-hydroxy-1,4-diazahexyl groups at positions 5 and 8.		6.55173dihydroxyanthraquinoneanalgesic;
antineoplastic agent
ml 7
ML-7 : An N-sulfonyldiazepane resullting from the formal condensation of 5-iodo-1-naphthylsulfonic acid with one of the nitrogens of 1,4-diazepane. It is a selective inhibitor of myosin light chain kinase (EC 2.7.11.18).		2.610N-sulfonyldiazepane;
organoiodine compound		EC 2.7.11.18 (myosin-light-chain kinase) inhibitor
ml 9
[no description available]		2.0310naphthalenes;
sulfonic acid derivative
modafinil
Modafinil: A benzhydryl acetamide compound, central nervous system stimulant, and CYP3A4 inducing agent that is used in the treatment of NARCOLEPSY and SLEEP WAKE DISORDERS.. modafinil : A racemate comprising equimolar amounts of armodafinil and (S)-modafinil. A central nervous system stimulant, it is used for the treatment of sleeping disorders such as narcolepsy, obstructive sleep apnoea, and shift-work sleep disorder. The optical enantiomers of modafinil have similar pharmacological actions in animals.. 2-[(diphenylmethyl)sulfinyl]acetamide : A sulfoxide that is dimethylsulfoxide in which two hydrogens attached to one of the methyl groups are replaced by phenyl groups, while one hydrogen attached to the other methyl group is replaced by a carbamoyl (aminocarbonyl) group.		2.0510monocarboxylic acid amide;
sulfoxide
moxisylyte
Moxisylyte: An alpha-adrenergic blocking agent that is used in Raynaud's disease. It is also used locally in the eye to reverse the mydriasis caused by phenylephrine and other sympathomimetic agents. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1312)		2.0510monoterpenoid
deet
N,N-diethyl-m-toluamide : A monocarboxylic acid amide resulting from the formal condensation of the carboxy group of m-toluic acid with the nitrogen of diethylamine. First developed by the U.S. Army in 1946 for use by military personnel in insect-infested areas, it is the most widely used insect repellent worldwide.		2.0510benzamides;
monocarboxylic acid amide		environmental contaminant;
insect repellent;
xenobiotic
nabumetone
Nabumetone: A butanone non-steroidal anti-inflammatory drug and cyclooxygenase-2 (COX2) inhibitor that is used in the management of pain associated with OSTEOARTHRITIS and RHEUMATOID ARTHRITIS.. nabumetone : A methyl ketone that is 2-butanone in which one of the methyl hydrogens at position 4 is replaced by a 6-methoxy-2-naphthyl group. A prodrug that is converted to the active metabolite, 6-methoxy-2-naphthylacetic acid, following oral administration. It is shown to have a slightly lower risk of gastrointestinal side effects than most other non-steroidal anti-inflammatory drugs.		2.0510methoxynaphthalene;
methyl ketone		cyclooxygenase 2 inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug
nafamostat
nafamostat: inhibitor of trypsin, plasmin, pancreatic kallikrein, plasma kallikrein & thrombin; strongly inhibits esterolytic activities of C1r & C1 esterase complement-mediated hemolysis; antineoplastic		3.2110benzoic acids;
guanidines
nalidixic acid
[no description available]		2.05101,8-naphthyridine derivative;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
DNA synthesis inhibitor
activins
Activins: Activins are produced in the pituitary, gonads, and other tissues. By acting locally, they stimulate pituitary FSH secretion and have diverse effects on cell differentiation and embryonic development. Activins are glycoproteins that are hetero- or homodimers of INHIBIN-BETA SUBUNITS.		2.5820
nefazodone
nefazodone: may be useful as an opiate adjunct		2.4320aromatic ether;
monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazoles		alpha-adrenergic antagonist;
analgesic;
antidepressant;
serotonergic antagonist;
serotonin uptake inhibitor
neostigmine
Neostigmine: A cholinesterase inhibitor used in the treatment of myasthenia gravis and to reverse the effects of muscle relaxants such as gallamine and tubocurarine. Neostigmine, unlike PHYSOSTIGMINE, does not cross the blood-brain barrier.. neostigmine : A quaternary ammonium ion comprising an anilinium ion core having three methyl substituents on the aniline nitrogen, and a 3-[(dimethylcarbamoyl)oxy] substituent at position 3. It is a parasympathomimetic which acts as a reversible acetylcholinesterase inhibitor.		2.2110quaternary ammonium ionantidote to curare poisoning;
EC 3.1.1.7 (acetylcholinesterase) inhibitor
nevirapine
Nevirapine: A potent, non-nucleoside reverse transcriptase inhibitor used in combination with nucleoside analogues for treatment of HIV INFECTIONS and AIDS.. nevirapine : A dipyridodiazepine that is 5,11-dihydro-6H-dipyrido[3,2-b:2',3'-e][1,4]diazepine which is substituted by methyl, oxo, and cyclopropyl groups at positions 4, 6, and 11, respectively. A non-nucleoside reverse transcriptase inhibitor with activity against HIV-1, it is used in combination with other antiretrovirals for the treatment of HIV infection.		2.4520cyclopropanes;
dipyridodiazepine		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nialamide
Nialamide: An MAO inhibitor that is used as an antidepressive agent.		2.0510organonitrogen compound;
organooxygen compound
nicardipine
Nicardipine: A potent calcium channel blockader with marked vasodilator action. It has antihypertensive properties and is effective in the treatment of angina and coronary spasms without showing cardiodepressant effects. It has also been used in the treatment of asthma and enhances the action of specific antineoplastic agents.. nicardipine : A racemate comprising equimolar amounts of (R)- and (S)-nicardipine. It is a calcium channel blocker which is used to treat hypertension.. 2-[benzyl(methyl)amino]ethyl methyl 2,6-dimethyl-4-(3-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine substituted by a methyl, {2-[benzyl(methyl)amino]ethoxy}carbonyl, 3-nitrophenyl, methoxycarbonyl and methyl groups at positions 2, 3, 4, 5 and 6, respectively.		2.0410benzenes;
C-nitro compound;
diester;
dihydropyridine;
methyl ester;
tertiary amino compound
niceritrol
Niceritrol: An ester of nicotinic acid that lowers cholesterol and triglycerides in total plasma and in the VLD- and LD-lipoprotein fractions.		2.0510organic molecular entity
niclosamide
Niclosamide: An antihelmintic that is active against most tapeworms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p48). niclosamide : A secondary carboxamide resulting from the formal condensation of the carboxy group of 5-chlorosalicylic acid with the amino group of 2-chloro-4-nitroaniline. It is an oral anthelmintic drug approved for use against tapeworm infections.		3.7620benzamides;
C-nitro compound;
monochlorobenzenes;
salicylanilides;
secondary carboxamide		anthelminthic drug;
anticoronaviral agent;
antiparasitic agent;
apoptosis inducer;
molluscicide;
piscicide;
STAT3 inhibitor
nifedipine
Nifedipine: A potent vasodilator agent with calcium antagonistic action. It is a useful anti-anginal agent that also lowers blood pressure.		2.7330C-nitro compound;
dihydropyridine;
methyl ester		calcium channel blocker;
human metabolite;
tocolytic agent;
vasodilator agent
niflumic acid
Niflumic Acid: An analgesic and anti-inflammatory agent used in the treatment of rheumatoid arthritis.		2.4720aromatic carboxylic acid;
pyridines
nilutamide
[no description available]		2.0510(trifluoromethyl)benzenes;
C-nitro compound;
imidazolidinone		androgen antagonist;
antineoplastic agent
nimesulide
nimesulide: structure. nimesulide : An aromatic ether having phenyl and 2-methylsulfonamido-5-nitrophenyl as the two aryl groups.		2.0510aromatic ether;
C-nitro compound;
sulfonamide		cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
nimodipine
Nimodipine: A calcium channel blockader with preferential cerebrovascular activity. It has marked cerebrovascular dilating effects and lowers blood pressure.. nimodipine : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a (2-methoxyethoxy)carbonyl group at position 3, a m-nitrophenyl group at position 4, and an isopropoxycarbonyl group at position 5. An L-type calcium channel blocker, it acts particularly on cerebral circulation, and is used both orally and intravenously for the prevention and treatment of subarachnoid hemorrhage from ruptured intracranial aneurysm.		2.44202-methoxyethyl ester;
C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
isopropyl ester		antihypertensive agent;
calcium channel blocker;
cardiovascular drug;
vasodilator agent
nisoldipine
Nisoldipine: A dihydropyridine calcium channel antagonist that acts as a potent arterial vasodilator and antihypertensive agent. It is also effective in patients with cardiac failure and angina.. nisoldipine : A racemate consisting of equimolar amounts of (R)- and (S)-nisoldipine. A calcium channel blocker, it is used in the treatment of hypertension and angina pectoris.. methyl 2-methylpropyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate : A dihydropyridine that is 1,4-dihydropyridine which is substituted by methyl groups at positions 2 and 6, a methoxycarbonyl group at position 3, an o-nitrophenyl group at position 4, and an isobutoxycarbonyl group at position 5. The racemate, a calcium channel blocker, is used in the treatment of hypertension and angina pectoris.		2.0510C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
methyl ester
nitidine
nitidine: RN given refers to parent cpd; synonym NSC 146397 refers to chloride; structure		2.1110phenanthridines
nitrazepam
Nitrazepam: A benzodiazepine derivative used as an anticonvulsant and hypnotic.. nitrazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one which is substituted at positions 5 and 7 by phenyl and nitro groups, respectively. It is used as a hypnotic for the short-term management of insomnia and for the treatment of epileptic spasms in infants (West's syndrome).		2.05101,4-benzodiazepinone;
C-nitro compound		anticonvulsant;
antispasmodic drug;
drug metabolite;
GABA modulator;
sedative
nitrendipine
Nitrendipine: A calcium channel blocker with marked vasodilator action. It is an effective antihypertensive agent and differs from other calcium channel blockers in that it does not reduce glomerular filtration rate and is mildly natriuretic, rather than sodium retentive.. nitrendipine : A dihydropyridine that is 1,4-dihydropyridine substituted by methyl groups at positions 2 and 6, a 3-nitrophenyl group at position 4, a ethoxycarbonyl group at position 3 and a methoxycarbonyl group at position 5. It is a calcium-channel blocker used in the treatment of hypertension.		2.4520C-nitro compound;
dicarboxylic acids and O-substituted derivatives;
diester;
dihydropyridine;
ethyl ester;
methyl ester		antihypertensive agent;
calcium channel blocker;
geroprotector;
vasodilator agent
nitroglycerin
Nitroglycerin: A volatile vasodilator which relieves ANGINA PECTORIS by stimulating GUANYLATE CYCLASE and lowering cytosolic calcium. It is also sometimes used for TOCOLYSIS and explosives.. nitroglycerol : A nitrate ester that is glycerol in which nitro group(s) replace the hydrogen(s) attached to one or more of the hydroxy groups.. nitroglycerin : A nitroglycerol that is glycerol in which the hydrogen atoms of all three hydroxy groups are replaced by nitro groups. It acts as a prodrug, releasing nitric oxide to open blood vessels and so alleviate heart pain.		2.0510nitroglycerolexplosive;
muscle relaxant;
nitric oxide donor;
prodrug;
tocolytic agent;
vasodilator agent;
xenobiotic
nizatidine
[no description available]		2.45201,3-thiazoles;
C-nitro compound;
carboxamidine;
organic sulfide;
tertiary amino compound		anti-ulcer drug;
cholinergic drug;
H2-receptor antagonist
masoprocol
nordihydroguaretic acid: antioxidant compound found in the creosote bush (Larrea tridentata)		2.0510catechols;
lignan;
tetrol		antioxidant;
ferroptosis inhibitor;
geroprotector;
plant metabolite
norfloxacin
Norfloxacin: A synthetic fluoroquinolone (FLUOROQUINOLONES) with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin inhibits bacterial DNA GYRASE.. norfloxacin : A quinolinemonocarboxylic acid with broad-spectrum antibacterial activity against most gram-negative and gram-positive bacteria. Norfloxacin is bactericidal and its mode of action depends on blocking of bacterial DNA replication by binding itself to an enzyme called DNA gyrase.		2.0510fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug;
DNA synthesis inhibitor;
environmental contaminant;
xenobiotic
nortriptyline
Nortriptyline: A metabolite of AMITRIPTYLINE that is also used as an antidepressive agent. Nortriptyline is used in major depression, dysthymia, and atypical depressions.. nortriptyline : An organic tricyclic compound that is 10,11-dihydro-5H-dibenzo[a,d][7]annulene substituted by a 3-(methylamino)propylidene group at position 5. It is an active metabolite of amitriptyline.		2.0510organic tricyclic compound;
secondary amine		adrenergic uptake inhibitor;
analgesic;
antidepressant;
antineoplastic agent;
apoptosis inducer;
drug metabolite
5-nitro-2-(3-phenylpropylamino)benzoic acid
5-nitro-2-(3-phenylpropylamino)benzoic acid: structure given in first source; chloride channel antagonist		2.0810nitrobenzoic acid
nu6102
NU6102: structure in first source		2.0310
ofloxacin
Ofloxacin: A synthetic fluoroquinolone antibacterial agent that inhibits the supercoiling activity of bacterial DNA GYRASE, halting DNA REPLICATION.. 9-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid : An oxazinoquinoline that is 2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinolin-7-one substituted by methyl, carboxy, fluoro, and 4-methylpiperazin-1-yl groups at positions 3, 6, 9, and 10, respectively.. ofloxacin : A racemate comprising equimolar amounts of levofloxacin and dextrofloxacin. It is a synthetic fluoroquinolone antibacterial agent which inhibits the supercoiling activity of bacterial DNA gyrase, halting DNA replication.		2.04103-oxo monocarboxylic acid;
N-arylpiperazine;
N-methylpiperazine;
organofluorine compound;
oxazinoquinoline
olomoucine
olomoucine: inhibits protein P34CDC2. olomoucine : A 9H-purine that is substituted by a (2-hydroxyethyl)nitrilo, benzylnitrilo and a methyl group at positions 2,6 and 9, respectively. It is a cyclin-dependent kinase inhibitor.		2.51202,6-diaminopurines;
ethanolamines		EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
omeprazole
Omeprazole: A 4-methoxy-3,5-dimethylpyridyl, 5-methoxybenzimidazole derivative of timoprazole that is used in the therapy of STOMACH ULCERS and ZOLLINGER-ELLISON SYNDROME. The drug inhibits an H(+)-K(+)-EXCHANGING ATPASE which is found in GASTRIC PARIETAL CELLS.. omeprazole : A racemate comprising equimolar amounts of (R)- and (S)-omeprazole.. 5-methoxy-2-{[(4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl}-1H-benzimidazole : A member of the class of benzimidazoles that is 1H-benzimidazole which is substituted by a [4-methoxy-3,5-dimethylpyridin-2-yl)methyl]sulfinyl group at position 2 and a methoxy group at position 5.		4.5251aromatic ether;
benzimidazoles;
pyridines;
sulfoxide
ondansetron
Ondansetron: A competitive serotonin type 3 receptor antagonist. It is effective in the treatment of nausea and vomiting caused by cytotoxic chemotherapy drugs, including cisplatin, and has reported anxiolytic and neuroleptic properties.		2.0510carbazoles
orphenadrine
Orphenadrine: A muscarinic antagonist used to treat drug-induced parkinsonism and to relieve pain from muscle spasm.. orphenadrine : A tertiary amino compound which is the phenyl-o-tolylmethyl ether of 2-(dimethylamino)ethanol.		2.0510ether;
tertiary amino compound		antidyskinesia agent;
antiparkinson drug;
H1-receptor antagonist;
muscarinic antagonist;
muscle relaxant;
NMDA receptor antagonist;
parasympatholytic
oxonic acid
Oxonic Acid: Antagonist of urate oxidase.		4.06401,3,5-triazines;
monocarboxylic acid
oxamniquine
Oxamniquine: An anthelmintic with schistosomicidal activity against Schistosoma mansoni, but not against other Schistosoma spp. Oxamniquine causes worms to shift from the mesenteric veins to the liver where the male worms are retained; the female worms return to the mesentery, but can no longer release eggs. (From Martindale, The Extra Pharmacopoeia, 31st ed, p121). oxamniquine : A racemate comprising equimolar amounts of (R)- and (S)-oxamniquine. An anthelmintic, it is administered orally for the treatment of schistomiasis caused by Schistosoma mansoni (but not by other Schistosoma species); intramuscular administration is no longer used as it causes severe pain at the injection site.. {2-[(isopropylamino)methyl]-7-nitro-1,2,3,4-tetrahydroquinolin-6-yl}methanol : A member of the class of quinolines that is 1,2,3,4-tetrahydroquinoline which is substituted at positions 2, 6, and 7 by (isopropylamino)methyl, hydroxymethyl, and nitro groups, respectively.		2.0510aromatic primary alcohol;
C-nitro compound;
quinolines;
secondary amino compound
oxaprozin
Oxaprozin: An oxazole-propionic acid derivative, cyclooxygenase inhibitor, and non-steroidal anti-inflammatory drug that is used in the treatment of pain and inflammation associated with of OSTEOARTHRITIS; RHEUMATOID ARTHRITIS; and ARTHRITIS, JUVENILE.. oxaprozin : A monocarboxylic acid that is a propionic acid derivative having a 4,5-diphenyl-1,3-oxazol-2-yl substituent at position 3. It is non-steroidal anti-inflammatory drug commonly used to relieve the pain and inflammatory responses associated with osteoarthritis and rheumatoid arthritis.		2.05101,3-oxazoles;
monocarboxylic acid		analgesic;
non-steroidal anti-inflammatory drug
oxazepam
Oxazepam: A benzodiazepine used in the treatment of anxiety, alcohol withdrawal, and insomnia.. oxazepam : A 1,4-benzodiazepinone that is 1,3-dihydro-2H-1,4-benzodiazepin-2-one substituted by a chloro group at position 7, a hydroxy group at position 3 and phenyl group at position 5.		2.45201,4-benzodiazepinone;
organochlorine compound		anxiolytic drug;
environmental contaminant;
xenobiotic
oxethazaine
[no description available]		2.0510amino acid amide
oxprenolol
Oxprenolol: A beta-adrenergic antagonist used in the treatment of hypertension, angina pectoris, arrhythmias, and anxiety.		2.0510aromatic ether
oxybenzone
oxybenzone : A hydroxybenzophenone that is benzophenone which is substituted at the 2- and 4-positions of one of the benzene rings by hydroxy and methoxy groups respectively.		2.0510hydroxybenzophenone;
monomethoxybenzene		dermatologic drug;
environmental contaminant;
protective agent;
ultraviolet filter;
xenobiotic
oxyphenbutazone
Oxyphenbutazone: A non-steroidal anti-inflammatory drug. Oxyphenbutazone eyedrops have been used abroad in the management of postoperative ocular inflammation, superficial eye injuries, and episcleritis. (From AMA, Drug Evaluations Annual, 1994, p2000) It had been used by mouth in rheumatic disorders such as ankylosing spondylitis, osteoarthritis, and rheumatoid arthritis but such use is no longer considered justified owing to the risk of severe hematological adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p27). oxyphenbutazone : A metabolite of phenylbutazone obtained by hydroxylation at position 4 of one of the phenyl rings. Commonly used (as its hydrate) to treat pain, swelling and stiffness associated with arthritis and gout, it was withdrawn from the market 1984 following association with blood dyscrasis and Stevens-Johnson syndrome.		2.0510phenols;
pyrazolidines		antimicrobial agent;
antineoplastic agent;
antipyretic;
drug metabolite;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic metabolite
aminosalicylic acid
Aminosalicylic Acid: An antitubercular agent often administered in association with ISONIAZID. The sodium salt of the drug is better tolerated than the free acid.. 4-aminosalicylic acid : An aminobenzoic acid that is salicylic acid substituted by an amino group at position 4.		2.0510aminobenzoic acid;
phenols		antitubercular agent
pamidronate
[no description available]		2.7130phosphonoacetic acid
pantoprazole
Pantoprazole: 2-pyridinylmethylsulfinylbenzimidazole proton pump inhibitor that is used in the treatment of GASTROESOPHAGEAL REFLUX and PEPTIC ULCER.. pantoprazole : A member of the class of benzimidazoles that is 1H-benzimidazole substituted by a difluoromethoxy group at position 5 and a [(3,4-dimethoxypyridin-2-yl)methyl]sulfinyl group at position 2.		3.1850aromatic ether;
benzimidazoles;
organofluorine compound;
pyridines;
sulfoxide		anti-ulcer drug;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
environmental contaminant;
xenobiotic
papaverine
Papaverine: An alkaloid found in opium but not closely related to the other opium alkaloids in its structure or pharmacological actions. It is a direct-acting smooth muscle relaxant used in the treatment of impotence and as a vasodilator, especially for cerebral vasodilation. The mechanism of its pharmacological actions is not clear, but it apparently can inhibit phosphodiesterases and it may have direct actions on calcium channels.. papaverine : A benzylisoquinoline alkaloid that is isoquinoline substituted by methoxy groups at positions 6 and 7 and a 3,4-dimethoxybenzyl group at position 1. It has been isolated from Papaver somniferum.		2.3110benzylisoquinoline alkaloid;
dimethoxybenzene;
isoquinolines		antispasmodic drug;
vasodilator agent
pd 153035
4-((3-bromophenyl)amino)-6,7-dimethoxyquinazoline: structure given in first source. PD-153035 : A member of the class of quinazolines carrying a 3-bromophenylamino substituent at position 4 and two methoxy substituents at positions 6 and 7.		2.9740aromatic amine;
aromatic ether;
bromobenzenes;
quinazolines;
secondary amino compound		EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
epidermal growth factor receptor antagonist
pd 169316
2-(4-nitrophenyl)-4-(4-fluorophenyl)-5-(4-pyridinyl)-1H-imidazole: p38 MAP kinase inhibitor		2.0310imidazoles
pd 98059
2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one: inhibits MAP kinase kinase (MEK) activity, p42 MAPK and p44 MAPK; structure in first source. 2-(2-amino-3-methoxyphenyl)chromen-4-one : A member of the class of monomethoxyflavones that is 3'-methoxyflavone bearing an additional amino substituent at position 2'.		3.83110aromatic amine;
monomethoxyflavone		EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector
pemoline
Pemoline: A central nervous system stimulant used in fatigue and depressive states and to treat hyperkinetic disorders in children.. pemoline : A member of the class of 1,3-oxazoles that is 1,3-oxazol-4(5H)-one which is substituted by an amino group at position 2 and by a phenyl group at position 5. A central nervous system stimulant, it was used to treat hyperactivity disorders in children, but withdrawn from use following reports of serious hepatotoxicity.		2.05101,3-oxazolescentral nervous system stimulant
pentobarbital
Pentobarbital: A short-acting barbiturate that is effective as a sedative and hypnotic (but not as an anti-anxiety) agent and is usually given orally. It is prescribed more frequently for sleep induction than for sedation but, like similar agents, may lose its effectiveness by the second week of continued administration. (From AMA Drug Evaluations Annual, 1994, p236). pentobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and sec-pentyl groups.		2.0510barbituratesGABAA receptor agonist
pentoxifylline
[no description available]		2.4420oxopurine
perazine
Perazine: A phenothiazine antipsychotic with actions and uses similar to those of CHLORPROMAZINE. Extrapyramidal symptoms may be more common than other side effects.. perazine : A phenothiazine derivative in which 10H-phenothiazinecarries a 3-(4-methylpiperazin-1-yl)propyl substituent at the N-10 position.		2.0510N-alkylpiperazine;
N-methylpiperazine;
phenothiazines		dopaminergic antagonist;
phenothiazine antipsychotic drug
perphenazine
Perphenazine: An antipsychotic phenothiazine derivative with actions and uses similar to those of CHLORPROMAZINE.. perphenazine : A phenothiazine derivative in which the phenothiazine tricycle carries a chloro substituent at the 2-position and a 3-[4-(2-hydroxyethyl)piperazin-1-yl]propyl group at N-10.		2.0510N-(2-hydroxyethyl)piperazine;
N-alkylpiperazine;
organochlorine compound;
phenothiazines		antiemetic;
dopaminergic antagonist;
phenothiazine antipsychotic drug
phenacetin
Saridon: contains phenacetin, caffeine, propyphenazone & pyrithyldione		2.4520acetamides;
aromatic ether		cyclooxygenase 3 inhibitor;
non-narcotic analgesic;
peripheral nervous system drug
phenobarbital
Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.		2.4520barbituratesanticonvulsant;
drug allergen;
excitatory amino acid antagonist;
sedative
phenolphthalein
Phenolphthalein: An acid-base indicator which is colorless in acid solution, but turns pink to red as the solution becomes alkaline. It is used medicinally as a cathartic.		2.0510phenols
phenoxybenzamine
Phenoxybenzamine: An alpha-adrenergic antagonist with long duration of action. It has been used to treat hypertension and as a peripheral vasodilator.		2.0510aromatic amine
phenylbutazone
Phenylbutazone: A butyl-diphenyl-pyrazolidinedione that has anti-inflammatory, antipyretic, and analgesic activities. It has been used in ANKYLOSING SPONDYLITIS; RHEUMATOID ARTHRITIS; and REACTIVE ARTHRITIS.. phenylbutazone : A member of the class of pyrazolidines that is 1,2-diphenylpyrazolidine-3,5-dione carrying a butyl group at the 4-position.		2.0510pyrazolidinesantirheumatic drug;
EC 1.1.1.184 [carbonyl reductase (NADPH)] inhibitor;
metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
peripheral nervous system drug
phloretin
[no description available]		2.4520dihydrochalconesantineoplastic agent;
plant metabolite
moxonidine
moxonidine: structure given in first source		2.0510organohalogen compound;
pyrimidines
pinacidil
Pinacidil: A guanidine that opens POTASSIUM CHANNELS producing direct peripheral vasodilatation of the ARTERIOLES. It reduces BLOOD PRESSURE and peripheral resistance and produces fluid retention. (Martindale The Extra Pharmacopoeia, 31st ed)		2.4620pyridines
pioglitazone
Pioglitazone: A thiazolidinedione and PPAR GAMMA agonist that is used in the treatment of TYPE 2 DIABETES MELLITUS.. pioglitazone : A member of the class of thiazolidenediones that is 1,3-thiazolidine-2,4-dione substituted by a benzyl group at position 5 which in turn is substituted by a 2-(5-ethylpyridin-2-yl)ethoxy group at position 4 of the phenyl ring. It exhibits hypoglycemic activity.		6.5952aromatic ether;
pyridines;
thiazolidinediones		antidepressant;
cardioprotective agent;
EC 2.7.1.33 (pantothenate kinase) inhibitor;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hypoglycemic agent;
insulin-sensitizing drug;
PPARgamma agonist;
xenobiotic
pipemidic acid
Pipemidic Acid: Antimicrobial against Gram negative and some Gram positive bacteria. It is protein bound and concentrated in bile and urine and used for gastrointestinal, biliary, and urinary infections.. pipemidic acid : A pyridopyrimidine that is 5-oxo-5,8-dihydropyrido[2,3-d]pyrimidine-6-carboxylic acid substituted at position 2 by a piperazin-1-yl group and at position 8 by an ethyl group. A synthetic broad-spectrum antibacterial, it is used for treatment of gastrointestinal, biliary, and urinary infections.		2.0510amino acid;
monocarboxylic acid;
N-arylpiperazine;
pyridopyrimidine;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor
piperazine
[no description available]		2.4620azacycloalkane;
piperazines;
saturated organic heteromonocyclic parent		anthelminthic drug
1-NA-PP1
[no description available]		2.0310pyrazolopyrimidinetyrosine kinase inhibitor
ag 1879
3-(4-chlorophenyl)-1-(1,1-dimethylethyl)-1H-pyrazolo(3,4-d)pyrimidin-4-amine: Fyn kinase inhibitor		3.6590aromatic amine;
monochlorobenzenes;
pyrazolopyrimidine		beta-adrenergic antagonist;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
geroprotector
pramoxine
pramoxine: RN given refers to parent cpd; structure. pramocaine : A member of the class of morpholines that is morpholine substituted at the nitrogen atom by a 3-(4-butoxyphenoxy)propyl group.		2.0410aromatic ether;
morpholines		local anaesthetic
praziquantel
azinox: Russian drug		2.830isoquinolines
prazosin
Prazosin: A selective adrenergic alpha-1 antagonist used in the treatment of HEART FAILURE; HYPERTENSION; PHEOCHROMOCYTOMA; RAYNAUD DISEASE; PROSTATIC HYPERTROPHY; and URINARY RETENTION.. prazosin : A member of the class of piperazines that is piperazine substituted by a furan-2-ylcarbonyl group and a 4-amino-6,7-dimethoxyquinazolin-2-yl group at positions 1 and 4 respectively.		9.5990aromatic ether;
furans;
monocarboxylic acid amide;
piperazines;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor
primaquine
Primaquine: An aminoquinoline that is given by mouth to produce a radical cure and prevent relapse of vivax and ovale malarias following treatment with a blood schizontocide. It has also been used to prevent transmission of falciparum malaria by those returning to areas where there is a potential for re-introduction of malaria. Adverse effects include anemias and GI disturbances. (From Martindale, The Extra Pharmacopeia, 30th ed, p404). primaquine : An N-substituted diamine that is pentane-1,4-diamine substituted by a 6-methoxyquinolin-8-yl group at the N(4) position. It is a drug used in the treatment of malaria and Pneumocystis pneumonia.		2.4620aminoquinoline;
aromatic ether;
N-substituted diamine		antimalarial
primidone
Primidone: A barbiturate derivative that acts as a GABA modulator and anti-epileptic agent. It is partly metabolized to PHENOBARBITAL in the body and owes some of its actions to this metabolite.. primidone : A pyrimidone that is dihydropyrimidine-4,6(1H,5H)-dione substituted by an ethyl and a phenyl group at position 5. It is used as an anticonvulsant for treatment of various types of seizures.		2.0510pyrimidoneanticonvulsant;
environmental contaminant;
xenobiotic
probenecid
Probenecid: The prototypical uricosuric agent. It inhibits the renal excretion of organic anions and reduces tubular reabsorption of urate. Probenecid has also been used to treat patients with renal impairment, and, because it reduces the renal tubular excretion of other drugs, has been used as an adjunct to antibacterial therapy.. probenecid : A sulfonamide in which the nitrogen of 4-sulfamoylbenzoic acid is substituted with two propyl groups.		2.4520benzoic acids;
sulfonamide		uricosuric drug
probucol
Probucol: A drug used to lower LDL and HDL cholesterol yet has little effect on serum-triglyceride or VLDL cholesterol. (From Martindale, The Extra Pharmacopoeia, 30th ed, p993).. probucol : A dithioketal that is propane-2,2-dithiol in which the hydrogens attached to both sulfur atoms are replaced by 3,5-di-tert-butyl-4-hydroxyphenyl groups. An anticholesteremic drug with antioxidant and anti-inflammatory properties, it is used to treat high levels of cholesterol in blood.		2.0510dithioketal;
polyphenol		anti-inflammatory drug;
anticholesteremic drug;
antilipemic drug;
antioxidant;
cardiovascular drug
procainamide
Procainamide: A class Ia antiarrhythmic drug that is structurally-related to PROCAINE.. procainamide : A benzamide that is 4-aminobenzamide substituted on the amide N by a 2-(diethylamino)ethyl group. It is a pharmaceutical antiarrhythmic agent used for the medical treatment of cardiac arrhythmias.		2.0510benzamidesanti-arrhythmia drug;
platelet aggregation inhibitor;
sodium channel blocker
procarbazine
Procarbazine: An antineoplastic agent used primarily in combination with mechlorethamine, vincristine, and prednisone (the MOPP protocol) in the treatment of Hodgkin's disease.. procarbazine : A benzamide obtained by formal condensation of the carboxy group of 4-[(2-methylhydrazino)methyl]benzoic acid with the amino group of isopropylamine. An antineoplastic chemotherapy drug used for treatment of Hodgkin's lymphoma. Metabolism yields azo-procarbazine and hydrogen peroxide, which results in the breaking of DNA strands.		2.9940benzamides;
hydrazines		antineoplastic agent
prochlorperazine
Prochlorperazine: A phenothiazine antipsychotic used principally in the treatment of NAUSEA; VOMITING; and VERTIGO. It is more likely than CHLORPROMAZINE to cause EXTRAPYRAMIDAL DISORDERS. (From Martindale, The Extra Pharmacopoeia, 30th ed, p612). prochlorperazine : A member of the class of phenothiazines that is 10H-phenothiazine having a chloro substituent at the 2-position and a 3-(4-methylpiperazin-1-yl)propyl group at the N-10 position.		2.0510N-alkylpiperazine;
N-methylpiperazine;
organochlorine compound;
phenothiazines		alpha-adrenergic antagonist;
antiemetic;
cholinergic antagonist;
dopamine receptor D2 antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic
procyclidine
Procyclidine: A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.. procyclidine : A tertiary alcohol that consists of propan-1-ol substituted by a cyclohexyl and a phenyl group at position 1 and a pyrrolidin-1-yl group at position 3.		2.0410pyrrolidines;
tertiary alcohol		antidyskinesia agent;
antiparkinson drug;
muscarinic antagonist
promethazine
Promethazine: A phenothiazine derivative with histamine H1-blocking, antimuscarinic, and sedative properties. It is used as an antiallergic, in pruritus, for motion sickness and sedation, and also in animals.. promethazine : A tertiary amine that is a substituted phenothiazine in which the ring nitrogen at position 10 is attached to C-3 of an N,N-dimethylpropan-2-amine moiety.		2.0510phenothiazines;
tertiary amine		anti-allergic agent;
anticoronaviral agent;
antiemetic;
antipruritic drug;
H1-receptor antagonist;
local anaesthetic;
sedative
propafenone
Propafenone: An antiarrhythmia agent that is particularly effective in ventricular arrhythmias. It also has weak beta-blocking activity.. propafenone : An aromatic ketone that is 3-(propylamino)propane-1,2-diol in which the hydrogen of the primary hydroxy group is replaced by a 2-(3-phenylpropanoyl)phenyl group. It is a class 1C antiarrhythmic drug with local anesthetic effects, and is used as the hydrochloride salt in the management of supraventricular and ventricular arrhythmias.		2.0410aromatic ketone;
secondary alcohol;
secondary amino compound		anti-arrhythmia drug
propidium
Propidium: Quaternary ammonium analog of ethidium; an intercalating dye with a specific affinity to certain forms of DNA and, used as diiodide, to separate them in density gradients; also forms fluorescent complexes with cholinesterase which it inhibits.		2.4420phenanthridines;
quaternary ammonium ion		fluorochrome;
intercalator
propofol
Propofol: An intravenous anesthetic agent which has the advantage of a very rapid onset after infusion or bolus injection plus a very short recovery period of a couple of minutes. (From Smith and Reynard, Textbook of Pharmacology, 1992, 1st ed, p206). Propofol has been used as ANTICONVULSANTS and ANTIEMETICS.. propofol : A phenol resulting from the formal substitution of the hydrogen at the 2 position of 1,3-diisopropylbenzene by a hydroxy group.		2.0510phenolsanticonvulsant;
antiemetic;
intravenous anaesthetic;
radical scavenger;
sedative
propranolol
Propranolol: A widely used non-cardioselective beta-adrenergic antagonist. Propranolol has been used for MYOCARDIAL INFARCTION; ARRHYTHMIA; ANGINA PECTORIS; HYPERTENSION; HYPERTHYROIDISM; MIGRAINE; PHEOCHROMOCYTOMA; and ANXIETY but adverse effects instigate replacement by newer drugs.. propranolol : A propanolamine that is propan-2-ol substituted by a propan-2-ylamino group at position 1 and a naphthalen-1-yloxy group at position 3.		2.4520naphthalenes;
propanolamine;
secondary amine		anti-arrhythmia drug;
antihypertensive agent;
anxiolytic drug;
beta-adrenergic antagonist;
environmental contaminant;
human blood serum metabolite;
vasodilator agent;
xenobiotic
pyridinolcarbamate
Pyridinolcarbamate: A drug that has been given by mouth in the treatment of atherosclerosis and other vascular disorders, hyperlipidemias, and thrombo-embolic disorders. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1408)		2.0510pyridines
pyrimethamine
Maloprim: contains above 2 cpds		2.0510aminopyrimidine;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
ranitidine
[no description available]		2.4520aralkylamine
opc 12759
rebamipide: structure in first source; RN refers to (+-)-isomer; inhibits gastric xanthine oxidase		2.0510secondary carboxamide
riluzole
Riluzole: A glutamate antagonist (RECEPTORS, GLUTAMATE) used as an anticonvulsant (ANTICONVULSANTS) and to prolong the survival of patients with AMYOTROPHIC LATERAL SCLEROSIS.		2.0510benzothiazoles
risperidone
Risperidone: A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.. risperidone : A member of the class of pyridopyrimidines that is 2-methyl-6,7,8,9-tetrahydropyrido[1,2-a]pyrimidin-4-one carrying an additional 2-[4-(6-fluoro-1,2-benzoxazol-3-yl)piperidin-1-yl]ethyl group at position 2.		2.05101,2-benzoxazoles;
heteroarylpiperidine;
organofluorine compound;
pyridopyrimidine		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
H1-receptor antagonist;
psychotropic drug;
second generation antipsychotic;
serotonergic antagonist
ritanserin
Ritanserin: A selective and potent serotonin-2 antagonist that is effective in the treatment of a variety of syndromes related to anxiety and depression. The drug also improves the subjective quality of sleep and decreases portal pressure.. ritanserin : A thiazolopyrimidine that is 5H-[1,3]thiazolo[3,2-a]pyrimidin-5-one which is substituted at position 7 by a methyl group and at position 6 by a 2-{4-[bis(4-fluorophenyl)methylidene]piperidin-1-yl}ethyl group. A potent and long-acting seratonin (5-hydroxytryptamine, 5-HT) antagonist of the subtype 5-HT2 (Ki = 0.39 nM), it is used in the treatment of a variety of disorders including anxiety, depression and schizophrenia. It has little sedative action.		2.0410organofluorine compound;
piperidines;
thiazolopyrimidine		antidepressant;
antipsychotic agent;
anxiolytic drug;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
serotonergic antagonist
rofecoxib
[no description available]		2.0510butenolide;
sulfone		analgesic;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
salicylamide
salamide: a major impurity of hydrochlorothiazide; structure in first source		2.0510phenols;
salicylamides		antirheumatic drug;
non-narcotic analgesic
sb 220025
SB 220025: inhibits p38 mitogen-activated protein kinase; structure in first source. SB220025 : Am member of the class of imidazoles carrying piperidin-4-yl, 4-fluophenyl and 2-aminopyrimidin-4-yl substituents at posiitons 1, 4 and 5 respectively.		2.0310aminopyrimidine;
imidazoles;
organofluorine compound;
piperidines		angiogenesis inhibitor;
anti-inflammatory agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
sb 239063
SB 239063: structure in first source. SB-239063 : A member of the class of imidazoles carrying 4-hydroxycyclohexyl, 4-fluorophenyl and 2-methoxypyrimidin-4-yl substituents at positions 1, 4 and 5 respectively.		2.0310imidazoles
sb 202190
4-(4-fluorophenyl)-2-(4-hydroxyphenyl)-5-(4-pyridyl)imidazole: structure given in first source; inhibits p38 MAP kinase		2.4620imidazoles;
organofluorine compound;
phenols;
pyridines		apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
scriptaid
scriptide: provokes translocation of GLUT4 to increase glucose uptake; structure in first source		2.0510isoquinolines
sevoflurane
Sevoflurane: A non-explosive inhalation anesthetic used in the induction and maintenance of general anesthesia. It does not cause respiratory irritation and may also prevent PLATELET AGGREGATION.. sevoflurane : An ether compound having fluoromethyl and 1,1,1,3,3,3-hexafluoroisopropyl as the two alkyl groups.		2.0510ether;
organofluorine compound		central nervous system depressant;
inhalation anaesthetic;
platelet aggregation inhibitor
sibutramine
sibutramine: serotonin and norepinephrine transporter inhibitor; Meridia is tradename for sibutramine hydrochloride		2.0510organochlorine compound;
tertiary amino compound		anti-obesity agent;
serotonin uptake inhibitor
sulfadiazine
Sulfadiazine: One of the short-acting SULFONAMIDES used in combination with PYRIMETHAMINE to treat toxoplasmosis in patients with acquired immunodeficiency syndrome and in newborns with congenital infections.. sulfadiazine : A sulfonamide consisting of pyrimidine with a 4-aminobenzenesulfonamido group at the 2-position.. diazine : The parent structure of the diazines.		2.0510pyrimidines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
antimicrobial agent;
antiprotozoal drug;
coccidiostat;
drug allergen;
EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
xenobiotic
risedronic acid
Risedronic Acid: A pyridine and diphosphonic acid derivative that acts as a CALCIUM CHANNEL BLOCKER and inhibits BONE RESORPTION.		2.7730pyridines
sotalol
Sotalol: An adrenergic beta-antagonist that is used in the treatment of life-threatening arrhythmias.. sotalol : A sulfonamide that is N-phenylmethanesulfonamide in which the phenyl group is substituted at position 4 by a 1-hydroxy-2-(isopropylamino)ethyl group. It has both beta-adrenoreceptor blocking (Vaughan Williams Class II) and cardiac action potential duration prolongation (Vaughan Williams Class III) antiarrhythmic properties. It is used (usually as the hydrochloride salt) for the management of ventricular and supraventricular arrhythmias.		2.4520ethanolamines;
secondary alcohol;
secondary amino compound;
sulfonamide		anti-arrhythmia drug;
beta-adrenergic antagonist;
environmental contaminant;
xenobiotic
4-phenylbutyric acid, sodium salt
sodium phenylbutyrate : The organic sodium salt of 4-phenylbutyric acid. A prodrug for phenylacetate, it is used to treat urea cycle disorders.		2.0510organic sodium saltEC 3.5.1.98 (histone deacetylase) inhibitor;
geroprotector;
neuroprotective agent;
orphan drug;
prodrug
stearic acid
octadecanoic acid : A C18 straight-chain saturated fatty acid component of many animal and vegetable lipids. As well as in the diet, it is used in hardening soaps, softening plastics and in making cosmetics, candles and plastics.		2.1310long-chain fatty acid;
saturated fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
human metabolite;
plant metabolite
imatinib
[no description available]		7.4620aromatic amine;
benzamides;
N-methylpiperazine;
pyridines;
pyrimidines		antineoplastic agent;
apoptosis inducer;
tyrosine kinase inhibitor
vorinostat
Vorinostat: A hydroxamic acid and anilide derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used in the treatment of CUTANEOUS T-CELL LYMPHOMA and SEZARY SYNDROME.. vorinostat : A dicarboxylic acid diamide comprising suberic (octanedioic) acid coupled to aniline and hydroxylamine. A histone deacetylase inhibitor, it is marketed under the name Zolinza for the treatment of cutaneous T cell lymphoma (CTCL).		7.04140dicarboxylic acid diamide;
hydroxamic acid		antineoplastic agent;
apoptosis inducer;
EC 3.5.1.98 (histone deacetylase) inhibitor
sulfadimethoxine
Sulfadimethoxine: A sulfanilamide that is used as an anti-infective agent.. sulfadimethoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 2- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position.		2.0510aromatic ether;
pyrimidines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
antimicrobial agent;
drug allergen;
environmental contaminant;
xenobiotic
sulfamerazine
[no description available]		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
drug allergen
sulfameter
Sulfameter: Long acting sulfonamide used in leprosy, urinary, and respiratory tract infections.. sulfamethoxydiazine : A sulfonamide consisting of pyrimidine having a methoxy substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
leprostatic drug;
renal agent
sulfamethazine
Sulfamethazine: A sulfanilamide anti-infective agent. It has a spectrum of antimicrobial action similar to other sulfonamides.. sulfamethazine : A sulfonamide consisting of pyrimidine with methyl substituents at the 4- and 6-positions and a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyrimidines;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
antiinfective agent;
antimicrobial agent;
carcinogenic agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
ligand;
xenobiotic
sulfamethizole
Sulfamethizole: A sulfathiazole antibacterial agent.. sulfamethizole : A sulfonamide consisting of a 1,3,4-thiadiazole nucleus with a methyl substituent at C-5 and a 4-aminobenzenesulfonamido group at C-2.		2.0510sulfonamide antibiotic;
sulfonamide;
thiadiazoles		antiinfective agent;
antimicrobial agent;
drug allergen;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor
sulfamethoxazole
Sulfamethoxazole: A bacteriostatic antibacterial agent that interferes with folic acid synthesis in susceptible bacteria. Its broad spectrum of activity has been limited by the development of resistance. (From Martindale, The Extra Pharmacopoeia, 30th ed, p208). sulfamethoxazole : An isoxazole (1,2-oxazole) compound having a methyl substituent at the 5-position and a 4-aminobenzenesulfonamido group at the 3-position.		2.0510isoxazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial agent;
antiinfective agent;
antimicrobial agent;
drug allergen;
EC 1.1.1.153 [sepiapterin reductase (L-erythro-7,8-dihydrobiopterin forming)] inhibitor;
EC 2.5.1.15 (dihydropteroate synthase) inhibitor;
environmental contaminant;
epitope;
P450 inhibitor;
xenobiotic
sulfanilamide
[no description available]		2.0510substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial agent;
drug allergen;
EC 4.2.1.1 (carbonic anhydrase) inhibitor
sulfanitran
[no description available]		2.0410sulfonamide
sulfaphenazole
Sulfaphenazole: A sulfonilamide anti-infective agent.. sulfaphenazole : A sulfonamide that is sulfanilamide in which the sulfonamide nitrogen is substituted by a 1-phenyl-1H-pyrazol-5-yl group. It is a selective inhibitor of cytochrome P450 (CYP) 2C9 isozyme, and antibacterial agent.		2.0510primary amino compound;
pyrazoles;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antibacterial drug;
EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor;
EC 1.14.13.67 (quinine 3-monooxygenase) inhibitor;
P450 inhibitor
sulfapyridine
Sulfapyridine: Antibacterial, potentially toxic, used to treat certain skin diseases.. sulfapyridine : A sulfonamide consisting of pyridine with a 4-aminobenzenesulfonamido group at the 2-position.		2.0510pyridines;
substituted aniline;
sulfonamide antibiotic;
sulfonamide		antiinfective agent;
dermatologic drug;
drug allergen;
environmental contaminant;
xenobiotic
sulfasalazine
Sulfasalazine: A drug that is used in the management of inflammatory bowel diseases. Its activity is generally considered to lie in its metabolic breakdown product, 5-aminosalicylic acid (see MESALAMINE) released in the colon. (From Martindale, The Extra Pharmacopoeia, 30th ed, p907). sulfasalazine : An azobenzene consisting of diphenyldiazene having a carboxy substituent at the 4-position, a hydroxy substituent at the 3-position and a 2-pyridylaminosulphonyl substituent at the 4'-position.		2.7830
sulfinpyrazone
Sulfinpyrazone: A uricosuric drug that is used to reduce the serum urate levels in gout therapy. It lacks anti-inflammatory, analgesic, and diuretic properties.		2.4520pyrazolidines;
sulfoxide		uricosuric drug
sulforaphane
sulforaphane: from Cardaria draba L.. sulforaphane : An isothiocyanate having a 4-(methylsulfinyl)butyl group attached to the nitrogen.		2.0710isothiocyanate;
sulfoxide		antineoplastic agent;
antioxidant;
EC 3.5.1.98 (histone deacetylase) inhibitor;
plant metabolite
2-(octylamino)-1-[4-(propan-2-ylthio)phenyl]-1-propanol
[no description available]		2.0510alkylbenzene
sulpiride
Sulpiride: A dopamine D2-receptor antagonist. It has been used therapeutically as an antidepressant, antipsychotic, and as a digestive aid. (From Merck Index, 11th ed). sulpiride : A member of the class of benzamides obtained from formal condensation between the carboxy group of 2-methoxy-5-sulfamoylbenzoic acid and the primary amino group of (1-ethylpyrrolidin-2-yl)methylamine.		2.0510benzamides;
N-alkylpyrrolidine;
sulfonamide		antidepressant;
antiemetic;
antipsychotic agent;
dopaminergic antagonist
suprofen
Suprofen: An IBUPROFEN-type anti-inflammatory analgesic and antipyretic. It inhibits prostaglandin synthesis and has been proposed as an anti-arthritic.. suprofen : An aromatic ketone that is thiophene substituted at C-2 by a 4-(1-carboxyethyl)benzoyl group.		2.0510aromatic ketone;
monocarboxylic acid;
thiophenes		antirheumatic drug;
drug allergen;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
peripheral nervous system drug
suramin
Suramin: A polyanionic compound with an unknown mechanism of action. It is used parenterally in the treatment of African trypanosomiasis and it has been used clinically with diethylcarbamazine to kill the adult Onchocerca. (From AMA Drug Evaluations Annual, 1992, p1643) It has also been shown to have potent antineoplastic properties.. suramin : A member of the class of phenylureas that is urea in which each of the amino groups has been substituted by a 3-({2-methyl-5-[(4,6,8-trisulfo-1-naphthyl)carbamoyl]phenyl}carbamoyl)phenyl group. An activator of both the rabbit skeletal muscle RyR1 and sheep cardiac RyR2 isoform ryanodine receptor channels, it has been used for the treatment of human African trypanosomiasis for over 100 years.		2.4720naphthalenesulfonic acid;
phenylureas;
secondary carboxamide		angiogenesis inhibitor;
antinematodal drug;
antineoplastic agent;
apoptosis inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
GABA antagonist;
GABA-gated chloride channel antagonist;
purinergic receptor P2 antagonist;
ryanodine receptor agonist;
trypanocidal drug
gatifloxacin
Gatifloxacin: A fluoroquinolone antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used as an ophthalmic solution for the treatment of BACTERIAL CONJUNCTIVITIS.. gatifloxacin : A monocarboxylic acid that is 4-oxo-1,4-dihydroquinoline-3-carboxylic acid which is substituted on the nitrogen by a cyclopropyl group and at positions 6, 7, and 8 by fluoro, 3-methylpiperazin-1-yl, and methoxy groups, respectively. Gatifloxacin is an antibiotic of the fourth-generation fluoroquinolone family, that like other members of that family, inhibits the bacterial topoisomerase type-II enzymes.		2.0510N-arylpiperazine;
organofluorine compound;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antiinfective agent;
antimicrobial agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
tegafur
[no description available]		4.2450organohalogen compound;
pyrimidines
temazepam
Temazepam: A benzodiazepine that acts as a GAMMA-AMINOBUTYRIC ACID modulator and anti-anxiety agent.		2.0510benzodiazepine
temozolomide
[no description available]		14.23143imidazotetrazine;
monocarboxylic acid amide;
triazene derivative		alkylating agent;
antineoplastic agent;
prodrug
terazosin
Terazosin: induces decreased blood pressure; used in the treatment of benign prostatic hyperplasia		2.0410furans;
piperazines;
primary amino compound;
quinazolines		alpha-adrenergic antagonist;
antihypertensive agent;
antineoplastic agent
terbutaline
Terbutaline: A selective beta-2 adrenergic agonist used as a bronchodilator and tocolytic.. terbutaline : A member of the class of phenylethanolamines that is catechol substituted at position 5 by a 2-(tert-butylamino)-1-hydroxyethyl group.		2.0510phenylethanolamines;
resorcinols		anti-asthmatic drug;
beta-adrenergic agonist;
bronchodilator agent;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
hypoglycemic agent;
sympathomimetic agent;
tocolytic agent
terfenadine
Terfenadine: A selective histamine H1-receptor antagonist devoid of central nervous system depressant activity. The drug was used for ALLERGY but withdrawn due to causing LONG QT SYNDROME.		2.4520diarylmethane
tetracaine
Tetracaine: A potent local anesthetic of the ester type used for surface and spinal anesthesia.. tetracaine : A benzoate ester in which 4-N-butylbenzoic acid and 2-(dimethylamino)ethanol have combined to form the ester bond; a local ester anaesthetic (ester caine) used for surface and spinal anaesthesia.		2.0510benzoate ester;
tertiary amino compound		local anaesthetic
tetraethylammonium
Tetraethylammonium: A potassium-selective ion channel blocker. (From J Gen Phys 1994;104(1):173-90)		2.4720quaternary ammonium ion
thalidomide
Thalidomide: A piperidinyl isoindole originally introduced as a non-barbiturate hypnotic, but withdrawn from the market due to teratogenic effects. It has been reintroduced and used for a number of immunological and inflammatory disorders. Thalidomide displays immunosuppressive and anti-angiogenic activity. It inhibits release of TUMOR NECROSIS FACTOR-ALPHA from monocytes, and modulates other cytokine action.. thalidomide : A racemate comprising equimolar amounts of R- and S-thalidomide.. 2-(2,6-dioxopiperidin-3-yl)-1H-isoindole-1,3(2H)-dione : A dicarboximide that is isoindole-1,3(2H)-dione in which the hydrogen attached to the nitrogen is substituted by a 2,6-dioxopiperidin-3-yl group.		7.46200phthalimides;
piperidones
thiabendazole
Tresaderm: dermatologic soln containing dexamethasone, thiabendazole & neomycin sulfate		2.05101,3-thiazoles;
benzimidazole fungicide;
benzimidazoles		antifungal agrochemical;
antinematodal drug
thioridazine
Thioridazine: A phenothiazine antipsychotic used in the management of PHYCOSES, including SCHIZOPHRENIA.. thioridazine : A phenothiazine derivative having a methylsulfanyl subsitituent at the 2-position and a (1-methylpiperidin-2-yl)ethyl] group at the N-10 position.		2.7330phenothiazines;
piperidines		alpha-adrenergic antagonist;
dopaminergic antagonist;
EC 1.8.1.12 (trypanothione-disulfide reductase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
tiaprofenic acid
tiaprofenic acid: RN given refers to parent cpd; structure. tiaprofenic acid : An aromatic ketone that is thiophene substituted at C-2 by benzoyl and at C-4 by a 1-carboxyethyl group.		2.0510aromatic ketone;
monocarboxylic acid;
thiophenes		drug allergen;
non-steroidal anti-inflammatory drug
ticlopidine
Ticlopidine: An effective inhibitor of platelet aggregation commonly used in the placement of STENTS in CORONARY ARTERIES.. ticlopidine : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group.		2.4820monochlorobenzenes;
thienopyridine		anticoagulant;
fibrin modulating drug;
hematologic agent;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
tinidazole
Tinidazole: A nitroimidazole alkylating agent that is used as an antitrichomonal agent against TRICHOMONAS VAGINALIS; ENTAMOEBA HISTOLYTICA; and GIARDIA LAMBLIA infections. It also acts as an antibacterial agent for the treatment of BACTERIAL VAGINOSIS and anaerobic bacterial infections.. tinidazole : 1H-imidazole substituted at C-1 by a (2-ethylsulfonyl)ethyl group, at C-2 by a methyl group and at C-5 by a nitro group. It is used as an antiprotozoal, antibacterial agent.		2.0410imidazolesantiamoebic agent;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
tiopronin
Tiopronin: Sulfhydryl acylated derivative of GLYCINE.		2.0510N-acyl-amino acid
tizanidine
tizanidine: RN given refers to parent cpd; structure. tizanidine : 2,1,3-Benzothiadiazole substituted at C-4 by a Delta(1)-imidazolin-2-ylamino group and at C-4 by a chloro group. It is an agonist at alpha2-adrenergic receptor sites.		2.0510benzothiadiazole;
imidazoles		alpha-adrenergic agonist;
muscle relaxant
tolazamide
Tolazamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE.. tolazamide : An N-sulfonylurea that is 1-tosylurea in which a hydrogen attached to the nitrogen at position 3 is replaced by an azepan-1-yl group. A hypoglycemic agent, it is used for the treatment of type 2 diabetes mellitus.		2.0510N-sulfonylureahypoglycemic agent;
potassium channel blocker
tolbutamide
Tolbutamide: A sulphonylurea hypoglycemic agent with actions and uses similar to those of CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). tolbutamide : An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position.		2.0510N-sulfonylureahuman metabolite;
hypoglycemic agent;
insulin secretagogue;
potassium channel blocker
tolperisone
Tolperisone: A centrally acting muscle relaxant that has been used for the symptomatic treatment of spasticity and muscle spasm. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1211)		2.0510aromatic ketone
n,n,n',n'-tetrakis(2-pyridylmethyl)ethylenediamine
N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine: a zinc ion chelating agent; structure given in first source. N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine : An N-substituted diamine that is ethylenediamine in which the four amino hydrogens are replaced by 2-pyridylmethyl groups.		2.110N-substituted diamine;
pyridines;
tertiary amino compound		apoptosis inducer;
chelator;
copper chelator
ultram
2-[(dimethylamino)methyl]-1-(3-methoxyphenyl)cyclohexanol : A tertiary alcohol that is cyclohexanol substituted at positions 1 and 2 by 3-methoxyphenyl and dimethylaminomethyl groups respectively.		2.4520aromatic ether;
tertiary alcohol;
tertiary amino compound
tranexamic acid
Tranexamic Acid: Antifibrinolytic hemostatic used in severe hemorrhage.		2.4520amino acid
trapidil
Trapidil: A coronary vasodilator agent.		2.0510triazolopyrimidines
trazodone
Trazodone: A serotonin uptake inhibitor that is used as an antidepressive agent. It has been shown to be effective in patients with major depressive disorders and other subsets of depressive disorders. It is generally more useful in depressive disorders associated with insomnia and anxiety. This drug does not aggravate psychotic symptoms in patients with schizophrenia or schizoaffective disorders. (From AMA Drug Evaluations Annual, 1994, p309). trazodone : An N-arylpiperazine in which one nitrogen is substituted by a 3-chlorophenyl group, while the other is substituted by a 3-(3-oxo[1,2,4]triazolo[4,3-a]pyridin-2(3H)-yl)propyl group.		2.0510monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
triazolopyridine		adrenergic antagonist;
antidepressant;
anxiolytic drug;
H1-receptor antagonist;
sedative;
serotonin uptake inhibitor
triazolam
Triazolam: A short-acting benzodiazepine used in the treatment of insomnia. Some countries temporarily withdrew triazolam from the market because of concerns about adverse reactions, mostly psychological, associated with higher dose ranges. Its use at lower doses with appropriate care and labeling has been reaffirmed by the FDA and most other countries.		2.4920triazolobenzodiazepinesedative
triclosan
[no description available]		2.0510aromatic ether;
dichlorobenzene;
monochlorobenzenes;
phenols		antibacterial agent;
antimalarial;
drug allergen;
EC 1.3.1.9 [enoyl-[acyl-carrier-protein] reductase (NADH)] inhibitor;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
fungicide;
persistent organic pollutant;
xenobiotic
triflupromazine
Triflupromazine: A phenothiazine used as an antipsychotic agent and as an antiemetic.. triflupromazine : A member of the class of phenothiazines that is 10H-phenothiazine having a trifluoromethyl subsitituent at the 2-position and a 3-(dimethylamino)propyl group at the N-10 position.		2.0510organofluorine compound;
phenothiazines;
tertiary amine		anticoronaviral agent;
antiemetic;
dopaminergic antagonist;
first generation antipsychotic
trimethadione
Trimethadione: An anticonvulsant effective in absence seizures, but generally reserved for refractory cases because of its toxicity. (From AMA Drug Evaluations Annual, 1994, p378). trimethadione : An oxazolidinone that is 1,3-oxazolidine-2,4-dione substituted by methyl groups at positions 3, 5 and 5. It is an antiepileptic agent.		2.0510oxazolidinoneanticonvulsant;
geroprotector
trimethoprim
Trimethoprim: A pyrimidine inhibitor of dihydrofolate reductase, it is an antibacterial related to PYRIMETHAMINE. It is potentiated by SULFONAMIDES and the TRIMETHOPRIM, SULFAMETHOXAZOLE DRUG COMBINATION is the form most often used. It is sometimes used alone as an antimalarial. TRIMETHOPRIM RESISTANCE has been reported.. trimethoprim : An aminopyrimidine antibiotic whose structure consists of pyrimidine 2,4-diamine and 1,2,3-trimethoxybenzene moieties linked by a methylene bridge.		2.4520aminopyrimidine;
methoxybenzenes		antibacterial drug;
diuretic;
drug allergen;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
environmental contaminant;
xenobiotic
troglitazone
Troglitazone: A chroman and thiazolidinedione derivative that acts as a PEROXISOME PROLIFERATOR-ACTIVATED RECEPTORS (PPAR) agonist. It was formerly used in the treatment of TYPE 2 DIABETES MELLITUS, but has been withdrawn due to hepatotoxicity.		2.0510chromanes;
thiazolidinone		anticoagulant;
anticonvulsant;
antineoplastic agent;
antioxidant;
EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
hypoglycemic agent;
platelet aggregation inhibitor;
vasodilator agent
tyrphostin a9
[no description available]		2.4110alkylbenzenegeroprotector
venlafaxine
venlafaxine : A tertiary amino compound that is N,N-dimethylethanamine substituted at position 1 by a 1-hydroxycyclohexyl and 4-methoxyphenyl group.		2.0510cyclohexanols;
monomethoxybenzene;
tertiary alcohol;
tertiary amino compound		adrenergic uptake inhibitor;
analgesic;
antidepressant;
dopamine uptake inhibitor;
environmental contaminant;
serotonin uptake inhibitor;
xenobiotic
vesnarinone
[no description available]		2.0510organic molecular entity
vigabatrin
[no description available]		2.0510gamma-amino acidanticonvulsant;
EC 2.6.1.19 (4-aminobutyrate--2-oxoglutarate transaminase) inhibitor
whi p180
[no description available]		2.0310
2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-((phenylamino)carbonyl)-2h-tetrazolium hydroxide
2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-((phenylamino)carbonyl)-2H-tetrazolium hydroxide: structure given in first source		2.0510
ici 204,219
zafirlukast: a leukotriene D4 receptor antagonist		2.0510carbamate ester;
indoles;
N-sulfonylcarboxamide		anti-asthmatic agent;
leukotriene antagonist
zm 336372
N-(5-(3-dimethylaminobenzamido)-2-methylphenyl)-4-hydroxybenzamide: an inhibitor of c-Raf; activates Raf-1; structure in first source		2.0310benzamides
zolpidem
Zolpidem: An imidazopyridine derivative and short-acting GABA-A receptor agonist that is used for the treatment of INSOMNIA.. zolpidem : An imidazo[1,2-a]pyridine compound having a 4-tolyl group at the 2-position, an N,N-dimethylcarbamoylmethyl group at the 3-position and a methyl substituent at the 6-position.		2.0510imidazopyridinecentral nervous system depressant;
GABA agonist;
sedative
guanidine hydrochloride
[no description available]		2.0510one-carbon compound;
organic chloride salt		protein denaturant
hydrocortisone acetate
hydrocortisone acetate: RN given refers to cpd without isomeric designation		2.0510cortisol ester;
tertiary alpha-hydroxy ketone
cortisone acetate
Cortisone Acetate: The acetate ester of cortisone that is used mainly for replacement therapy in adrenocortical insufficiency and in the treatment of many allergic and inflammatory disorders.		2.0510corticosteroid hormone
mitomycin
Mitomycin: An antineoplastic antibiotic produced by Streptomyces caespitosus. It is one of the bi- or tri-functional ALKYLATING AGENTS causing cross-linking of DNA and inhibition of DNA synthesis.. mitomycin : A family of aziridine-containing natural products isolated from Streptomyces caespitosus or Streptomyces lavendulae.		2.0510mitomycinalkylating agent;
antineoplastic agent
corticosterone
[no description available]		2.251011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone		human metabolite;
mouse metabolite
prednisolone
Prednisolone: A glucocorticoid with the general properties of the corticosteroids. It is the drug of choice for all conditions in which routine systemic corticosteroid therapy is indicated, except adrenal deficiency states.. prednisolone : A glucocorticoid that is prednisone in which the oxo group at position 11 has been reduced to the corresponding beta-hydroxy group. It is a drug metabolite of prednisone.		9.9942311beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
drug metabolite;
environmental contaminant;
immunosuppressive agent;
xenobiotic
estriol
hormonin: estrogen replacement; each tablet contains 600 ug micronized 17beta-estradiol, 270 ug estriol and 1.4 mg estrone. chlorapatite : A phosphate mineral with the formula Ca5(PO4)3Cl.		2.051016alpha-hydroxy steroid;
17beta-hydroxy steroid;
3-hydroxy steroid		estrogen;
human metabolite;
human xenobiotic metabolite;
mouse metabolite
reserpine
Reserpine: An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria. Reserpine inhibits the uptake of norepinephrine into storage vesicles resulting in depletion of catecholamines and serotonin from central and peripheral axon terminals. It has been used as an antihypertensive and an antipsychotic as well as a research tool, but its adverse effects limit its clinical use.. reserpine : An alkaloid found in the roots of Rauwolfia serpentina and R. vomitoria.		2.4520alkaloid ester;
methyl ester;
yohimban alkaloid		adrenergic uptake inhibitor;
antihypertensive agent;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
first generation antipsychotic;
plant metabolite;
xenobiotic
cephaloridine
Cephaloridine: A cephalosporin antibiotic.. cefaloridine : A cephalosporin compound having pyridinium-1-ylmethyl and 2-thienylacetamido side-groups. A first-generation semisynthetic derivative of cephalosporin C.		2.0510beta-lactam antibiotic allergen;
cephalosporin;
semisynthetic derivative		antibacterial drug
phentolamine
Phentolamine: A nonselective alpha-adrenergic antagonist. It is used in the treatment of hypertension and hypertensive emergencies, pheochromocytoma, vasospasm of RAYNAUD DISEASE and frostbite, clonidine withdrawal syndrome, impotence, and peripheral vascular disease.. phentolamine : A substituted aniline that is 3-aminophenol in which the hydrogens of the amino group are replaced by 4-methylphenyl and 4,5-dihydro-1H-imidazol-2-ylmethyl groups respectively. An alpha-adrenergic antagonist, it is used for the treatment of hypertension.		2.0510imidazoles;
phenols;
substituted aniline;
tertiary amino compound		alpha-adrenergic antagonist;
vasodilator agent
sorbitol
D-glucitol : The D-enantiomer of glucitol (also known as D-sorbitol).		2.0510glucitolcathartic;
Escherichia coli metabolite;
food humectant;
human metabolite;
laxative;
metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite;
sweetening agent
thymidine
[no description available]		5.5861pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
metabolite;
mouse metabolite
floxuridine
Floxuridine: An antineoplastic antimetabolite that is metabolized to fluorouracil when administered by rapid injection; when administered by slow, continuous, intra-arterial infusion, it is converted to floxuridine monophosphate. It has been used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.. floxuridine : A pyrimidine 2'-deoxyribonucleoside compound having 5-fluorouracil as the nucleobase; used to treat hepatic metastases of gastrointestinal adenocarcinomas and for palliation in malignant neoplasms of the liver and gastrointestinal tract.		2.0510nucleoside analogue;
organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
radiosensitizing agent
piperonyl butoxide
[no description available]		2.0510benzodioxolespesticide synergist
bromouracil
Bromouracil: 5-Bromo-2,4(1H,3H)-pyrimidinedione. Brominated derivative of uracil that acts as an antimetabolite, substituting for thymine in DNA. It is used mainly as an experimental mutagen, but its deoxyriboside (BROMODEOXYURIDINE) is used to treat neoplasms.. 5-bromouracil : A pyrimidine having keto groups at the 2- and 4-positions and a bromo group at the 5-position. Used mainly as an experimental mutagen.		2.0510nucleobase analogue;
pyrimidines		mutagen
3,3',5-triiodothyroacetic acid
tiratricol : A monocarboxylic acid that is (4-hydroxy-3,5-diiodophenyl)acetic acid in which the phenolic hydroxy group has been replaced by a 4-hydroxy-3-iodophenoxy group. It is a thyroid hormone analogue that has been used in the treatment of thyroid hormone resistance syndrome.		2.0510
hydroxyproline
Hydroxyproline: A hydroxylated form of the imino acid proline. A deficiency in ASCORBIC ACID can result in impaired hydroxyproline formation.. hydroxyproline : A proline derivative that is proline substituted by at least one hydroxy group.		4.08504-hydroxyproline;
L-alpha-amino acid zwitterion		human metabolite;
mouse metabolite;
plant metabolite
histamine dihydrochloride
Ceplene: Tradename for histamine dihydrochloride.		2.0510
thyroxine
Thyroxine: The major hormone derived from the thyroid gland. Thyroxine is synthesized via the iodination of tyrosines (MONOIODOTYROSINE) and the coupling of iodotyrosines (DIIODOTYROSINE) in the THYROGLOBULIN. Thyroxine is released from thyroglobulin by proteolysis and secreted into the blood. Thyroxine is peripherally deiodinated to form TRIIODOTHYRONINE which exerts a broad spectrum of stimulatory effects on cell metabolism.. thyroxine : An iodothyronine compound having iodo substituents at the 3-, 3'-, 5- and 5'-positions.		4.68612-halophenol;
iodophenol;
L-phenylalanine derivative;
non-proteinogenic L-alpha-amino acid;
thyroxine zwitterion;
thyroxine		antithyroid drug;
human metabolite;
mouse metabolite;
thyroid hormone
dextroamphetamine
Dextroamphetamine: The d-form of AMPHETAMINE. It is a central nervous system stimulant and a sympathomimetic. It has also been used in the treatment of narcolepsy and of attention deficit disorders and hyperactivity in children. Dextroamphetamine has multiple mechanisms of action including blocking uptake of adrenergics and dopamine, stimulating release of monamines, and inhibiting monoamine oxidase. It is also a drug of abuse and a psychotomimetic.. (S)-amphetamine : A 1-phenylpropan-2-amine that has S configuration.		2.05101-phenylpropan-2-amineadrenergic agent;
adrenergic uptake inhibitor;
dopamine uptake inhibitor;
dopaminergic agent;
neurotoxin;
sympathomimetic agent
carbachol
Carbachol: A slowly hydrolyzed CHOLINERGIC AGONIST that acts at both MUSCARINIC RECEPTORS and NICOTINIC RECEPTORS.		2.4720ammonium salt;
carbamate ester		cardiotonic drug;
miotic;
muscarinic agonist;
nicotinic acetylcholine receptor agonist;
non-narcotic analgesic
norethindrone acetate
norethisterone acetate : A 3-oxo Delta(4)-steroid that is norethisterone in which the hydroxy group has been converted to its acetate ester.		2.05103-oxo-Delta(4) steroid;
acetate ester;
terminal acetylenic compound		progestin;
synthetic oral contraceptive
spironolactone
Spironolactone: A potassium sparing diuretic that acts by antagonism of aldosterone in the distal renal tubules. It is used mainly in the treatment of refractory edema in patients with congestive heart failure, nephrotic syndrome, or hepatic cirrhosis. Its effects on the endocrine system are utilized in the treatments of hirsutism and acne but they can lead to adverse effects. (From Martindale, The Extra Pharmacopoeia, 30th ed, p827). spironolactone : A steroid lactone that is 17alpha-pregn-4-ene-21,17-carbolactone substituted by an oxo group at position 3 and an alpha-acetylsulfanyl group at position 7.		2.97403-oxo-Delta(4) steroid;
oxaspiro compound;
steroid lactone;
thioester		aldosterone antagonist;
antihypertensive agent;
diuretic;
environmental contaminant;
xenobiotic
prednisolone acetate
prednisolone acetate: RN given refers to cpd with locant for acetate group in position 21 & (11 beta)-isomer		3.4311corticosteroid hormone
cyclobarbital
cyclobarbital: was heading 1977-94 (see under BARBITURATES 1977-90); CYCLOBARBITONE, HEXEMAL, & TETRAHYDROPHENOBARBITAL were see CYCLOBARBITAL 1977-94; use BARBITURATES to search CYCLOBARBITAL 1977-94; short to intermediate duration barbiturate used as hypnotic and sedative		2.0510barbiturates
aldosterone
[no description available]		2.411011beta-hydroxy steroid;
18-oxo steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid hormone;
mineralocorticoid;
primary alpha-hydroxy ketone;
steroid aldehyde		human metabolite;
mouse metabolite
allobarbital
allobarbital: was heading 1976-94 (see under BARBITURATES 1976-90); ALLOBARBITONE, DIALLYLBARBITAL, DIALLYLBARBITURIC ACID, & DIALLYLMAL were see ALLOBARBITAL 1976-94; use BARBITURATES to search ALLOBARBITAL 1976-94; a barbiturate derivative with effects of intermediate duration; at lower doses, it is used as a sedative; at higher doses, it displays hypnotic effects		2.0510barbiturates
penicillamine
Penicillamine: 3-Mercapto-D-valine. The most characteristic degradation product of the penicillin antibiotics. It is used as an antirheumatic and as a chelating agent in Wilson's disease.. penicillamine : An alpha-amino acid having the structure of valine substituted at the beta position with a sulfanyl group.		2.0510non-proteinogenic alpha-amino acid;
penicillamine		antirheumatic drug;
chelator;
copper chelator;
drug allergen
trichlorfon
Trichlorfon: An organochlorophosphate cholinesterase inhibitor that is used as an insecticide for the control of flies and roaches. It is also used in anthelmintic compositions for animals. (From Merck, 11th ed). trichlorfon : A phosphonic ester that is dimethyl phosphonate in which the hydrogen atom attched to the phosphorous is substituted by a 2,2,2-trichloro-1-hydroxyethyl group.		2.0510organic phosphonate;
organochlorine compound;
phosphonic ester		agrochemical;
anthelminthic drug;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
insecticide
prednisone
Prednisone: A synthetic anti-inflammatory glucocorticoid derived from CORTISONE. It is biologically inert and converted to PREDNISOLONE in the liver.. prednisone : A synthetic glucocorticoid drug that is particularly effective as an immunosuppressant, and affects virtually all of the immune system. Prednisone is a prodrug that is converted by the liver into prednisolone (a beta-hydroxy group instead of the oxo group at position 11), which is the active drug and also a steroid.		16.343411-oxo steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antineoplastic agent;
immunosuppressive agent;
prodrug
estrone
Hydroxyestrones: Estrone derivatives substituted with one or more hydroxyl groups in any position. They are important metabolites of estrone and other estrogens.		2.051017-oxo steroid;
3-hydroxy steroid;
phenolic steroid;
phenols		antineoplastic agent;
bone density conservation agent;
estrogen;
human metabolite;
mouse metabolite
fluprednisolone
Fluprednisolone: A synthetic glucocorticoid with anti-inflammatory properties.		2.0210fluorinated steroid
oxandrolone
Oxandrolone: A synthetic hormone with anabolic and androgenic properties.		2.051017beta-hydroxy steroid;
3-oxo steroid;
anabolic androgenic steroid;
oxa-steroid		anabolic agent;
androgen
dehydroepiandrosterone
Dehydroepiandrosterone: A major C19 steroid produced by the ADRENAL CORTEX. It is also produced in small quantities in the TESTIS and the OVARY. Dehydroepiandrosterone (DHEA) can be converted to TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE. Most of DHEA is sulfated (DEHYDROEPIANDROSTERONE SULFATE) before secretion.. dehydroepiandrosterone : An androstanoid that is androst-5-ene substituted by a beta-hydroxy group at position 3 and an oxo group at position 17. It is a naturally occurring steroid hormone produced by the adrenal glands.		2.051017-oxo steroid;
3beta-hydroxy-Delta(5)-steroid;
androstanoid		androgen;
human metabolite;
mouse metabolite
nad
[no description available]		2.0510NADgeroprotector
dichlororibofuranosylbenzimidazole
Dichlororibofuranosylbenzimidazole: An RNA polymerase II transcriptional inhibitor. This compound terminates transcription prematurely by selective inhibition of RNA synthesis. It is used in research to study underlying mechanisms of cellular regulation.		2.0310
penicillin g
Penicillin G: A penicillin derivative commonly used in the form of its sodium or potassium salts in the treatment of a variety of infections. It is effective against most gram-positive bacteria and against gram-negative cocci. It has also been used as an experimental convulsant because of its actions on GAMMA-AMINOBUTYRIC ACID mediated synaptic transmission.. benzylpenicillin : A penicillin in which the substituent at position 6 of the penam ring is a phenylacetamido group.		2.4520penicillin allergen;
penicillin		antibacterial drug;
drug allergen;
epitope
pilocarpine
Pilocarpine: A slowly hydrolyzed muscarinic agonist with no nicotinic effects. Pilocarpine is used as a miotic and in the treatment of glaucoma.. (+)-pilocarpine : The (+)-enantiomer of pilocarpine.		2.8730pilocarpineantiglaucoma drug
pentylenetetrazole
Pentylenetetrazole: A pharmaceutical agent that displays activity as a central nervous system and respiratory stimulant. It is considered a non-competitive GAMMA-AMINOBUTYRIC ACID antagonist. Pentylenetetrazole has been used experimentally to study seizure phenomenon and to identify pharmaceuticals that may control seizure susceptibility.. pentetrazol : An organic heterobicyclic compound that is 1H-tetrazole in which the hydrogens at positions 1 and 5 are replaced by a pentane-1,5-diyl group. A central and respiratory stimulant, it was formerly used for the treatment of cough and other respiratory tract disorders, cardiovascular disorders including hypotension, and pruritis.		2.610organic heterobicyclic compound;
organonitrogen heterocyclic compound
triiodothyronine
Triiodothyronine: A T3 thyroid hormone normally synthesized and secreted by the thyroid gland in much smaller quantities than thyroxine (T4). Most T3 is derived from peripheral monodeiodination of T4 at the 5' position of the outer ring of the iodothyronine nucleus. The hormone finally delivered and used by the tissues is mainly T3.. 3,3',5-triiodo-L-thyronine : An iodothyronine compound having iodo substituents at the 3-, 3'- and 5-positions. Although some is produced in the thyroid, most of the 3,3',5-triiodo-L-thyronine in the body is generated by mono-deiodination of L-thyroxine in the peripheral tissues. Its metabolic activity is about 3 to 5 times that of L-thyroxine. The sodium salt is used in the treatment of hypothyroidism.		4.36412-halophenol;
amino acid zwitterion;
iodophenol;
iodothyronine		human metabolite;
mouse metabolite;
thyroid hormone
carbon tetrachloride
Carbon Tetrachloride: A solvent for oils, fats, lacquers, varnishes, rubber waxes, and resins, and a starting material in the manufacturing of organic compounds. Poisoning by inhalation, ingestion or skin absorption is possible and may be fatal. (Merck Index, 11th ed). tetrachloromethane : A chlorocarbon that is methane in which all the hydrogens have been replaced by chloro groups.		3.3860chlorocarbon;
chloromethanes		hepatotoxic agent;
refrigerant
cantharidin
Cantharidin: A toxic compound, isolated from the Spanish fly or blistering beetle (Lytta (Cantharis) vesicatoria) and other insects. It is a potent and specific inhibitor of protein phosphatases 1 (PP1) and 2A (PP2A). This compound can produce severe skin inflammation, and is extremely toxic if ingested orally.. cantharidin : A monoterpenoid with an epoxy-bridged cyclic dicarboxylic anhydride structure secreted by many species of blister beetle, and most notably by the Spanish fly, Lytta vesicatoria. Natural toxin inhibitor of protein phosphatases 1 and 2A.		2.1310cyclic dicarboxylic anhydride;
monoterpenoid		EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
herbicide
alanine
Alanine: A non-essential amino acid that occurs in high levels in its free state in plasma. It is produced from pyruvate by transamination. It is involved in sugar and acid metabolism, increases IMMUNITY, and provides energy for muscle tissue, BRAIN, and the CENTRAL NERVOUS SYSTEM.. alanine : An alpha-amino acid that consists of propionic acid bearing an amino substituent at position 2.		4.460alanine zwitterion;
alanine;
L-alpha-amino acid;
proteinogenic amino acid;
pyruvate family amino acid		EC 4.3.1.15 (diaminopropionate ammonia-lyase) inhibitor;
fundamental metabolite
serine
Serine: A non-essential amino acid occurring in natural form as the L-isomer. It is synthesized from GLYCINE or THREONINE. It is involved in the biosynthesis of PURINES; PYRIMIDINES; and other amino acids.. serine : An alpha-amino acid that is alanine substituted at position 3 by a hydroxy group.		3.3260L-alpha-amino acid;
proteinogenic amino acid;
serine family amino acid;
serine zwitterion;
serine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
desoxycorticosterone acetate
Desoxycorticosterone Acetate: The 21-acetate derivative of desoxycorticosterone.		2.2510corticosteroid hormone
chloramphenicol
Amphenicol: Chloramphenicol and its derivatives.		2.0510C-nitro compound;
carboxamide;
diol;
organochlorine compound		antibacterial drug;
antimicrobial agent;
Escherichia coli metabolite;
geroprotector;
Mycoplasma genitalium metabolite;
protein synthesis inhibitor
aspartic acid
Aspartic Acid: One of the non-essential amino acids commonly occurring in the L-form. It is found in animals and plants, especially in sugar cane and sugar beets. It may be a neurotransmitter.. aspartic acid : An alpha-amino acid that consists of succinic acid bearing a single alpha-amino substituent. L-aspartic acid : The L-enantiomer of aspartic acid.		4.0550aspartate family amino acid;
aspartic acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
mouse metabolite;
neurotransmitter
glutamine
Glutamine: A non-essential amino acid present abundantly throughout the body and is involved in many metabolic processes. It is synthesized from GLUTAMIC ACID and AMMONIA. It is the principal carrier of NITROGEN in the body and is an important energy source for many cells.. L-glutamine : An optically active form of glutamine having L-configuration.. glutamine : An alpha-amino acid that consists of butyric acid bearing an amino substituent at position 2 and a carbamoyl substituent at position 4.		2.0510amino acid zwitterion;
glutamine family amino acid;
glutamine;
L-alpha-amino acid;
polar amino acid zwitterion;
proteinogenic amino acid		EC 1.14.13.39 (nitric oxide synthase) inhibitor;
Escherichia coli metabolite;
human metabolite;
metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
lysine
Lysine: An essential amino acid. It is often added to animal feed.. lysine : A diamino acid that is caproic (hexanoic) acid bearing two amino substituents at positions 2 and 6.. L-lysine : An L-alpha-amino acid; the L-isomer of lysine.		3.2960aspartate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
lysine;
organic molecular entity;
proteinogenic amino acid		algal metabolite;
anticonvulsant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
cetrimonium bromide
cetyltrimethylammonium bromide : The organic bromide salt that is the bromide salt of cetyltrimethylammonium; one of the components of the topical antiseptic cetrimide.		2.0510organic bromide salt;
quaternary ammonium salt		detergent;
surfactant
cyanides
Cyanides: Inorganic salts of HYDROGEN CYANIDE containing the -CN radical. The concept also includes isocyanides. It is distinguished from NITRILES, which denotes organic compounds containing the -CN radical.. cyanides : Salts and C-organyl derivatives of hydrogen cyanide, HC#N.. isocyanide : The isomer HN(+)#C(-) of hydrocyanic acid, HC#N, and its hydrocarbyl derivatives RNC (RN(+)#C(-)).. cyanide : A pseudohalide anion that is the conjugate base of hydrogen cyanide.		2.110pseudohalide anionEC 1.9.3.1 (cytochrome c oxidase) inhibitor
vincristine
[no description available]		2.4520acetate ester;
formamides;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent;
drug;
microtubule-destabilising agent;
plant metabolite;
tubulin modulator
physostigmine
Physostigmine: A cholinesterase inhibitor that is rapidly absorbed through membranes. It can be applied topically to the conjunctiva. It also can cross the blood-brain barrier and is used when central nervous system effects are desired, as in the treatment of severe anticholinergic toxicity.		2.0510carbamate ester;
indole alkaloid		antidote to curare poisoning;
EC 3.1.1.8 (cholinesterase) inhibitor;
miotic
sucrose
Saccharum: A plant genus of the family POACEAE widely cultivated in the tropics for the sweet cane that is processed into sugar.		2.0510glycosyl glycosidealgal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
osmolyte;
Saccharomyces cerevisiae metabolite;
sweetening agent
ethinyl estradiol
Ethinyl Estradiol: A semisynthetic alkylated ESTRADIOL with a 17-alpha-ethinyl substitution. It has high estrogenic potency when administered orally, and is often used as the estrogenic component in ORAL CONTRACEPTIVES.. 17alpha-ethynylestradiol : A 3-hydroxy steroid that is estradiol substituted by a ethynyl group at position 17. It is a xenoestrogen synthesized from estradiol and has been shown to exhibit high estrogenic potency on oral administration.		2.452017-hydroxy steroid;
3-hydroxy steroid;
terminal acetylenic compound		xenoestrogen
testosterone propionate
Testosterone Propionate: An ester of TESTOSTERONE with a propionate substitution at the 17-beta position.. androgen : A sex hormone that stimulates or controls the development and maintenance of masculine characteristics in vertebrates by binding to androgen receptors.		2.0510steroid ester
9,10-dimethyl-1,2-benzanthracene
9,10-Dimethyl-1,2-benzanthracene: Polycyclic aromatic hydrocarbon found in tobacco smoke that is a potent carcinogen.. 7,12-dimethyltetraphene : A tetraphene having methyl substituents at the 7- and 12-positions. It is a potent carcinogen and is present in tobacco smoke.		2.1710ortho-fused polycyclic arene;
tetraphenes		carcinogenic agent
apomorphine
Apomorphine: A derivative of morphine that is a dopamine D2 agonist. It is a powerful emetic and has been used for that effect in acute poisoning. It has also been used in the diagnosis and treatment of parkinsonism, but its adverse effects limit its use.		2.0510aporphine alkaloidalpha-adrenergic drug;
antidyskinesia agent;
antiparkinson drug;
dopamine agonist;
emetic;
serotonergic drug
aminopyrine
Aminopyrine: A pyrazolone with analgesic, anti-inflammatory, and antipyretic properties but has risk of AGRANULOCYTOSIS. A breath test with 13C-labeled aminopyrine has been used as a non-invasive measure of CYTOCHROME P-450 metabolic activity in LIVER FUNCTION TESTS.. aminophenazone : A pyrazolone that is 1,2-dihydro-3H-pyrazol-3-one substituted by a dimethylamino group at position 4, methyl groups at positions 1 and 5 and a phenyl group at position 2. It exhibits analgesic, anti-inflammatory, and antipyretic properties.		2.0510pyrazolone;
tertiary amino compound		antipyretic;
environmental contaminant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
methyltestosterone
Methyltestosterone: A synthetic hormone used for androgen replacement therapy and as an hormonal antineoplastic agent (ANTINEOPLASTIC AGENTS, HORMONAL).. methyltestosterone : A 17beta-hydroxy steroid that is testosterone bearing a methyl group at the 17alpha position.		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
enone		anabolic agent;
androgen;
antineoplastic agent
tetrabenazine
9,10-dimethoxy-3-isobutyl-1,3,4,6,7,11b-hexahydro-2H-pyrido[2,1-a]isoquinolin-2-one : A benzoquinolizine that is 1,2,3,4,4a,9,10,10a-octahydrophenanthrene in which the carbon at position 10a is replaced by a nitrogen and which is substituted by an isobutyl group at position 2, an oxo group at position 3, and methoxy groups at positions 6 and 7.		2.5220benzoquinolizine;
cyclic ketone;
tertiary amino compound
adenosine diphosphate
Adenosine Diphosphate: Adenosine 5'-(trihydrogen diphosphate). An adenine nucleotide containing two phosphate groups esterified to the sugar moiety at the 5'-position.		2.4220adenosine 5'-phosphate;
purine ribonucleoside 5'-diphosphate		fundamental metabolite;
human metabolite
cephalothin
Cephalothin: A cephalosporin antibiotic.. cefalotin : A semisynthetic, first-generation cephalosporin antibiotic with acetoxymethyl and (2-thienylacetyl)nitrilo moieties at positions 3 and 7, respectively, of the core structure. Administered parenterally during surgery and to treat a wide spectrum of blood infections.		2.0510azabicycloalkene;
beta-lactam antibiotic allergen;
carboxylic acid;
cephalosporin;
semisynthetic derivative;
thiophenes		antibacterial drug;
antimicrobial agent
uridine
[no description available]		2.4420uridinesdrug metabolite;
fundamental metabolite;
human metabolite
kanamycin a
Kanamycin: Antibiotic complex produced by Streptomyces kanamyceticus from Japanese soil. Comprises 3 components: kanamycin A, the major component, and kanamycins B and C, the minor components.. kanamycin : Kanamycin is a naturally occurring antibiotic complex from Streptomyces kanamyceticus that consists of several components: kanamycin A, the major component (also usually designated as kanamycin), and kanamycins B, C, D and X the minor components.		2.0510kanamycinsbacterial metabolite
bromodeoxyuridine
Bromodeoxyuridine: A nucleoside that substitutes for thymidine in DNA and thus acts as an antimetabolite. It causes breaks in chromosomes and has been proposed as an antiviral and antineoplastic agent. It has been given orphan drug status for use in the treatment of primary brain tumors.		3.360pyrimidine 2'-deoxyribonucleosideantimetabolite;
antineoplastic agent
galactose
galactopyranose : The pyranose form of galactose.		2.8130D-galactose;
galactopyranose		Escherichia coli metabolite;
mouse metabolite
carbostyril
Quinolones: A group of derivatives of naphthyridine carboxylic acid, quinoline carboxylic acid, or NALIDIXIC ACID.. quinolin-2(1H)-one : A quinolone that is 1,2-dihydroquinoline substituted by an oxo group at position 2.		9.25173monohydroxyquinoline;
quinolone		bacterial xenobiotic metabolite
phenylephrine
Phenylephrine: An alpha-1 adrenergic agonist used as a mydriatic, nasal decongestant, and cardiotonic agent.. phenylephrine : A member of the class of the class of phenylethanolamines that is (1R)-2-(methylamino)-1-phenylethan-1-ol carrying an additional hydroxy substituent at position 3 on the phenyl ring.		2.0510phenols;
phenylethanolamines;
secondary amino compound		alpha-adrenergic agonist;
cardiotonic drug;
mydriatic agent;
nasal decongestant;
protective agent;
sympathomimetic agent;
vasoconstrictor agent
levodopa
Levodopa: The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system.. L-dopa : An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinson's disease		2.7730amino acid zwitterion;
dopa;
L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		allelochemical;
antidyskinesia agent;
antiparkinson drug;
dopaminergic agent;
hapten;
human metabolite;
mouse metabolite;
neurotoxin;
plant growth retardant;
plant metabolite;
prodrug
edetic acid
Edetic Acid: A chelating agent that sequesters a variety of polyvalent cations such as CALCIUM. It is used in pharmaceutical manufacturing and as a food additive.		2.9210ethylenediamine derivative;
polyamino carboxylic acid;
tetracarboxylic acid		anticoagulant;
antidote;
chelator;
copper chelator;
geroprotector
tyrosine
Tyrosine: A non-essential amino acid. In animals it is synthesized from PHENYLALANINE. It is also the precursor of EPINEPHRINE; THYROID HORMONES; and melanin.. tyrosine : An alpha-amino acid that is phenylalanine bearing a hydroxy substituent at position 4 on the phenyl ring.		8.74570amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
tyrosine		EC 1.3.1.43 (arogenate dehydrogenase) inhibitor;
fundamental metabolite;
micronutrient;
nutraceutical
adenosine monophosphate
Adenosine Monophosphate: Adenine nucleotide containing one phosphate group esterified to the sugar moiety in the 2'-, 3'-, or 5'-position.		3.3510adenosine 5'-phosphate;
purine ribonucleoside 5'-monophosphate		adenosine A1 receptor agonist;
cofactor;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
EC 3.1.3.11 (fructose-bisphosphatase) inhibitor;
fundamental metabolite;
micronutrient;
nutraceutical
niridazole
Niridazole: An antischistosomal agent that has become obsolete.		2.05101,3-thiazoles;
C-nitro compound
methylene blue
Methylene Blue: A compound consisting of dark green crystals or crystalline powder, having a bronze-like luster. Solutions in water or alcohol have a deep blue color. Methylene blue is used as a bacteriologic stain and as an indicator. It inhibits GUANYLATE CYCLASE, and has been used to treat cyanide poisoning and to lower levels of METHEMOGLOBIN.. methylene blue : An organic chloride salt having 3,7-bis(dimethylamino)phenothiazin-5-ium as the counterion. A commonly used dye that also exhibits antioxidant, antimalarial, antidepressant and cardioprotective properties.		2.0510organic chloride saltacid-base indicator;
antidepressant;
antimalarial;
antimicrobial agent;
antioxidant;
cardioprotective agent;
EC 1.4.3.4 (monoamine oxidase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
EC 4.6.1.2 (guanylate cyclase) inhibitor;
fluorochrome;
histological dye;
neuroprotective agent;
physical tracer
leucine
Leucine: An essential branched-chain amino acid important for hemoglobin formation.. leucine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isobutyl group.		3.1350amino acid zwitterion;
L-alpha-amino acid;
leucine;
proteinogenic amino acid;
pyruvate family amino acid		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
ethyl methanesulfonate
Ethyl Methanesulfonate: An antineoplastic agent with alkylating properties. It also acts as a mutagen by damaging DNA and is used experimentally for that effect.. ethyl methanesulfonate : A methanesulfonate ester resulting from the formal condensation of methanesulfonic acid with ethanol.		7.4820methanesulfonate esteralkylating agent;
antineoplastic agent;
carcinogenic agent;
genotoxin;
mutagen;
teratogenic agent
methacholine chloride
Methacholine Chloride: A quaternary ammonium parasympathomimetic agent with the muscarinic actions of ACETYLCHOLINE. It is hydrolyzed by ACETYLCHOLINESTERASE at a considerably slower rate than ACETYLCHOLINE and is more resistant to hydrolysis by nonspecific CHOLINESTERASES so that its actions are more prolonged. It is used as a parasympathomimetic bronchoconstrictor agent and as a diagnostic aid for bronchial asthma. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1116)		5.0731quaternary ammonium salt
aniline
[no description available]		2.4820anilines;
primary arylamine
carbaryl
Carbaryl: A carbamate insecticide and parasiticide. It is a potent anticholinesterase agent belonging to the carbamate group of reversible cholinesterase inhibitors. It has a particularly low toxicity from dermal absorption and is used for control of head lice in some countries.. carbaryl : A carbamate ester obtained by the formal condensation of 1-naphthol with methylcarbamic acid.		2.0510carbamate ester;
naphthalenes		acaricide;
agrochemical;
carbamate insecticide;
EC 3.1.1.7 (acetylcholinesterase) inhibitor;
EC 3.1.1.8 (cholinesterase) inhibitor;
plant growth retardant
lactose
Lactose: A disaccharide of GLUCOSE and GALACTOSE in human and cow milk. It is used in pharmacy for tablets, in medicine as a nutrient, and in industry.. lactose : A glycosylglucose disaccharide, found most notably in milk, that consists of D-galactose and D-glucose fragments bonded through a beta-1->4 glycosidic linkage. The glucose fragment can be in either the alpha- or beta-pyranose form, whereas the galactose fragment can only have the beta-pyranose form.. beta-lactose : The beta-anomer of lactose.		2.0510lactose
methionine
Methionine: A sulfur-containing essential L-amino acid that is important in many body functions.. methionine : A sulfur-containing amino acid that is butyric acid bearing an amino substituent at position 2 and a methylthio substituent at position 4.		3.3160aspartate family amino acid;
L-alpha-amino acid;
methionine zwitterion;
methionine;
proteinogenic amino acid		antidote to paracetamol poisoning;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical
1,2-dipalmitoylphosphatidylcholine
1,2-Dipalmitoylphosphatidylcholine: Synthetic phospholipid used in liposomes and lipid bilayers to study biological membranes. It is also a major constituent of PULMONARY SURFACTANTS.		2.7630
phenylalanine
Phenylalanine: An essential aromatic amino acid that is a precursor of MELANIN; DOPAMINE; noradrenalin (NOREPINEPHRINE), and THYROXINE.. L-phenylalanine : The L-enantiomer of phenylalanine.. phenylalanine : An aromatic amino acid that is alanine in which one of the methyl hydrogens is substituted by a phenyl group.		4.0540amino acid zwitterion;
erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid;
phenylalanine;
proteinogenic amino acid		algal metabolite;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
Escherichia coli metabolite;
human xenobiotic metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
Mebutamate
[no description available]		2.0510organic molecular entity
desoxycorticosterone
Desoxycorticosterone: A steroid metabolite that is the 11-deoxy derivative of CORTICOSTERONE and the 21-hydroxy derivative of PROGESTERONE		2.071020-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
mineralocorticoid;
primary alpha-hydroxy ketone		human metabolite;
mouse metabolite
colchicine
(S)-colchicine : A colchicine that has (S)-configuration. It is a secondary metabolite, has anti-inflammatory properties and is used to treat gout, crystal-induced joint inflammation, familial Mediterranean fever, and many other conditions.		5.2860alkaloid;
colchicine		anti-inflammatory agent;
gout suppressant;
mutagen
oxacillin
Oxacillin: An antibiotic similar to FLUCLOXACILLIN used in resistant staphylococci infections.. oxacillin : A penicillin antibiotic carrying a 5-methyl-3-phenylisoxazole-4-carboxamide group at position 6beta.		2.0610penicillinantibacterial agent;
antibacterial drug
cycloheximide
Cycloheximide: Antibiotic substance isolated from streptomycin-producing strains of Streptomyces griseus. It acts by inhibiting elongation during protein synthesis.. cycloheximide : A dicarboximide that is 4-(2-hydroxyethyl)piperidine-2,6-dione in which one of the hydrogens attached to the carbon bearing the hydroxy group is replaced by a 3,5-dimethyl-2-oxocyclohexyl group. It is an antibiotic produced by the bacterium Streptomyces griseus.		3.2860antibiotic fungicide;
cyclic ketone;
dicarboximide;
piperidine antibiotic;
piperidones;
secondary alcohol		anticoronaviral agent;
bacterial metabolite;
ferroptosis inhibitor;
neuroprotective agent;
protein synthesis inhibitor
egtazic acid
Egtazic Acid: A chelating agent relatively more specific for calcium and less toxic than EDETIC ACID.. ethylene glycol bis(2-aminoethyl)tetraacetic acid : A diether that is ethylene glycol in which the hydrogens of the hydroxy groups have been replaced by 2-[bis(carboxymethyl)amino]ethyl group respectively.		2.0810diether;
tertiary amino compound;
tetracarboxylic acid		chelator
chloroform
Chloroform: A commonly used laboratory solvent. It was previously used as an anesthetic, but was banned from use in the U.S. due to its suspected carcinogenicity.. chloroform : A one-carbon compound that is methane in which three of the hydrogens are replaced by chlorines.		2.0310chloromethanes;
one-carbon compound		carcinogenic agent;
central nervous system drug;
inhalation anaesthetic;
non-polar solvent;
refrigerant
norethindrone
Norethindrone: A synthetic progestational hormone with actions similar to those of PROGESTERONE but functioning as a more potent inhibitor of ovulation. It has weak estrogenic and androgenic properties. The hormone has been used in treating amenorrhea, functional uterine bleeding, endometriosis, and for CONTRACEPTION.. norethisterone : A 17beta-hydroxy steroid that is testosterone in which the hydrogen at position 17 is replaced by an ethynyl group and in which the methyl group attached to position 10 is replaced by hydrogen.		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
terminal acetylenic compound;
tertiary alcohol		progestin;
synthetic oral contraceptive
norethynodrel
Norethynodrel: A synthetic progestational hormone with actions and uses similar to those of PROGESTERONE. It has been used in the treatment of functional uterine bleeding and ENDOMETRIOSIS. As a contraceptive (CONTRACEPTIVE AGENTS), it has usually been administered in combination with MESTRANOL.		2.0510oxo steroid
benziodarone
benziodarone: minor descriptor (75-89); on-line & INDEX MEDICUS search BENZOFURANS (68-89) & IODOBENZOATES (74)		2.0510aromatic ketone
ampicillin
Ampicillin: Semi-synthetic derivative of penicillin that functions as an orally active broad-spectrum antibiotic.. ampicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-phenylacetamido group.		2.0510beta-lactam antibiotic;
penicillin allergen;
penicillin		antibacterial drug
mannitol
[no description available]		2.4620mannitolallergen;
antiglaucoma drug;
compatible osmolytes;
Escherichia coli metabolite;
food anticaking agent;
food bulking agent;
food humectant;
food stabiliser;
food thickening agent;
hapten;
metabolite;
osmotic diuretic;
sweetening agent
cytarabine
[no description available]		19.5115457beta-D-arabinoside;
monosaccharide derivative;
pyrimidine nucleoside		antimetabolite;
antineoplastic agent;
antiviral agent;
immunosuppressive agent
asparagine
Asparagine: A non-essential amino acid that is involved in the metabolic control of cell functions in nerve and brain tissue. It is biosynthesized from ASPARTIC ACID and AMMONIA by asparagine synthetase. (From Concise Encyclopedia Biochemistry and Molecular Biology, 3rd ed). asparagine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 2-amino-2-oxoethyl group.		2.4920amino acid zwitterion;
asparagine;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
histidine
Histidine: An essential amino acid that is required for the production of HISTAMINE.. L-histidine : The L-enantiomer of the amino acid histidine.. histidine : An alpha-amino acid that is propanoic acid bearing an amino substituent at position 2 and a 1H-imidazol-4-yl group at position 3.		5.2331amino acid zwitterion;
histidine;
L-alpha-amino acid;
polar amino acid zwitterion;
proteinogenic amino acid		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
medroxyprogesterone acetate
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
corticosteroid;
steroid ester		adjuvant;
androgen;
antineoplastic agent;
antioxidant;
female contraceptive drug;
inhibitor;
progestin;
synthetic oral contraceptive
sulfobromophthalein sodium
bromosulfophthalein sodium : An organic sodium salt that is the disodium salt of bromosulfophthalein.. bromosulfophthalein : An organosulfonic acid that consists of phthalide bearing four bromo substituents at positions 4, 5, 6 and 7 as well as two 4-hydroxy-3-sulfophenyl groups both located at position 1.		2.0410organic sodium saltdye
valine
Valine: A branched-chain essential amino acid that has stimulant activity. It promotes muscle growth and tissue repair. It is a precursor in the penicillin biosynthetic pathway.. valine : A branched-chain amino acid that consists of glycine in which one of the hydrogens attached to the alpha-carbon is substituted by an isopropyl group.. L-valine : The L-enantiomer of valine.		5.4470L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
pyruvate family amino acid;
valine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
threonine
Threonine: An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins.. threonine : An alpha-amino acid in which one of the hydrogens attached to the alpha-carbon of glycine is substituted by a 1-hydroxyethyl group.		4.2160amino acid zwitterion;
aspartate family amino acid;
L-alpha-amino acid;
proteinogenic amino acid;
threonine		algal metabolite;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
mestranol
[no description available]		2.051017beta-hydroxy steroid;
aromatic ether;
terminal acetylenic compound		prodrug;
xenoestrogen
methaqualone
Methaqualone: A quinazoline derivative with hypnotic and sedative properties. It has been withdrawn from the market in many countries because of problems with abuse. (From Martindale, The Extra Pharmacopoeia, 30th ed, p604). methaqualone : A member of the class of quinazolines that is quinazolin-4-one substituted at positions 2 and 3 by methyl and o-tolyl groups respectively. A depressant that increases the activity of the GABA receptors in the brain and nervous system, it is used as a sedative and hypnotic medication. It became popular as a recreational drug and club drug in the late 1960s and 1970s.		2.0510quinazolinesGABA agonist;
sedative
trypan blue
VisionBlue: A trypan blue ophthalmic solution.		2.0510
cordycepin
[no description available]		2.05103'-deoxyribonucleoside;
adenosines		antimetabolite;
nucleoside antibiotic
tryptophan
Tryptophan: An essential amino acid that is necessary for normal growth in infants and for NITROGEN balance in adults. It is a precursor of INDOLE ALKALOIDS in plants. It is a precursor of SEROTONIN (hence its use as an antidepressant and sleep aid). It can be a precursor to NIACIN, albeit inefficiently, in mammals.. tryptophan : An alpha-amino acid that is alanine bearing an indol-3-yl substituent at position 3.		2.7630erythrose 4-phosphate/phosphoenolpyruvate family amino acid;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid;
tryptophan zwitterion;
tryptophan		antidepressant;
Escherichia coli metabolite;
human metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
plant metabolite;
Saccharomyces cerevisiae metabolite
isoleucine
Isoleucine: An essential branched-chain aliphatic amino acid found in many proteins. It is an isomer of LEUCINE. It is important in hemoglobin synthesis and regulation of blood sugar and energy levels.. isoleucine : A 2-amino-3-methylpentanoic acid having either (2R,3R)- or (2S,3S)-configuration.. L-isoleucine : The L-enantiomer of isoleucine.		3.6890aspartate family amino acid;
isoleucine;
L-alpha-amino acid zwitterion;
L-alpha-amino acid;
proteinogenic amino acid		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
arginine
Arginine: An essential amino acid that is physiologically active in the L-form.. arginine : An alpha-amino acid that is glycine in which the alpha-is substituted by a 3-guanidinopropyl group.		2.9840arginine;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		biomarker;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical
ethylene
Plastipore: high density polyethylene sponge biocompatible material; used as posts in dental bridges		4.6111alkene;
gas molecular entity		plant hormone;
refrigerant
acetonitrile
acetonitrile: RN given refers to unlabeled cpd. acetonitrile : A nitrile that is hydrogen cyanide in which the hydrogen has been replaced by a methyl group.		2.2110aliphatic nitrile;
volatile organic compound		EC 3.5.1.4 (amidase) inhibitor;
NMR chemical shift reference compound;
polar aprotic solvent
methylene chloride
Methylene Chloride: A chlorinated hydrocarbon that has been used as an inhalation anesthetic and acts as a narcotic in high concentrations. Its primary use is as a solvent in manufacturing and food technology.. dichloromethane : A member of the class of chloromethanes that is methane in which two of the hydrogens have been replaced by chlorine. A dense, non-flammible colourless liquid at room temperature (b.p. 40degreeC, d = 1.33) which is immiscible with water, it is widely used as a solvent, a paint stripper, and for the removal of caffeine from coffee and tea.		2.4110chloromethanes;
volatile organic compound		carcinogenic agent;
polar aprotic solvent;
refrigerant
trichloroacetic acid
Trichloroacetic Acid: A strong acid used as a protein precipitant in clinical chemistry and also as a caustic for removing warts.. trichloroacetic acid : A monocarboxylic acid that is acetic acid in which all three methyl hydrogens are substituted by chlorine.		2.0510monocarboxylic acid;
organochlorine compound		carcinogenic agent;
metabolite;
mouse metabolite
triamcinolone acetonide
Triamcinolone Acetonide: An esterified form of TRIAMCINOLONE. It is an anti-inflammatory glucocorticoid used topically in the treatment of various skin disorders. Intralesional, intramuscular, and intra-articular injections are also administered under certain conditions.. triamcinolone acetonide : A synthetic glucocorticoid that is the 16,17-acetonide of triamcinolone. Used to treat various skin infections.		2.051011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
cyclic ketal;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone		anti-allergic agent;
anti-inflammatory drug
allylpropymal
allylpropymal: RN given refers to parent cpd. aprobarbital : A member of the class of barbiturates that is pyrimidine-2,4,6(1H,3H,5H)-trione substituted by an isopropyl and a prop-1-en-3-yl group at position 5.		2.0510barbiturates
butobarbital
butobarbital: Butobarbital should be distinguished from Butabarbital (a synonym for Secbutabarbital)		2.0510barbiturates
tromethamine
Tromethamine: An organic amine proton acceptor. It is used in the synthesis of surface-active agents and pharmaceuticals; as an emulsifying agent for cosmetic creams and lotions, mineral oil and paraffin wax emulsions, as a biological buffer, and used as an alkalizer. (From Merck, 11th ed; Martindale, The Extra Pharmacopoeia, 30th ed, p1424)		2.5920primary amino compound;
triol		buffer
trichloroethylene
Trichloroethylene: A highly volatile inhalation anesthetic used mainly in short surgical procedures where light anesthesia with good analgesia is required. It is also used as an industrial solvent. Prolonged exposure to high concentrations of the vapor can lead to cardiotoxicity and neurological impairment.. triol : A chemical compound containing three hydroxy groups.		2.0510chloroethenesinhalation anaesthetic;
mouse metabolite
acrylic acid
acrylic acid: RN given refers to parent cpd. acrylic acid : A alpha,beta-unsaturated monocarboxylic acid that is ethene substituted by a carboxy group.		2.1110alpha,beta-unsaturated monocarboxylic acidmetabolite
dichloroacetic acid
[no description available]		5.2431monocarboxylic acid;
organochlorine compound		astringent;
marine metabolite
methylmethacrylate
Methylmethacrylate: The methyl ester of methacrylic acid. It polymerizes easily to form POLYMETHYL METHACRYLATE. It is used as a bone cement.. methyl methacrylate : An enoate ester having methacrylic acid as the carboxylic acid component and methanol as the alcohol component.		2.2510enoate ester;
methyl ester		allergen;
polymerisation monomer
dehydrocholic acid
Dehydrocholic Acid: A semisynthetic bile acid made from cholic acid. It is used as a cholagogue, hydrocholeretic, diuretic, and as a diagnostic aid.. 3,7,12-trioxo-5beta-cholanic acid : An oxo-5beta-cholanic acid in which three oxo substituents are located at positions 3, 7 and 12 on the cholanic acid skeleton.		2.051012-oxo steroid;
3-oxo-5beta-steroid;
7-oxo steroid;
oxo-5beta-cholanic acid		gastrointestinal drug
taurocholic acid
Taurocholic Acid: The product of conjugation of cholic acid with taurine. Its sodium salt is the chief ingredient of the bile of carnivorous animals. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as a cholagogue and cholerectic.. taurocholate : An organosulfonate oxoanion that is the conjugate base of taurocholic acid.. taurocholic acid : A bile acid taurine conjugate of cholic acid that usually occurs as the sodium salt of bile in mammals.		2.4920amino sulfonic acid;
bile acid taurine conjugate		human metabolite
methylprednisolone
Methylprednisolone: A PREDNISOLONE derivative with similar anti-inflammatory action.. 6alpha-methylprednisolone : The 6alpha-stereoisomer of 6-methylprednisolone.		5.621306-methylprednisolone;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		adrenergic agent;
anti-inflammatory drug;
antiemetic;
environmental contaminant;
neuroprotective agent;
xenobiotic
rotenone
Derris: A plant genus of the family FABACEAE. The root is a source of rotenoids (ROTENONE) and flavonoids. Some species of Pongamia have been reclassified to this genus and some to MILLETTIA. Some species of Deguelia have been reclassified to this genus.. rotenoid : Members of the class of tetrahydrochromenochromene that consists of a cis-fused tetrahydrochromeno[3,4-b]chromene skeleton and its substituted derivatives. The term was originally restricted to natural products, but is now also used to describe semi-synthetic and fully synthetic compounds.		2.0410organic heteropentacyclic compound;
rotenones		antineoplastic agent;
metabolite;
mitochondrial NADH:ubiquinone reductase inhibitor;
phytogenic insecticide;
piscicide;
toxin
isosorbide dinitrate
Isosorbide Dinitrate: A vasodilator used in the treatment of ANGINA PECTORIS. Its actions are similar to NITROGLYCERIN but with a slower onset of action.		2.0510glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
n-vinyl-2-pyrrolidinone
N-vinyl-2-pyrrolidinone: monomer of POVIDONE; structure given in first source		2.2510pyrrolidin-2-ones
quinoxalines
quinoxaline : A naphthyridine in which the nitrogens are at positions 1 and 4.		5.541mancude organic heterobicyclic parent;
naphthyridine;
ortho-fused heteroarene
synephrine
[no description available]		2.0510ethanolamines;
phenethylamine alkaloid;
phenols		alpha-adrenergic agonist;
plant metabolite
benzoyl peroxide
Benzoyl Peroxide: A peroxide derivative that has been used topically for BURNS and as a dermatologic agent in the treatment of ACNE and POISON IVY DERMATITIS. It is used also as a bleach in the food industry.		2.0510carbonyl compound
trehalose
alpha,alpha-trehalose : A trehalose in which both glucose residues have alpha-configuration at the anomeric carbon.		2.0510trehaloseEscherichia coli metabolite;
geroprotector;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
pyridostigmine bromide
Pyridostigmine Bromide: A cholinesterase inhibitor with a slightly longer duration of action than NEOSTIGMINE. It is used in the treatment of myasthenia gravis and to reverse the actions of muscle relaxants.		2.5520pyridinium salt
monobenzone
monobenzone: structure. monobenzone : The monobenzyl ether of hydroquinone. It is used as a topical drug for medical depigmentation.		3.2510benzyl etherallergen;
dermatologic drug;
melanin synthesis inhibitor
caprolactam
Caprolactam: Cyclic amide of caproic acid used in manufacture of synthetic fibers of the polyamide type. Can cause local irritation.. epsilon-caprolactam : A member of the class of caprolactams that is azepane substituted by an oxo group at position 2.		10.3631caprolactamshuman blood serum metabolite
chlorobenzene
[no description available]		2.0510monochlorobenzenessolvent
pyrroles
1H-pyrrole : A tautomer of pyrrole that has the double bonds at positions 2 and 4.. pyrrole : A five-membered monocyclic heteroarene comprising one NH and four CH units which forms the parent compound of the pyrrole group of compounds. Its five-membered ring structure has three tautomers. A 'closed class'.. azole : Any monocyclic heteroarene consisting of a five-membered ring containing nitrogen. Azoles can also contain one or more other non-carbon atoms, such as nitrogen, sulfur or oxygen.		21.5533340pyrrole;
secondary amine
furan
furan : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing four carbons and one oxygen, with formula C4H4O. It is a toxic, flammable, low-boiling (31degreeC) colourless liquid.		2.0510furans;
mancude organic heteromonocyclic parent;
monocyclic heteroarene		carcinogenic agent;
hepatotoxic agent;
Maillard reaction product
thiophenes
Thiophenes: A monocyclic heteroarene furan in which the oxygen atom is replaced by a sulfur.. thiophenes : Compounds containing at least one thiophene ring.		6.4971mancude organic heteromonocyclic parent;
monocyclic heteroarene;
thiophenes;
volatile organic compound		non-polar solvent
isopropyl myristate
isopropyl myristate: used for microemulsions; structure		4.6111fatty acid ester
ergotamine
Ergotamine: A vasoconstrictor found in ergot of Central Europe. It is a serotonin agonist that has been used as an oxytocic agent and in the treatment of MIGRAINE DISORDERS.. ergotamine : A peptide ergot alkaloid that is dihydroergotamine in which a double bond replaces the single bond between positions 9 and 10.		2.0510peptide ergot alkaloidalpha-adrenergic agonist;
mycotoxin;
non-narcotic analgesic;
oxytocic;
serotonergic agonist;
vasoconstrictor agent
neostigmine bromide
neostigmine bromide : The bromide salt of neostigmine.		2.0510bromide salt
phenformin
Phenformin: A biguanide hypoglycemic agent with actions and uses similar to those of METFORMIN. Although it is generally considered to be associated with an unacceptably high incidence of lactic acidosis, often fatal, it is still available in some countries. (From Martindale, The Extra Pharmacopoeia, 30th ed, p290). phenformin : A member of the class of biguanides that is biguanide in which one of the terminal nitrogen atoms is substituted by a 2-phenylethyl group. It was used as an anti-diabetic drug but was later withdrawn from the market due to potential risk of lactic acidosis.		4.140biguanidesantineoplastic agent;
geroprotector;
hypoglycemic agent
mephobarbital
Mephobarbital: A barbiturate that is metabolized to PHENOBARBITAL. It has been used for similar purposes, especially in EPILEPSY, but there is no evidence mephobarbital offers any advantage over PHENOBARBITAL.. mephobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at N-1 by a methyl group and at C-5 by ethyl and phenyl groups.		2.0510barbituratesanticonvulsant
hexachlorobenzene
Hexachlorobenzene: An agricultural fungicide and seed treatment agent.. hexachlorobenzene : A member of the class of chlorobenzenes that is benzene in which all of the hydrogens are replaced by chlorines. An agricultural fungicide introduced in the mid-1940s and formerly used as a seed treatment, its use has been banned since 1984 under the Stockholm Convention on Persistent Organic Pollutants.		2.0510aromatic fungicide;
chlorobenzenes		antifungal agrochemical;
carcinogenic agent;
persistent organic pollutant
trinitrotoluene
Trinitrotoluene: A 2,4,6-trinitrotoluene, which is an explosive chemical that can cause skin irritation and other toxic consequences.. 2,4,6-trinitrotoluene : A trinitrotoluene having the nitro groups at positions 2, 4 and 6.		2.0510trinitrotolueneexplosive
framycetin
Framycetin: A component of NEOMYCIN that is produced by Streptomyces fradiae. On hydrolysis it yields neamine and neobiosamine B. (From Merck Index, 11th ed). framycetin : A tetracyclic antibacterial agent derived from neomycin, being a glycoside ester of neamine and neobiosamine B.		2.0510aminoglycosideallergen;
antibacterial drug;
Escherichia coli metabolite
pyrazolanthrone
pyrazolanthrone: JNK (c-Jun N-terminal kinase) inhibitor; structure in first source. anthra[1,9-cd]pyrazol-6(2H)-one : A member of the class of anthrapyrazoles that is anthra[1,9-cd]pyrazole substituted at position 6 by an oxo group. An inhibitor of c-Jun N-terminal kinase.		3.3460anthrapyrazole;
aromatic ketone;
cyclic ketone		antineoplastic agent;
c-Jun N-terminal kinase inhibitor;
geroprotector
1,4-naphthoquinone
naphthoquinone : A polycyclic aromatic ketone metabolite of naphthalene.. 1,4-naphthoquinone : The parent structure of the family of 1,4-naphthoquinones, in which the oxo groups of the quinone moiety are at positions 1 and 4 of the naphthalene ring. Derivatives have pharmacological properties.		2.03101,4-naphthoquinones
meglumine
Meglumine: 1-Deoxy-1-(methylamino)-D-glucitol. A derivative of sorbitol in which the hydroxyl group in position 1 is replaced by a methylamino group. Often used in conjunction with iodinated organic compounds as contrast medium.. N-methylglucamine : A hexosamine that is D-glucitol in which the hydroxy group at position 1 is substituted by the nitrogen of a methylamino group. A crystalline base, it is used in preparing salts of certain acids for use as diagnostic radiopaque media, while its antimonate is used as an antiprotozoal in the treatment of leishmaniasis.		2.0510hexosamine;
secondary amino compound
cinchophen
cinchophen: was heading 1963-94; ACIPHENOCHINOLIUM was see CHINOPHEN 1978-94; use QUINOLINES to search CINCHOPHEN 1966-94		2.0510quinolines
1-naphthylamine
1-Naphthylamine: A suspected industrial carcinogen (and listed as such by OSHA). Its N-hydroxy metabolite is strongly carcinogenic and mutagenic.. naphthylamine : A primary arylamine that is naphthalene substituted by an amino group at unspecified position.. 1-naphthylamine : A naphthylamine that is naphthalene substituted by an amino group at position 1.		2.1310naphthylaminehuman xenobiotic metabolite
2-naphthol
2-naphthol: RN given refers to parent cpd. 2-naphthol : A naphthol carrying a hydroxy group at position 2.. naphthols : Any hydroxynaphthalene derivative that has a single hydroxy substituent.		2.1510naphtholantinematodal drug;
genotoxin;
human urinary metabolite;
human xenobiotic metabolite;
mouse metabolite;
radical scavenger
yohimbine
Yohimbine: A plant alkaloid with alpha-2-adrenergic blocking activity. Yohimbine has been used as a mydriatic and in the treatment of ERECTILE DYSFUNCTION.. yohimbine : An indole alkaloid with alpha2-adrenoceptor antagonist activity. It is produced by Corynanthe johimbe and Rauwolfia serpentina.		2.0510methyl 17-hydroxy-20xi-yohimban-16-carboxylatealpha-adrenergic antagonist;
dopamine receptor D2 antagonist;
serotonergic antagonist
mequinol
mequinol: depigmenting agent; RN given refers to parent cpd		3.5920methoxybenzenes;
phenols		metabolite
quinestrol
Quinestrol: The 3-cyclopentyl ether of ETHINYL ESTRADIOL. After gastrointestinal absorption, it is stored in ADIPOSE TISSUE, slowly released, and metabolized principally to the parent compound. It has been used in ESTROGEN REPLACEMENT THERAPY. (From AMA Drug Evaluations Annual, 1992, p1011)		2.051017-hydroxy steroid;
terminal acetylenic compound		xenoestrogen
dydrogesterone
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid		progestin
catechin
Catechin: An antioxidant flavonoid, occurring especially in woody plants as both (+)-catechin and (-)-epicatechin (cis) forms.. catechin : Members of the class of hydroxyflavan that have a flavan-3-ol skeleton and its substituted derivatives.. rac-catechin : A racemate comprising equimolar amounts of (+)- and (-)-catechin. (+)-catechin : The (+)-enantiomer of catechin and a polyphenolic antioxidant plant metabolite.		2.4720catechinantioxidant;
plant metabolite
perylene
Perylene: A 20-carbon dibenz(de,kl)anthracene that can be viewed as a naphthalene fused to a phenalene or as dinaphthalene. It is used as fluorescent lipid probe in the cytochemistry of membranes and is a polycyclic hydrocarbon pollutant in soil and water. Derivatives may be carcinogenic.. perylene : An ortho- and peri-fused polycyclic arene comprising of five benzene rings that is anthracene in which the d,e and k,l sides are fused to benzene rings.		2.0510ortho- and peri-fused polycyclic arene;
perylenes
quinazolines
Quinazolines: A group of aromatic heterocyclic compounds that contain a bicyclic structure with two fused six-membered aromatic rings, a benzene ring and a pyrimidine ring.. quinazoline : A mancude organic heterobicyclic parent that is naphthalene in which the carbon atoms at positions 1 and 3 have been replaced by nitrogen atoms.. quinazolines : Any organic heterobicyclic compound based on a quinazoline skeleton and its substituted derivatives.		14.011172azaarene;
mancude organic heterobicyclic parent;
ortho-fused heteroarene;
quinazolines
acridines
Acridines: Compounds that include the structure of acridine.. acridine : A polycyclic heteroarene that is anthracene in which one of the central CH groups is replaced by a nitrogen atom.		3.1450acridines;
mancude organic heterotricyclic parent;
polycyclic heteroarene		genotoxin
indazoles
Indazoles: A group of heterocyclic aromatic organic compounds consisting of the fusion of BENZENE and PYRAZOLES.		10.44272indazole
benzoxazoles
1,3-benzoxazole : A benzoxazole in which the benzene ring is fused to a 1,3-oxazole ring across positions 4 and 5.. benzoxazole : Compounds based on a fused 1,2- or 1,3-oxazole and benzene bicyclic ring skeleton.		4.61111,3-benzoxazoles;
mancude organic heterobicyclic parent
adamantane
Adamantane: A tricyclo bridged hydrocarbon.		3.6590adamantanes;
polycyclic alkane
cyclopentane
Cyclopentanes: A group of alicyclic hydrocarbons with the general formula R-C5H9.. cyclopentanes : Cyclopentane and its derivatives formed by substitution.		2.5920cycloalkane;
cyclopentanes;
volatile organic compound		non-polar solvent
isoxazoles
Isoxazoles: Azoles with an OXYGEN and a NITROGEN next to each other at the 1,2 positions, in contrast to OXAZOLES that have nitrogens at the 1,3 positions.. isoxazole : A monocyclic heteroarene with a structure consisting of a 5-membered ring containing three carbon atoms and an oxygen and nitrogen atom adjacent to each other. It is the parent of the class of isoxazoles.. isoxazoles : Oxazoles in which the N and O atoms are adjacent.		5.8260isoxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
oxazoles
Oxazoles: Five-membered heterocyclic ring structures containing an oxygen in the 1-position and a nitrogen in the 3-position, in distinction from ISOXAZOLES where they are at the 1,2 positions.. 1,3-oxazole : A five-membered monocyclic heteroarene that is an analogue of cyclopentadiene with O in place of CH2 at position 1 and N in place of CH at position 3.. oxazole : An azole based on a five-membered heterocyclic aromatic skeleton containing one N and one O atom.		3.87301,3-oxazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
thiazoles
[no description available]		23.58593721,3-thiazoles;
mancude organic heteromonocyclic parent;
monocyclic heteroarene
pyrimidine
pyrimidine : The parent compound of the pyrimidines; a diazine having the two nitrogens at the 1- and 3-positions.		2.7230diazine;
pyrimidines		Daphnia magna metabolite
pyrazines
Pyrazines: A heterocyclic aromatic organic compound with the chemical formula C4H4N2.. pyrazine : A diazine that is benzene in which the carbon atoms at positions 1 and 4 have been replaced by nitrogen atoms.		12.83445diazine;
pyrazines		Daphnia magna metabolite
ephedrine
Ephedrine: A phenethylamine found in EPHEDRA SINICA. PSEUDOEPHEDRINE is an isomer. It is an alpha- and beta-adrenergic agonist that may also enhance release of norepinephrine. It has been used for asthma, heart failure, rhinitis, and urinary incontinence, and for its central nervous system stimulatory effects in the treatment of narcolepsy and depression. It has become less extensively used with the advent of more selective agonists.. (-)-ephedrine : A phenethylamine alkaloid that is 2-phenylethanamine substituted by a methyl group at the amino nitrogen and a methyl and a hydroxy group at position 2 and 1 respectively.		2.0510phenethylamine alkaloid;
phenylethanolamines		bacterial metabolite;
environmental contaminant;
nasal decongestant;
plant metabolite;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
hydrazine
diamine : Any polyamine that contains two amino groups.		4.8250azane;
hydrazines		EC 4.3.1.10 (serine-sulfate ammonia-lyase) inhibitor
chlormadinone acetate
Chlormadinone Acetate: An orally active synthetic progestational hormone used often in combinations as an oral contraceptive (CONTRACEPTIVES, ORAL).		2.0510corticosteroid hormone
2,3-dimercaptosuccinic acid
[no description available]		2.0510
evans blue
Evans Blue: An azo dye used in blood volume and cardiac output measurement by the dye dilution method. It is very soluble, strongly bound to plasma albumin, and disappears very slowly.. Evans blue : An organic sodium salt that is the tetrasodium salt of 6,6'-{(3,3'-dimethyl[1,1'-biphenyl]-4,4'-diyl)bis[diazene-2,1-diyl]}bis(4-amino-5-hydroxynaphthalene-1,3-disulfonate). It is sometimes used as a counterstain, especially in fluorescent methods to suppress background autofluorescence.		3.9340organic sodium saltfluorochrome;
histological dye;
sodium channel blocker;
teratogenic agent
monocrotaline
Monocrotaline: A pyrrolizidine alkaloid and a toxic plant constituent that poisons livestock and humans through the ingestion of contaminated grains and other foods. The alkaloid causes pulmonary artery hypertension, right ventricular hypertrophy, and pathological changes in the pulmonary vasculature. Significant attenuation of the cardiopulmonary changes are noted after oral magnesium treatment.		5.57151pyrrolizidine alkaloid
testosterone enanthate
[no description available]		2.0510heptanoate ester;
sterol ester		androgen
aminophylline
Aminophylline: A drug combination that contains THEOPHYLLINE and ethylenediamine. It is more soluble in water than theophylline but has similar pharmacologic actions. It's most common use is in bronchial asthma, but it has been investigated for several other applications.. aminophylline : A mixture comprising of theophylline and ethylenediamine in a 2:1 ratio.		2.0510mixturebronchodilator agent;
cardiotonic drug
azacitidine
Azacitidine: A pyrimidine analogue that inhibits DNA methyltransferase, impairing DNA methylation. It is also an antimetabolite of cytidine, incorporated primarily into RNA. Azacytidine has been used as an antineoplastic agent.. 5-azacytidine : An N-glycosyl-1,3,5-triazine that is 4-amino-1,3,5-triazin-2(1H)-one substituted by a beta-D-ribofuranosyl residue via an N-glycosidic linkage. An antineoplastic agent, it is used in the treatment of myeloid leukaemia.		10.13202N-glycosyl-1,3,5-triazine;
nucleoside analogue		antineoplastic agent
phenyramidol
phenyramidol: considered as a drug that possibly causes hepatotoxicity		2.0510aminopyridine
carbutamide
Carbutamide: A sulfonylurea antidiabetic agent with similar actions and uses to CHLORPROPAMIDE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p277)		2.0510benzenes;
sulfonamide
perfluorobutane
perfluorobutane: component of the echo contrast agent, BR14, which consists of perfluorobutane gas microbubbles. perflubutane : A fluorocarbon that is butane in which all of the hydrogens have been replaced by fluorines. Microbubbles of preflubutane are used in the ultrasound contrast agent BR14.		2.0510fluoroalkane;
fluorocarbon;
gas molecular entity		ultrasound contrast agent
nandrolone decanoate
Nandrolone Decanoate: Decanoic acid ester of nandrolone that is used as an anabolic agent to prevent or treat WASTING SYNDROME associated with severe chronic illness or HIV infection (HIV WASTING SYNDROME). It may also be used in the treatment of POSTMENOPAUSAL OSTEOPOROSIS.		2.0510steroid ester
aminoimidazole carboxamide
Aminoimidazole Carboxamide: An imidazole derivative which is a metabolite of the antineoplastic agents BIC and DIC. By itself, or as the ribonucleotide, it is used as a condensation agent in the preparation of nucleosides and nucleotides. Compounded with orotic acid, it is used to treat liver diseases.. 5-aminoimidazole-4-carboxamide : An aminoimidazole in which the amino group is at C-5 with a carboxamido group at C-4.		2.5820aminoimidazole;
monocarboxylic acid amide		mouse metabolite
bucladesine
[no description available]		2.05103',5'-cyclic purine nucleotide;
butanamides;
butyrate ester		agonist;
cardiotonic drug;
vasodilator agent
betamethasone
Betamethasone: A glucocorticoid given orally, parenterally, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. Its lack of mineralocorticoid properties makes betamethasone particularly suitable for treating cerebral edema and congenital adrenal hyperplasia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p724)		2.723011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		anti-asthmatic agent;
anti-inflammatory drug;
immunosuppressive agent
perflubron
perflubron: potential anti-obesity compound; reduces food adsorption; 8-carbon perfluorocarbon radiopaque compound; an oral contrast agent for use with MRI to enhance delineation of the bowel distinguishing it from adjacent organs. perflubron : A haloalkane that is perfluorooctane in which a fluorine attached to one of the terminal carbons has been replaced by a bromine.		2.0510haloalkane;
organobromine compound;
perfluorinated compound		blood substitute;
radioopaque medium
cyproterone acetate
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
chlorinated steroid;
steroid ester		androgen antagonist;
geroprotector;
progestin
lithocholic acid
Lithocholic Acid: A bile acid formed from chenodeoxycholate by bacterial action, usually conjugated with glycine or taurine. It acts as a detergent to solubilize fats for absorption and is itself absorbed. It is used as cholagogue and choleretic.. lithocholic acid : A monohydroxy-5beta-cholanic acid with a alpha-hydroxy substituent at position 3. It is a bile acid obtained from chenodeoxycholic acid by bacterial action.. lithocholate : A bile acid anion that is the conjugate base of lithocholic acid.		2.1110bile acid;
C24-steroid;
monohydroxy-5beta-cholanic acid		geroprotector;
human metabolite;
mouse metabolite
nandrolone
Nandrolone: C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of ESTRADIOL to resemble TESTOSTERONE but less one carbon at the 19 position.. nandrolone : A 3-oxo Delta(4)-steroid that is estr-4-en-3-one substituted by a beta-hydroxy group at position 17.		2.041017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
anabolic androgenic steroid		human metabolite
hydantoins
Hydantoins: Compounds based on imidazolidine dione. Some derivatives are ANTICONVULSANTS.. imidazolidine-2,4-dione : An imidazolidinone with oxo groups at position 2 and 4.		2.3110imidazolidine-2,4-dione
fluorobenzenes
Fluorobenzenes: Derivatives of BENZENE that contain FLUORINE.. monofluorobenzene : The simplest member of the class of monofluorobenzenes that is benzene carrying a single fluoro substituent.. fluorobenzenes : Any fluoroarene that is a benzene or a substituted benzene carrying at least one fluoro group.		2.4620monofluorobenzenesNMR chemical shift reference compound
dextropropoxyphene
Dextropropoxyphene: A narcotic analgesic structurally related to METHADONE. Only the dextro-isomer has an analgesic effect; the levo-isomer appears to exert an antitussive effect.. propoxyphene : A racemate of the (1R,2R)- and (1S,2R)- diastereoisomers.. dextropropoxyphene : The (1S,2R)-(+)-diastereoisomer of propoxyphene.		2.05101-benzyl-3-(dimethylamino)-2-methyl-1-phenylpropyl propanoatemu-opioid receptor agonist;
opioid analgesic
limestone
Calcium Carbonate: Carbonic acid calcium salt (CaCO3). An odorless, tasteless powder or crystal that occurs in nature. It is used therapeutically as a phosphate buffer in hemodialysis patients and as a calcium supplement.. calcium carbonate : A calcium salt with formula CCaO3.		3.4811calcium salt;
carbonate salt;
inorganic calcium salt;
one-carbon compound		antacid;
fertilizer;
food colouring;
food firming agent
glycyrrhetinic acid
[no description available]		2.0510cyclic terpene ketone;
hydroxy monocarboxylic acid;
pentacyclic triterpenoid		immunomodulator;
plant metabolite
chenodeoxycholic acid
Chenodeoxycholic Acid: A bile acid, usually conjugated with either glycine or taurine. It acts as a detergent to solubilize fats for intestinal absorption and is reabsorbed by the small intestine. It is used as cholagogue, a choleretic laxative, and to prevent or dissolve gallstones.. chenodeoxycholic acid : A dihydroxy-5beta-cholanic acid that is (5beta)-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 7 respectively.. chenodeoxycholate : Conjugate base of chenodeoxycholic acid; major species at pH 7.3.		2.4520bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
fusarium
Fusarium: A mitosporic Hypocreales fungal genus, various species of which are important parasitic pathogens of plants and a variety of vertebrates. Teleomorphs include GIBBERELLA.		2.0310
berbamine
[no description available]		4.6961phenylpropanoid
indirubin
[no description available]		3.0240
cepharanthine
cepharanthine: isoquinoline alkaloid from tubers of STEPHANIA; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation. cepharanthine : A bisbenzylisoquinoline alkaloid from tubers of Stephania; stimulates recovery of immunologic function in lymphatic system after administration of antineoplastic agents or x-irradiation.		3.1910bisbenzylisoquinoline alkaloid;
isoquinolines
dihydralazine
Dihydralazine: 1,4-Dihydrazinophthalazine. An antihypertensive agent with actions and uses similar to those of HYDRALAZINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p354)		2.0510phthalazines
reticulin
Reticulin: A scleroprotein fibril consisting mostly of type III collagen. Reticulin fibrils are extremely thin, with a diameter of between 0.5 and 2 um. They are involved in maintaining the structural integrity in a variety of organs.		4.6732benzylisoquinoline alkaloid;
benzyltetrahydroisoquinoline;
isoquinolinol		plant metabolite
phenylpropanolamine
Phenylpropanolamine: A sympathomimetic that acts mainly by causing release of NOREPINEPHRINE but also has direct agonist activity at some adrenergic receptors. It is most commonly used as a nasal vasoconstrictor and an appetite depressant.. phenylpropanolamine : An amphetamine in which the parent 1-phenylpropan-2-amine skeleton is substituted at position 1 with an hydroxy group. A decongestant and appetite suppressant, it is commonly used in prescription and over-the-counter cough and cold preparations.. (-)-norephedrine : An amphetamine that is propylbenzene substituted by a hydroxy group at position 1 and by an amino group at position 2 (the 1R,2S-stereoisomer). It is a plant alkaloid.		2.0510amphetamines;
phenethylamine alkaloid		plant metabolite
alpha-aminopyridine
alpha-aminopyridine: RN given refers to parent cpd; structure in Merck Index, 9th ed, #485. aminopyridine : Compounds containing a pyridine skeleton substituted by one or more amine groups.		6.99151
thiazolidines
Thiazolidines: Reduced (protonated) form of THIAZOLES. They can be oxidized to THIAZOLIDINEDIONES.		2.830thiazolidine
oleanolic acid
[no description available]		2.0410hydroxy monocarboxylic acid;
pentacyclic triterpenoid		plant metabolite
dihydroergotamine
Dihydroergotamine: A 9,10alpha-dihydro derivative of ERGOTAMINE. It is used as a vasoconstrictor, specifically for the therapy of MIGRAINE DISORDERS.. dihydroergotamine : Ergotamine in which a single bond replaces the double bond between positions 9 and 10. A semisynthetic ergot alkaloid with weaker oxytocic and vasoconstrictor properties than ergotamine, it is used (as the methanesulfonic or tartaric acid salts) for the treatment of migraine and orthostatic hypotension.		2.0510ergot alkaloid;
semisynthetic derivative		dopamine agonist;
non-narcotic analgesic;
serotonergic agonist;
sympatholytic agent;
vasoconstrictor agent
podophyllotoxin
Podophyllum: A genus of poisonous American herbs, family BERBERIDACEAE. The roots yield PODOPHYLLOTOXIN and other pharmacologically important agents. The plant was formerly used as a cholagogue and cathartic. It is different from the European mandrake, MANDRAGORA.		2.0510furonaphthodioxole;
lignan;
organic heterotetracyclic compound		antimitotic;
antineoplastic agent;
keratolytic drug;
microtubule-destabilising agent;
plant metabolite;
tubulin modulator
hesperidin
Hesperidin: A flavanone glycoside found in CITRUS fruit peels.. hesperidin : A disaccharide derivative that consists of hesperetin substituted by a 6-O-(alpha-L-rhamnopyranosyl)-beta-D-glucopyranosyl moiety at position 7 via a glycosidic linkage.		2.05103'-hydroxyflavanones;
4'-methoxyflavanones;
dihydroxyflavanone;
disaccharide derivative;
flavanone glycoside;
monomethoxyflavanone;
rutinoside		mutagen
medroxyprogesterone
[no description available]		2.041017alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(4) steroid;
tertiary alpha-hydroxy ketone		contraceptive drug;
progestin;
synthetic oral contraceptive
gluconic acid
gluconic acid: zinc gluconate has anti-inflammatory activity; RN given refers to (D)-isomer; all RRs refers to (D)-isomer unless otherwise noted. ketogluconic acid : A gluconic acid that contains a ketonic carbonyl group.. D-gluconic acid : A gluconic acid having D-configuration.		2.110gluconic acidchelator;
Penicillium metabolite
copper gluconate
Gluconates: Derivatives of gluconic acid (the structural formula HOCH2(CHOH)4COOH), including its salts and esters.		2.110organic molecular entity
azomycin
azomycin: RN given refers to parent cpd with specified locant; structure		2.2110C-nitro compound;
imidazoles		antitubercular agent
syringic acid
syringic acid: RN given refers to parent cpd; structure in third source. syringic acid : A dimethoxybenzene that is 3,5-dimethyl ether derivative of gallic acid.		2.1710benzoic acids;
dimethoxybenzene;
phenols		plant metabolite
chlormethiazole
Chlormethiazole: A sedative and anticonvulsant often used in the treatment of alcohol withdrawal. Chlormethiazole has also been proposed as a neuroprotective agent. The mechanism of its therapeutic activity is not entirely clear, but it does potentiate GAMMA-AMINOBUTYRIC ACID receptors response and it may also affect glycine receptors.		2.0510thiazoles
perillyl alcohol
perillyl alcohol: inhibits geranylgeranyl transferase; structure in first source. perillyl alcohol : A limonene monoterpenoid consists of a cyclohexene ring substituted by a hydroxymethyl and a prop-1-en-2-yl group at positions 1 and 4 respectively. It is a constituent of a variety of essential oils including lavender.		2.0210limonene monoterpenoidplant metabolite;
volatile oil component
methamphetamine
Methamphetamine: A central nervous system stimulant and sympathomimetic with actions and uses similar to DEXTROAMPHETAMINE. The smokable form is a drug of abuse and is referred to as crank, crystal, crystal meth, ice, and speed.. methamphetamine : A member of the class of amphetamines in which the amino group of (S)-amphetamine carries a methyl substituent.		3.5620amphetamines;
secondary amine		central nervous system stimulant;
environmental contaminant;
neurotoxin;
psychotropic drug;
xenobiotic
maleimide
[no description available]		2.2510dicarboximide;
maleimides		EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
muscone
muscone: structure in first source		4.6111
malondialdehyde
Malondialdehyde: The dialdehyde of malonic acid.. malonaldehyde : A dialdehyde that is propane substituted by two oxo groups at the terminal carbon atoms respectively. A biomarker of oxidative damage to lipids caused by smoking, it exists in vivo mainly in the enol form.		2.9330dialdehydebiomarker
myristic acid
Myristic Acid: A saturated 14-carbon fatty acid occurring in most animal and vegetable fats, particularly butterfat and coconut, palm, and nutmeg oils. It is used to synthesize flavor and as an ingredient in soaps and cosmetics. (From Dorland, 28th ed). tetradecanoic acid : A straight-chain, fourteen-carbon, long-chain saturated fatty acid mostly found in milk fat.. tetradecanoate : A long-chain fatty acid anion that is the conjugate base of myristic acid; major species at pH 7.3.		4.0640long-chain fatty acid;
straight-chain saturated fatty acid		algal metabolite;
Daphnia magna metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
human metabolite
lucanthone hydrochloride
Schistosomicides: Agents that act systemically to kill adult schistosomes.		2.5320
gentian violet
Gentian Violet: A dye that is a mixture of violet rosanilinis with antibacterial, antifungal, and anthelmintic properties.. crystal violet : An organic chloride salt that is the monochloride salt of crystal violet cation. It has been used in creams for the topical treatment of bacterial and fungal infections, being effective against some Gram-positive bacteria (notably Staphylococcus species) and some pathogenic fungi (including Candida species) but use declined following reports of animal carcinogenicity. It has also been used for dying wood, silk, and paper, as well as a histological stain.		2.7330organic chloride saltanthelminthic drug;
antibacterial agent;
antifungal agent;
antiseptic drug;
histological dye
hematoporphyrin
Hematoporphyrins: Iron-free derivatives of heme with 4 methyl groups, 2 hydroxyethyl groups and 2 propionic acid groups attached to the pyrrole rings. Some of these PHOTOSENSITIZING AGENTS are used in the PHOTOTHERAPY of malignant NEOPLASMS.. hematoporphyrin : A dicarboxylic acid that is protoporphyrin in which the vinyl groups at positions 7 and 12 are replaced by 1-hydroxyethyl groups.		2.0510
lactulose
[no description available]		2.0510glycosylfructosegastrointestinal drug;
laxative
3-hydroxyflavone
3-hydroxyflavone: structure given in first source. flavonol : A monohydroxyflavone that is the 3-hydroxy derivative of flavone.		7.0710flavonols;
monohydroxyflavone
diphenylamine
Diphenylamine: In humans it may be irritating to mucous membranes. Methemoglobinemia has been produced experimentally. In veterinary use, it is one of active ingredients in topical agents for prevention and treatment of screwworm infestation. An indicator in tests for nitrate poisoning.. diphenylamine : An aromatic amine containing two phenyl substituents. It has been used as a fungicide for the treatment of superficial scald in apples and pears, but is no longer approved for this purpose within the European Union.		2.0510aromatic amine;
bridged diphenyl fungicide;
secondary amino compound		antifungal agrochemical;
antioxidant;
carotogenesis inhibitor;
EC 1.3.99.29 [phytoene desaturase (zeta-carotene-forming)] inhibitor;
ferroptosis inhibitor;
radical scavenger
megestrol acetate
[no description available]		2.051020-oxo steroid;
3-oxo-Delta(4) steroid;
acetate ester;
steroid ester		antineoplastic agent;
appetite enhancer;
contraceptive drug;
progestin;
synthetic oral contraceptive
acetylcysteine
N-acetyl-L-cysteine : An N-acetyl-L-amino acid that is the N-acetylated derivative of the natural amino acid L-cysteine.		5.8790acetylcysteine;
L-cysteine derivative;
N-acetyl-L-amino acid		antidote to paracetamol poisoning;
antiinfective agent;
antioxidant;
antiviral drug;
ferroptosis inhibitor;
geroprotector;
human metabolite;
mucolytic;
radical scavenger;
vulnerary
erythromycin stearate
[no description available]		2.0510aminoglycoside
erythromycin
Erythromycin: A bacteriostatic antibiotic macrolide produced by Streptomyces erythreus. Erythromycin A is considered its major active component. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin : Any of several wide-spectrum macrolide antibiotics obtained from actinomycete Saccharopolyspora erythraea (formerly known as Streptomyces erythraeus).. erythromycin A : An erythromycin that consists of erythronolide A having 2,6-dideoxy-3-C-methyl-3-O-methyl-alpha-L-ribo-hexopyranosyl and 3,4,6-trideoxy-3-(dimethylamino)-beta-D-xylo-hexopyranosyl residues attahced at positions 4 and 6 respectively.		3.8640cyclic ketone;
erythromycin
dehydroepiandrosterone sulfate
Dehydroepiandrosterone Sulfate: The circulating form of a major C19 steroid produced primarily by the ADRENAL CORTEX. DHEA sulfate serves as a precursor for TESTOSTERONE; ANDROSTENEDIONE; ESTRADIOL; and ESTRONE.. dehydroepiandrosterone sulfate : A steroid sulfate that is the 3-sulfooxy derivative of dehydroepiandrosterone.		2.041017-oxo steroid;
steroid sulfate		EC 2.7.1.33 (pantothenate kinase) inhibitor;
human metabolite;
mouse metabolite
ethylnitrosourea
Ethylnitrosourea: A nitrosourea compound with alkylating, carcinogenic, and mutagenic properties.. N-ethyl-N-nitrosourea : A member of the class of N-nitrosoureas that is urea in which one of the nitrogens is substituted by ethyl and nitroso groups.		2.0310N-nitrosoureasalkylating agent;
carcinogenic agent;
genotoxin;
mutagen
vinblastine
[no description available]		2.4520
deoxycytidine
[no description available]		13.623211pyrimidine 2'-deoxyribonucleosideEscherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
estradiol valerate
[no description available]		2.0510steroid ester
undecane
undecane : A straight-chain alkane with 11 carbon atoms.		2.0310alkane
durapatite
Durapatite: The mineral component of bones and teeth; it has been used therapeutically as a prosthetic aid and in the prevention and treatment of osteoporosis.. hydroxylapatite : A phosphate mineral with the formula Ca5(PO4)3(OH).		2.2510
arsenic trioxide
Arsenic Trioxide: An inorganic compound with the chemical formula As2O3 that is used for the treatment of ACUTE PROMYELOCYTIC LEUKEMIA in patients who have relapsed from, or are resistant to, conventional drug therapy.		9.03370
vancomycin
Vancomycin: Antibacterial obtained from Streptomyces orientalis. It is a glycopeptide related to RISTOCETIN that inhibits bacterial cell wall assembly and is toxic to kidneys and the inner ear.. vancomycin : A complex glycopeptide from Streptomyces orientalis. It inhibits a specific step in the synthesis of the peptidoglycan layer in the Gram-positive bacteria Staphylococcus aureus and Clostridium difficile.		2.9940glycopeptideantibacterial drug;
antimicrobial agent;
bacterial metabolite
glycyrrhizic acid
glycyrrhizinic acid : A triterpenoid saponin that is the glucosiduronide derivative of 3beta-hydroxy-11-oxoolean-12-en-30-oic acid.		2.4820enone;
glucosiduronic acid;
pentacyclic triterpenoid;
tricarboxylic acid;
triterpenoid saponin		EC 3.4.21.5 (thrombin) inhibitor;
plant metabolite
d-alpha tocopherol
Vitamin E: A generic descriptor for all TOCOPHEROLS and TOCOTRIENOLS that exhibit ALPHA-TOCOPHEROL activity. By virtue of the phenolic hydrogen on the 2H-1-benzopyran-6-ol nucleus, these compounds exhibit varying degree of antioxidant activity, depending on the site and number of methyl groups and the type of ISOPRENOIDS.. tocopherol : A collective name for a group of closely related lipids that contain a chroman-6-ol nucleus substituted at position 2 by a methyl group and by a saturated hydrocarbon chain consisting of three isoprenoid units. They are designated as alpha-, beta-, gamma-, and delta-tocopherol depending on the number and position of additional methyl substituents on the aromatic ring. Tocopherols occur in vegetable oils and vegetable oil products, almost exclusively with R,R,R configuration. Tocotrienols differ from tocopherols only in having three double bonds in the hydrocarbon chain.. vitamin E : Any member of a group of fat-soluble chromanols that exhibit biological activity against vitamin E deficiency. The vitamers in this class consists of a chroman-6-ol core which is substituted at position 2 by a methyl group and (also at position 2) either a saturated or a triply-unsaturated hydrocarbon chain consisting of three isoprenoid units. The major function of vitamin E is to act as a natural antioxidant by scavenging free radicals and molecular oxygen.. (R,R,R)-alpha-tocopherol : An alpha-tocopherol that has R,R,R configuration. The naturally occurring stereoisomer of alpha-tocopherol, it is found particularly in sunflower and olive oils.		4.8271alpha-tocopherolalgal metabolite;
antiatherogenic agent;
anticoagulant;
antioxidant;
antiviral agent;
EC 2.7.11.13 (protein kinase C) inhibitor;
immunomodulator;
micronutrient;
nutraceutical;
plant metabolite
tocopherols
[no description available]		2.0210
1,2-epoxyhexane
[no description available]		4.6111
nitrofen
nitrofen: structure		2.5220organic molecular entityEC 1.3.3.4 (protoporphyrinogen oxidase) inhibitor;
herbicide
pristane
pristane: structure. pristane : A norterpene that is an acyclic saturated hydrocarbon derived from phytane by loss of its C-16 terminal methyl group.		2.610long-chain alkane;
norterpene		biomarker;
immunological adjuvant
dronabinol
Dronabinol: A psychoactive compound extracted from the resin of Cannabis sativa (marihuana, hashish). The isomer delta-9-tetrahydrocannabinol (THC) is considered the most active form, producing characteristic mood and perceptual changes associated with this compound.. Delta(9)-tetrahydrocannabinol : A diterpenoid that is 6a,7,8,10a-tetrahydro-6H-benzo[c]chromene substituted at position 1 by a hydroxy group, positions 6, 6 and 9 by methyl groups and at position 3 by a pentyl group. The principal psychoactive constituent of the cannabis plant, it is used for treatment of anorexia associated with AIDS as well as nausea and vomiting associated with cancer chemotherapy.		2.0510benzochromene;
diterpenoid;
phytocannabinoid;
polyketide		cannabinoid receptor agonist;
epitope;
hallucinogen;
metabolite;
non-narcotic analgesic
amiloride
Amiloride: A pyrazine compound inhibiting SODIUM reabsorption through SODIUM CHANNELS in renal EPITHELIAL CELLS. This inhibition creates a negative potential in the luminal membranes of principal cells, located in the distal convoluted tubule and collecting duct. Negative potential reduces secretion of potassium and hydrogen ions. Amiloride is used in conjunction with DIURETICS to spare POTASSIUM loss. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p705). amiloride : A member of the class of pyrazines resulting from the formal monoacylation of guanidine with the carboxy group of 3,5-diamino-6-chloropyrazine-2-carboxylic acid.		4.0840aromatic amine;
guanidines;
organochlorine compound;
pyrazines		diuretic;
sodium channel blocker
pimozide
Pimozide: A diphenylbutylpiperidine that is effective as an antipsychotic agent and as an alternative to HALOPERIDOL for the suppression of vocal and motor tics in patients with Tourette syndrome. Although the precise mechanism of action is unknown, blockade of postsynaptic dopamine receptors has been postulated. (From AMA Drug Evaluations Annual, 1994, p403). pimozide : A member of the class of benzimidazoles that is 1,3-dihydro-2H-benzimidazol-2-one in which one of the nitrogens is substituted by a piperidin-4-yl group, which in turn is substituted on the nitrogen by a 4,4-bis(p-fluorophenyl)butyl group.		2.0510benzimidazoles;
heteroarylpiperidine;
organofluorine compound		antidyskinesia agent;
dopaminergic antagonist;
first generation antipsychotic;
H1-receptor antagonist;
serotonergic antagonist
phenethyl isothiocyanate
phenethyl isothiocyanate: a dietary liver aldehyde dehydrogenase inhibitor; promotes urinary bladder carcinoma. phenethyl isothiocyanate : An isothiocyanate having a phenethyl group attached to the nitrogen. It is a naturally occurring compound found in some cruciferous vegetables (e.g. watercress) and is known to possess anticancer properties.		2.9740isothiocyanateantineoplastic agent;
EC 1.2.1.3 [aldehyde dehydrogenase (NAD(+))] inhibitor;
metabolite
fluorescein
Fluorescein: A phthalic indicator dye that appears yellow-green in normal tear film and bright green in a more alkaline medium such as the aqueous humor.. fluorescein (lactone form) : A xanthene dye that is highly fluorescent, detectable even when present in minute quantities. Used forensically to detect traces of blood, in analytical chemistry as an indicator in silver nitrate titrations and in microscopy.		2.02102-benzofurans;
gamma-lactone;
organic heteropentacyclic compound;
oxaspiro compound;
polyphenol;
xanthene dye		fluorescent dye;
radioopaque medium
thioflavin t
thioflavin T: RN given refers to chloride; structure. thioflavine T : An organic chloride salt having 2-[4-(dimethylamino)phenyl]-3,6-dimethyl-1,3-benzothiazol-3-ium as the counterion. It is widely used to visualise and quantify the presence of amyloids, both in vitro and in vivo.		2.1110organic chloride saltfluorochrome;
geroprotector;
histological dye
fucose
Fucose: A six-member ring deoxysugar with the chemical formula C6H12O5. It lacks a hydroxyl group on the carbon at position 6 of the molecule.. L-fucopyranose : The pyranose form of L-fucose.. fucose : Any deoxygalactose that is deoxygenated at the 6-position.		2.5220fucopyranose;
L-fucose		Escherichia coli metabolite;
mouse metabolite
sulfadoxine
Sulfadoxine: A long acting sulfonamide that is used, usually in combination with other drugs, for respiratory, urinary tract, and malarial infections.. sulfadoxine : A sulfonamide consisting of pyrimidine having methoxy substituents at the 5- and 6-positions and a 4-aminobenzenesulfonamido group at the 4-position. In combination with the antiprotozoal pyrimethamine (CHEBI:8673) it is used as an antimalarial.		2.0510pyrimidines;
sulfonamide		antibacterial drug;
antimalarial
sulfur hexafluoride
Sulfur Hexafluoride: Sulfur hexafluoride. An inert gas used mainly as a test gas in respiratory physiology. Other uses include its injection in vitreoretinal surgery to restore the vitreous chamber and as a tracer in monitoring the dispersion and deposition of air pollutants.. sulfur hexafluoride : A sulfur coordination entity consisting of six fluorine atoms attached to a central sulfur atom. It is the most potent greenhouse gas currently known, with a global warming potential of 23,900 times that of CO2 over a 100 year period (SF6 has an estimated lifetime in the atmosphere of between 800 and 3,000 years).		6.321sulfur coordination entitygreenhouse gas;
NMR chemical shift reference compound;
ultrasound contrast agent
acadesine
[no description available]		2.49201-ribosylimidazolecarboxamide;
aminoimidazole;
nucleoside analogue		antineoplastic agent;
platelet aggregation inhibitor
stavudine
Stavudine: A dideoxynucleoside analog that inhibits reverse transcriptase and has in vitro activity against HIV.. stavudine : A nucleoside analogue obtained by formal dehydration across positions 2 and 3 of thymidine. An inhibitor of HIV-1 reverse transcriptase		2.0510dihydrofuran;
nucleoside analogue;
organic molecular entity		antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
doxifluridine
doxifluridine : A pyrimidine 5'-deoxyribonucleoside that is 5-fluorouridine in which the hydroxy group at the 5' position is replaced by a hydrogen. It is an oral prodrug of the antineoplastic agent 5-fluorouracil. Designed to circumvent the rapid degradation of 5-fluorouracil by dihydropyrimidine dehydrogenase in the gut wall, it is converted into 5-fluorouracil in the presence of pyrimidine nucleoside phosphorylase.		2.0510organofluorine compound;
pyrimidine 5'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
prodrug
sabinene
sabinene: RN given refers to cpd without isomeric designation. sabinene : A thujene that is a bicyclic monoterpene isolated from the essential oils of various plant species.		2.0610thujeneplant metabolite
iproclozide
iproclozide: structure		2.0510aromatic ether
streptomycin
[no description available]		2.0510antibiotic antifungal drug;
antibiotic fungicide;
streptomycins		antibacterial drug;
antifungal agrochemical;
antimicrobial agent;
antimicrobial drug;
bacterial metabolite;
protein synthesis inhibitor
cladribine
[no description available]		14.82202organochlorine compound;
purine 2'-deoxyribonucleoside		antineoplastic agent;
immunosuppressive agent
carbenicillin disodium
[no description available]		2.0510organic sodium salt
dehydroemetine
dehydroemetine: was MH 1991-94 (see under EMETINE 1976-90); use EMETINE to search DEHYDROEMETINE 1976-94; amebicide, derivative of emetine. dehydroemetine : A pyridoisoquinoline which was developed in response to the cardiovascular toxicity associated with emetine and results from the dehydrogenation of the heterotricylic ring of emetine. It is an antiprotozoal agent and displays antimalarial, antiamoebic, and antileishmanial properties.		2.0510aromatic ether;
isoquinolines;
pyridoisoquinoline		antileishmanial agent;
antimalarial;
antiprotozoal drug
benorilate
benorilate: was heading 1980-94 (see under SALICYLATES 1980-90); was BENORYLATE see under SALICYLATES 1975-79; BENORYLATE was see BENORILATE 1980-94; use SALICYLATES to search BENORILATE 1980-90 & BENORYLATE 1975-79; an ester of aspirin and paracetamol with analgesic, antipyretic, and anti-inflammatory activity used in the treatment of rheumatoid diseases; it has less severe side effects than aspirin		2.0510carbonyl compound
trimetazidine
Trimetazidine: A vasodilator used in angina of effort or ischemic heart disease.		2.0510aromatic amine
buthionine sulfoximine
Buthionine Sulfoximine: A synthetic amino acid that depletes glutathione by irreversibly inhibiting gamma-glutamylcysteine synthetase. Inhibition of this enzyme is a critical step in glutathione biosynthesis. It has been shown to inhibit the proliferative response in human T-lymphocytes and inhibit macrophage activation. (J Biol Chem 1995;270(33):1945-7). 2-amino-4-(S-butylsulfonimidoyl)butanoic acid : A non-proteinogenic alpha-amino acid that is homocysteine in which the thiol group carries an oxo, imino and butyl groups.. S-butyl-DL-homocysteine (S,R)-sulfoximine : A sulfoximide that is the sulfoximine derivative of an analogue of DL-methionine in which the S-methyl group is replaced by S-butyl.		2.7430diastereoisomeric mixture;
homocysteines;
non-proteinogenic alpha-amino acid;
sulfoximide		EC 6.3.2.2 (glutamate--cysteine ligase) inhibitor;
ferroptosis inducer
floxacillin
Floxacillin: Antibiotic analog of CLOXACILLIN.. flucloxacillin : A penicillin compound having a 6beta-[3-(2-chloro-6-fluorophenyl)-5-methyl-1,2-oxazole-4-carboxamido] side-chain.		2.4520penicillin allergen;
penicillin		antibacterial drug
vidarabine
adenine arabinoside : A purine nucleoside in which adenine is attached to arabinofuranose via a beta-N(9)-glycosidic bond.		9.49212beta-D-arabinoside;
purine nucleoside		antineoplastic agent;
bacterial metabolite;
nucleoside antibiotic
enbucrilate
Enbucrilate: A tissue adhesive that is applied as a monomer to moist tissue and polymerizes to form a bond. It is slowly biodegradable and used in all kinds of surgery, including dental.		2.1510alpha,beta-unsaturated monocarboxylic acid;
nitrile
tiadenol
tiadenol: structure		2.0510aliphatic sulfide
lutetium
Lutetium: An element of the rare earth family of metals. It has the atomic symbol Lu, atomic number 71, and atomic weight 175.		2.2510d-block element atom;
lanthanoid atom
palladium
Palladium: A chemical element having an atomic weight of 106.4, atomic number of 46, and the symbol Pd. It is a white, ductile metal resembling platinum, and following it in abundance and importance of applications. It is used in dentistry in the form of gold, silver, and copper alloys.. palladium : Chemical element (nickel group element atom) with atomic number 46.		2.1310metal allergen;
nickel group element atom;
platinum group metal atom
platinum
Platinum: A heavy, soft, whitish metal, resembling tin, with atomic number 78, atomic weight 195.084, symbol Pt. It is used in manufacturing equipment for laboratory and industrial use. It occurs as a black powder (platinum black) and as a spongy substance (spongy platinum) and may have been known in Pliny's time as alutiae.		2.5820elemental platinum;
nickel group element atom;
platinum group metal atom
ruthenium
Ruthenium: A hard, brittle, grayish-white rare earth metal with an atomic symbol Ru, atomic number 44, and atomic weight 101.07. It is used as a catalyst and hardener for PLATINUM and PALLADIUM.		2.1710iron group element atom;
platinum group metal atom
silver
Silver: An element with the atomic symbol Ag, atomic number 47, and atomic weight 107.87. It is a soft metal that is used medically in surgical instruments, dental prostheses, and alloys. Long-continued use of silver salts can lead to a form of poisoning known as ARGYRIA.		5.3731copper group element atom;
elemental silver		Escherichia coli metabolite
thulium
Thulium: An element of the rare earth family of metals. It has the atomic symbol Tm, atomic number 69, and atomic weight 168.93.		4.6111f-block element atom;
lanthanoid atom
titanium
Titanium: A dark-gray, metallic element of widespread distribution but occurring in small amounts with atomic number, 22, atomic weight, 47.867 and symbol, Ti; specific gravity, 4.5; used for fixation of fractures.		5.7451titanium group element atom
chromium
Chromium: A trace element that plays a role in glucose metabolism. It has the atomic symbol Cr, atomic number 24, and atomic weight 52. According to the Fourth Annual Report on Carcinogens (NTP85-002,1985), chromium and some of its compounds have been listed as known carcinogens.. chromium ion : An chromium atom having a net electric charge.. chromium atom : A chromium group element atom that has atomic number 24.		2.1310chromium group element atom;
metal allergen		micronutrient
gadolinium
Gadolinium: An element of the rare earth family of metals. It has the atomic symbol Gd, atomic number 64, and atomic weight 157.25. Its oxide is used in the control rods of some nuclear reactors.		2.0510f-block element atom;
lanthanoid atom
gold
Gold: A yellow metallic element with the atomic symbol Au, atomic number 79, and atomic weight 197. It is used in jewelry, goldplating of other metals, as currency, and in dental restoration. Many of its clinical applications, such as ANTIRHEUMATIC AGENTS, are in the form of its salts.		8.4460copper group element atom;
elemental gold
uranium
Uranium: A radioactive element of the actinide series of metals. It has an atomic symbol U, atomic number 92, and atomic weight 238.03. U-235 is used as the fissionable fuel in nuclear weapons and as fuel in nuclear power reactors.		4.6111actinoid atom;
f-block element atom;
monoatomic uranium
cupric chloride
cupric chloride: RN given refers to unlabeled parent cpd. copper(II) chloride : An inorganic chloride of copper in which the metal is in the +2 oxidation state.		2.1710copper molecular entity;
inorganic chloride		EC 5.3.3.5 (cholestenol Delta-isomerase) inhibitor
zalcitabine
Zalcitabine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication at low concentrations, acting as a chain-terminator of viral DNA by binding to reverse transcriptase. Its principal toxic side effect is axonal degeneration resulting in peripheral neuropathy.. zalcitabine : A pyrimidine 2',3'-dideoxyribonucleoside compound having cytosine as the nucleobase.		2.0510pyrimidine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
phosphoric acid, trisodium salt
[no description available]		2.0710sodium phosphate
camptothecin
NSC 100880: carboxylate (opened lactone) form of camptothecin; RN refers to (S)-isomer; structure given in first source		10.13233delta-lactone;
pyranoindolizinoquinoline;
quinoline alkaloid;
tertiary alcohol		antineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
genotoxin;
plant metabolite
deuterium
Deuterium: The stable isotope of hydrogen. It has one neutron and one proton in the nucleus.		3.9321dihydrogen
fluorine
Fluorine: A nonmetallic, diatomic gas that is a trace element and member of the halogen family. It is used in dentistry as fluoride (FLUORIDES) to prevent dental caries.		2.1310diatomic fluorine;
gas molecular entity		NMR chemical shift reference compound
galactose
aldohexose : A hexose with a (potential) aldehyde group at one end.		4.6111
phosphoryl chloride
phosphoryl chloride: structure		2.0610phosphorus coordination entity
ozone
Ozone: The unstable triatomic form of oxygen, O3. It is a powerful oxidant that is produced for various chemical and industrial uses. Its production is also catalyzed in the ATMOSPHERE by ULTRAVIOLET RAY irradiation of oxygen or other ozone precursors such as VOLATILE ORGANIC COMPOUNDS and NITROGEN OXIDES. About 90% of the ozone in the atmosphere exists in the stratosphere (STRATOSPHERIC OZONE).. ozone : An elemental molecule with formula O3. An explosive, pale blue gas (b.p. -112degreeC) that has a characteristic, pungent odour, it is continuously produced in the upper atmosphere by the action of solar ultraviolet radiation on atmospheric oxygen. It is an antimicrobial agent used in the production of bottled water, as well as in the treatment of meat, poultry and other foodstuffs.		4.6111elemental molecule;
gas molecular entity;
reactive oxygen species;
triatomic oxygen		antiseptic drug;
disinfectant;
electrophilic reagent;
greenhouse gas;
mutagen;
oxidising agent;
tracer
trolamine salicylate
Arthritis: Acute or chronic inflammation of JOINTS.		4.140
stanozolol
Stanozolol: A synthetic steroid that has anabolic and androgenic properties. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1194). stanozolol : An organic heteropentacyclic compound resulting from the formal condensation of the 3-keto-aldehyde moiety of oxymetholone with hydrazine. Like oxymetholone, it is a synthetic anabolic steroid. It has both anabolic and androgenic properties, and has been used to treat hereditary angioedema and various vascular disorders. It has also been widely abused by professional athletes.		2.051017beta-hydroxy steroid;
anabolic androgenic steroid;
organic heteropentacyclic compound;
tertiary alcohol		anabolic agent;
androgen
clodronic acid
Clodronic Acid: A diphosphonate which affects calcium metabolism. It inhibits bone resorption and soft tissue calcification.. clodronic acid : An organochlorine compound that is methylene chloride in which both hydrogens are replaced by phosphonic acid groups. It inhibits bone resorption and soft tissue calcification, and is used (often as the disodium salt tetrahydrate) as an adjunct in the treatment of severe hypercalcaemia associated with malignancy, and in the management of osteolytic lesions and bone pain associated with skeletal metastases.		2.45201,1-bis(phosphonic acid);
one-carbon compound;
organochlorine compound		antineoplastic agent;
bone density conservation agent
ammonium chloride
Ammonium Chloride: An acidifying agent that has expectorant and diuretic effects. Also used in etching and batteries and as a flux in electroplating.. ammonium chloride : An inorganic chloride having ammonium as the counterion.		3.6830ammonium salt;
inorganic chloride		ferroptosis inhibitor
ethionine
L-ethionine : An S-ethylhomocysteine that has S-configuration at the chiral centre.		2.4820S-ethylhomocysteineantimetabolite;
carcinogenic agent
titanium dioxide
titanium dioxide: used medically as protectant against externally caused irritation & sunlight; high concentrations of dust may cause irritation to respiratory tract; RN given refers to titanium oxide (TiO2); structure. titanium dioxide : A titanium oxide with the formula TiO2. A naturally occurring oxide sourced from ilmenite, rutile and anatase, it has a wide range of applications.		3.0840titanium oxidesfood colouring
tiletamine hydrochloride
Cyclohexanones: Cyclohexane ring substituted by one or more ketones in any position.. cyclohexanones : Any alicyclic ketone based on a cyclohexane skeleton and its substituted derivatives thereof.		2.4420
xipamide
Xipamide: A sulfamoylbenzamide analog of CLOPAMIDE. It is diuretic and saluretic with antihypertensive activity. It is bound to PLASMA PROTEINS, thus has a delayed onset and prolonged action.		2.0510benzamides
selegiline
Selegiline: A selective, irreversible inhibitor of Type B monoamine oxidase that is used for the treatment of newly diagnosed patients with PARKINSON DISEASE, and for the treatment of depressive disorders. The compound without isomeric designation is Deprenyl.		2.0510selegiline;
terminal acetylenic compound		geroprotector
levamisole
Levamisole: An antihelminthic drug that has been tried experimentally in rheumatic disorders where it apparently restores the immune response by increasing macrophage chemotaxis and T-lymphocyte function. Paradoxically, this immune enhancement appears to be beneficial in rheumatoid arthritis where dermatitis, leukopenia, and thrombocytopenia, and nausea and vomiting have been reported as side effects. (From Smith and Reynard, Textbook of Pharmacology, 1991, p435-6). levamisole : A 6-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazole that has S configuration. It is used (generally as the monohydrochloride salt) to treat parasitic worm infections in pigs, sheep and cattle and was formerly used in humans as an adjuvant to chemotherapy for the treatment of various cancers. It is also widely used as an adulterant to coccaine.		2.05106-phenyl-2,3,5,6-tetrahydroimidazo[2,1-b][1,3]thiazoleantinematodal drug;
antirheumatic drug;
EC 3.1.3.1 (alkaline phosphatase) inhibitor;
immunological adjuvant;
immunomodulator
clemastine
Clemastine: A histamine H1 antagonist used as the hydrogen fumarate in hay fever, rhinitis, allergic skin conditions, and pruritus. It causes drowsiness.. clemastine : 2-[(2R)-1-Methylpyrrolidin-2-yl]ethanol in which the hydrogen of the hydroxy group is substituted by a 1-(4-chlorophenyl)-1-phenylethyl group (R configuration). An antihistamine with antimuscarinic and moderate sedative properties, it is used as its fumarate salt for the symptomatic relief of allergic conditions such as rhinitis, urticaria, conjunctivitis and in pruritic (severe itching) skin conditions.		2.1310monochlorobenzenes;
N-alkylpyrrolidine		anti-allergic agent;
antipruritic drug;
H1-receptor antagonist;
muscarinic antagonist
thiamphenicol
[no description available]		2.0510monocarboxylic acid amide;
sulfone		antimicrobial agent;
immunosuppressive agent
pizotyline
Pizotyline: Serotonin antagonist used against MIGRAINE DISORDERS and vascular headaches.. pizotifen : A benzocycloheptathiophene that is 9,10-dihydro-4H-benzo[4,5]cyclohepta[1,2-b]thiophene 4-ylidene)-1-methylpiperidine which is joined from the 4 position to the 4 position of an N-methylpiperidine moiety by a double bond. It is a sedating antihistamine, with strong serotonin antagonist and weak antimuscarinic activity. It is generally used as the malate salt for the treatment of migraine and the prevention of headache attacks during cluster periods.		2.0510benzocycloheptathiophenehistamine antagonist;
muscarinic antagonist;
serotonergic antagonist
cromolyn sodium
Cromolyn Sodium: A chromone complex that acts by inhibiting the release of chemical mediators from sensitized MAST CELLS. It is used in the prophylactic treatment of both allergic and exercise-induced asthma, but does not affect an established asthmatic attack.. disodium cromoglycate : An organic sodium salt that is the disodium salt of cromoglycic acid.		2.0510organic sodium saltanti-asthmatic drug;
drug allergen
isosorbide-5-mononitrate
isosorbide-5-mononitrate: for prevention of angina pectoris; structure given in first source; a Russian drug		2.0510glucitol derivative;
nitrate ester		nitric oxide donor;
vasodilator agent
tetradecanoylphorbol acetate
Tetradecanoylphorbol Acetate: A phorbol ester found in CROTON OIL with very effective tumor promoting activity. It stimulates the synthesis of both DNA and RNA.. phorbol ester : Esters of phorbol, originally found in croton oil (from Croton tiglium, of the family Euphorbiaceae). A number of phorbol esters possess activity as tumour promoters and activate the mechanisms associated with cell growth. Some of these are used in experiments as activators of protein kinase C.. phorbol 13-acetate 12-myristate : A phorbol ester that is phorbol in which the hydroxy groups at the cyclopropane ring juction (position 13) and the adjacent carbon (position 12) have been converted into the corresponding acetate and myristate esters. It is a major active constituent of the seed oil of Croton tiglium. It has been used as a tumour promoting agent for skin carcinogenesis in rodents and is associated with increased cell proliferation of malignant cells. However its function is controversial since a decrease in cell proliferation has also been observed in several cancer cell types.		4.3641acetate ester;
diester;
phorbol ester;
tertiary alpha-hydroxy ketone;
tetradecanoate ester		antineoplastic agent;
apoptosis inducer;
carcinogenic agent;
mitogen;
plant metabolite;
protein kinase C agonist;
reactive oxygen species generator
danazol
Danazol: A synthetic steroid with antigonadotropic and anti-estrogenic activities that acts as an anterior pituitary suppressant by inhibiting the pituitary output of gonadotropins. It possesses some androgenic properties. Danazol has been used in the treatment of endometriosis and some benign breast disorders.		2.051017beta-hydroxy steroid;
terminal acetylenic compound		anti-estrogen;
estrogen antagonist;
geroprotector
lisuride
Lisuride: An ergot derivative that acts as an agonist at dopamine D2 receptors (DOPAMINE AGONISTS). It may also act as an antagonist at dopamine D1 receptors, and as an agonist at some serotonin receptors (SEROTONIN RECEPTOR AGONISTS).		3.1710monocarboxylic acid amideantidyskinesia agent;
antiparkinson drug;
dopamine agonist;
serotonergic agonist
iodine
[no description available]		2.110halide anion;
monoatomic iodine		human metabolite
daunorubicin
Daunorubicin: A very toxic anthracycline aminoglycoside antineoplastic isolated from Streptomyces peucetius and others, used in treatment of LEUKEMIA and other NEOPLASMS.. anthracycline : Anthracyclines are polyketides that have a tetrahydronaphthacenedione ring structure attached by a glycosidic linkage to the amino sugar daunosamine.. daunorubicin : A natural product found in Actinomadura roseola.		11.4395aminoglycoside antibiotic;
anthracycline;
p-quinones;
tetracenequinones		antineoplastic agent;
bacterial metabolite
razoxane
Razoxane: An antimitotic agent with immunosuppressive properties.		2.5220N-alkylpiperazine
fludarabine phosphate
fludarabine phosphate: structure given in first source. fludarabine phosphate : A purine arabinonucleoside monophosphate having 2-fluoroadenine as the nucleobase. A prodrug, it is rapidly dephosphorylated to 2-fluoro-ara-A and then phosphorylated intracellularly by deoxycytidine kinase to the active triphosphate, 2-fluoro-ara-ATP. Once incorporated into DNA, 2-fluoro-ara-ATP functions as a DNA chain terminator. It is used for the treatment of adult patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to, or whose disease has progressed during, treatment with at least one standard alkylating-agent containing regimenas.		3.8330nucleoside analogue;
organofluorine compound;
purine arabinonucleoside monophosphate		antimetabolite;
antineoplastic agent;
antiviral agent;
DNA synthesis inhibitor;
immunosuppressive agent;
prodrug
phosphotyrosine
Phosphotyrosine: An amino acid that occurs in endogenous proteins. Tyrosine phosphorylation and dephosphorylation plays a role in cellular signal transduction and possibly in cell growth control and carcinogenesis.. O(4)-phospho-L-tyrosine : A non-proteinogenic L-alpha-amino acid that is L-tyrosine phosphorylated at the phenolic hydroxy group.		11.98320L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid;
O(4)-phosphotyrosine		Escherichia coli metabolite;
immunogen
carbimazole
Carbimazole: An imidazole antithyroid agent. Carbimazole is metabolized to METHIMAZOLE, which is responsible for the antithyroid activity.. carbimazole : A member of the class of imidazoles that is methimazole in which the nitrogen bearing a hydrogen is converted into its ethoxycarbonyl derivative. A prodrug for methimazol, carbimazole is used for the treatment of hyperthyroidism.		2.05101,3-dihydroimidazole-2-thiones;
carbamate ester		antithyroid drug;
prodrug
bromocriptine
Bromocriptine: A semisynthetic ergotamine alkaloid that is a dopamine D2 agonist. It suppresses prolactin secretion.		2.0510indole alkaloidantidyskinesia agent;
antiparkinson drug;
dopamine agonist;
hormone antagonist
ergocristine
ergocristine: an ergot alkaloid; one of the three components of ergotoxine; has alpha blocking action, stimulates smooth muscles & antagonizes serotonin; used as oxytocic & in peripheral disorders; minor descriptor (77-86); on-line & INDEX MEDICUS search EROLINES (77-86); RN given refers to ((5'alpha)-isomer). ergocristine : Ergotaman bearing benzyl, hydroxy, and isopropyl groups at the 5', 12' and 2' positions, respectively, and oxo groups at positions 3', 6', and 18. It is a natural ergot alkaloid.		2.0410ergot alkaloid
phenyl acetate
phenyl acetate: The ester formed between phenol and acetic acid. Don't confuse with phenylacetic acid derivatives listed under PHENYLACETATES.. phenyl acetate : An acetate ester obtained by the formal condensation of phenol with acetic acid.		2.5720benzenes;
phenyl acetates
cetylpyridinium chloride anhydrous
tserigel: according to first source contains polyvinylbutyral & cetylpyridinium chloride; UD only lists cetylpyridinium chloride as constituent. cetylpyridinium chloride : A pyridinium salt that has N-hexadecylpyridinium as the cation and chloride as the anion. It has antiseptic properties and is used in solutions or lozenges for the treatment of minor infections of the mouth and throat.		2.0510chloride salt;
organic chloride salt		antiseptic drug;
surfactant
triamcinolone
Triamcinolone: A glucocorticoid given, as the free alcohol or in esterified form, orally, intramuscularly, by local injection, by inhalation, or applied topically in the management of various disorders in which corticosteroids are indicated. (From Martindale, The Extra Pharmacopoeia, 30th ed, p739). triamcinolone : A C21-steroid hormone that is 1,4-pregnadiene-3,20-dione carrying four hydroxy substituents at positions 11beta, 16alpha, 17alpha and 21 as well as a fluoro substituent at position 9. Used in the form of its 16,17-acetonide to treat various skin infections.		2.051011beta-hydroxy steroid;
16alpha-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid hormone;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		anti-allergic agent;
anti-inflammatory drug
oxyphenisatin
[no description available]		2.0510indoles
tetrachloroethylene
Tetrachloroethylene: A chlorinated hydrocarbon used as an industrial solvent and cooling liquid in electrical transformers. It is a potential carcinogen.		2.0510chlorocarbon;
chloroethenes		nephrotoxic agent
ursodeoxycholic acid
Ursodeoxycholic Acid: An epimer of chenodeoxycholic acid. It is a mammalian bile acid found first in the bear and is apparently either a precursor or a product of chenodeoxycholate. Its administration changes the composition of bile and may dissolve gallstones. It is used as a cholagogue and choleretic.. ursodeoxycholic acid : A bile acid found in the bile of bears (Ursidae) as a conjugate with taurine. Used therapeutically, it prevents the synthesis and absorption of cholesterol and can lead to the dissolution of gallstones.. ursodeoxycholate : A bile acid anion that is the conjugate base of ursodeoxycholic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.		2.0510bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
benzonidazole
benzonidazole: used in treatment of Chagas' disease. benznidazole : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2-nitroimidazol-1-yl)acetic acid with the aromatic amino group of benzylamine. Used for treatment of Chagas disease.		2.2110C-nitro compound;
imidazoles;
monocarboxylic acid amide		antiprotozoal drug
butachlor
butachlor : An aromatic amide that is 2-choro-N-(2,6-diethylphenyl)acetamide in which the amide nitrogen has been replaced by a butoxymethyl group.		2.0510aromatic amide;
organochlorine compound;
tertiary carboxamide		environmental contaminant;
herbicide;
xenobiotic
du-21220
Ritodrine: An adrenergic beta-2 agonist used to control PREMATURE LABOR.. 4-[2-[[1-hydroxy-1-(4-hydroxyphenyl)propan-2-yl]amino]ethyl]phenol : A secondary amino compound that is 4-(2-amino-1-hydroxypropyl)phenol in which one of the hydrogens attached to the nitrogen is replaced by a 2-(4-hydroxyphenyl)ethyl group.		2.0410benzyl alcohols;
polyphenol;
secondary alcohol;
secondary amino compound
transferrin
Transferrin: An iron-binding beta1-globulin that is synthesized in the LIVER and secreted into the blood. It plays a central role in the transport of IRON throughout the circulation. A variety of transferrin isoforms exist in humans, including some that are considered markers for specific disease states.		3.3960
rose bengal b disodium salt
[no description available]		2.0510
alkenes
[no description available]		2.1310
glutamic acid
Glutamic Acid: A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.. glutamic acid : An alpha-amino acid that is glutaric acid bearing a single amino substituent at position 2.		3.6690glutamic acid;
glutamine family amino acid;
L-alpha-amino acid;
proteinogenic amino acid		Escherichia coli metabolite;
ferroptosis inducer;
micronutrient;
mouse metabolite;
neurotransmitter;
nutraceutical
cefazolin
Cefazolin: A semisynthetic cephalosporin analog with broad-spectrum antibiotic action due to inhibition of bacterial cell wall synthesis. It attains high serum levels and is excreted quickly via the urine.. cefazolin : A first-generation cephalosporin compound having [(5-methyl-1,3,4-thiadiazol-2-yl)sulfanyl]methyl and (1H-tetrazol-1-ylacetyl)amino side-groups at positions 3 and 7 respectively.		2.0510beta-lactam antibiotic allergen;
cephalosporin;
tetrazoles;
thiadiazoles		antibacterial drug
amoxicillin
Amoxicillin: A broad-spectrum semisynthetic antibiotic similar to AMPICILLIN except that its resistance to gastric acid permits higher serum levels with oral administration.. amoxicillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-amino-2-(4-hydroxyphenyl)acetamido group.		2.0510penicillin allergen;
penicillin		antibacterial drug
timolol
(S)-timolol (anhydrous) : The (S)-(-) (more active) enantiomer of timolol. A beta-adrenergic antagonist, both the hemihydrate and the maleate salt are used in the mangement of glaucoma, hypertension, angina pectoris and myocardial infarction, and for the prevention of migraine.		2.4520timololanti-arrhythmia drug;
antiglaucoma drug;
antihypertensive agent;
beta-adrenergic antagonist
nicergoline
Nicergoline: An ergot derivative that has been used as a cerebral vasodilator and in peripheral vascular disease. It may ameliorate cognitive deficits in CEREBROVASCULAR DISORDERS.		2.0510organic heterotetracyclic compound;
organonitrogen heterocyclic compound
oxcarbazepine
Oxcarbazepine: A carbamazepine derivative that acts as a voltage-gated sodium channel blocker. It is used for the treatment of PARTIAL SEIZURES with or without secondary generalization. It is also an inducer of CYTOCHROME P-450 CYP3A4.. oxcarbazepine : A dibenzoazepine derivative, having a carbamoyl group at the ring nitrogen, substituted with an oxo group at C-4 of the azepeine ring which is also hydrogenated at C-4 and C-5. It is a anticholinergic anticonvulsant and mood stabilizing drug, used primarily in the treatment of epilepsy.		2.0510cyclic ketone;
dibenzoazepine		anticonvulsant;
drug allergen
vidarabine phosphate
Vidarabine Phosphate: An adenosine monophosphate analog in which ribose is replaced by an arabinose moiety. It is the monophosphate ester of VIDARABINE with antiviral and possibly antineoplastic properties.		3.8330
amineptin
amineptin: used in treatment of neuroses with psychoasthenic, anxio-phobic & depressive manifestations; synonym S 1694 refers to HCl; structure. amineptine : A carbocyclic fatty acid that is 5-aminoheptanoic acid in which one of the hydrogens attached to the nitrogen is replaced by a 10,11-dihydro-5H-dibenzo[a,d][7]annulen-5-yl group. A tricyclic antidepressant, it was never approved in the US and was withdrawn from the French market in 1999 due to concerns over abuse, dependence and severe acne.		2.0510amino acid;
carbocyclic fatty acid;
carbotricyclic compound;
secondary amino compound		antidepressant;
dopamine uptake inhibitor
zidovudine
Zidovudine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by an azido group. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. The compound is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA during reverse transcription. It improves immunologic function, partially reverses the HIV-induced neurological dysfunction, and improves certain other clinical abnormalities associated with AIDS. Its principal toxic effect is dose-dependent suppression of bone marrow, resulting in anemia and leukopenia.. zidovudine : A pyrimidine 2',3'-dideoxyribonucleoside compound having a 3'-azido substituent and thymine as the nucleobase.		2.4520azide;
pyrimidine 2',3'-dideoxyribonucleoside		antimetabolite;
antiviral drug;
HIV-1 reverse transcriptase inhibitor
pirprofen
pirprofen: anti-inflammatory agent used in therapy of rheumatoid arthritis; prostaglandin synthetase inhibitor; more potent than indomethacin; structure		2.0510pyrroline
tobramycin
Tobramycin: An aminoglycoside, broad-spectrum antibiotic produced by Streptomyces tenebrarius. It is effective against gram-negative bacteria, especially the PSEUDOMONAS species. It is a 10% component of the antibiotic complex, NEBRAMYCIN, produced by the same species.. tobramycin : A amino cyclitol glycoside that is kanamycin B lacking the 3-hydroxy substituent from the 2,6-diaminoglucose ring.		2.0510amino cyclitol glycosideantibacterial agent;
antimicrobial agent;
toxin
paclitaxel
Taxus: Genus of coniferous yew trees or shrubs, several species of which have medicinal uses. Notable is the Pacific yew, Taxus brevifolia, which is used to make the anti-neoplastic drug taxol (PACLITAXEL).		11.56414taxane diterpenoid;
tetracyclic diterpenoid		antineoplastic agent;
human metabolite;
metabolite;
microtubule-stabilising agent
etoposide
[no description available]		11.75564beta-D-glucoside;
furonaphthodioxole;
organic heterotetracyclic compound		antineoplastic agent;
DNA synthesis inhibitor
substance p
[no description available]		2.0810peptideneurokinin-1 receptor agonist;
neurotransmitter;
vasodilator agent
dobutamine
Dobutamine: A catecholamine derivative with specificity for BETA-1 ADRENERGIC RECEPTORS. It is commonly used as a cardiotonic agent after CARDIAC SURGERY and during DOBUTAMINE STRESS ECHOCARDIOGRAPHY.. dobutamine : A catecholamine that is 4-(3-aminobutyl)phenol in which one of the hydrogens attached to the nitrogen is substituted by a 2-(3,4-dihydroxyphenyl)ethyl group. A beta1-adrenergic receptor agonist that has cardiac stimulant action without evoking vasoconstriction or tachycardia, it is used as the hydrochloride to increase the contractility of the heart in the management of acute heart failure.		2.0510catecholamine;
secondary amine		beta-adrenergic agonist;
cardiotonic drug;
sympathomimetic agent
ribavirin
Rebetron: Rebetron is tradename		2.48201-ribosyltriazole;
aromatic amide;
monocarboxylic acid amide;
primary carboxamide		anticoronaviral agent;
antiinfective agent;
antimetabolite;
antiviral agent;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
amikacin
Amikacin: A broad-spectrum antibiotic derived from KANAMYCIN. It is reno- and oto-toxic like the other aminoglycoside antibiotics.. amikacin : An amino cyclitol glycoside that is kanamycin A acylated at the N-1 position by a 4-amino-2-hydroxybutyryl group.		2.0510alpha-D-glucoside;
amino cyclitol glycoside;
aminoglycoside;
carboxamide		antibacterial drug;
antimicrobial agent;
nephrotoxin
ticrynafen
Ticrynafen: A novel diuretic with uricosuric action. It has been proposed as an antihypertensive agent.. tienilic acid : An aromatic ketone that is 2,3-dichlorophenoxyacetic acid in which the hydrogen at position 4 on the benzene ring is replaced by a thiophenecarbonyl group. A loop diuretic used to treat hypertension, it was withdrawn from the market in 1982 due to links with hepatitis.		2.0510aromatic ether;
aromatic ketone;
dichlorobenzene;
monocarboxylic acid;
thiophenes		antihypertensive agent;
hepatotoxic agent;
loop diuretic
methyldopa
Methyldopa: An alpha-2 adrenergic agonist that has both central and peripheral nervous system effects. Its primary clinical use is as an antihypertensive agent.. alpha-methyl-L-dopa : A derivative of L-tyrosine having a methyl group at the alpha-position and an additional hydroxy group at the 3-position on the phenyl ring.		2.5320L-tyrosine derivative;
non-proteinogenic L-alpha-amino acid		alpha-adrenergic agonist;
antihypertensive agent;
hapten;
peripheral nervous system drug;
sympatholytic agent
bezafibrate
[no description available]		2.0510aromatic ether;
monocarboxylic acid amide;
monocarboxylic acid;
monochlorobenzenes		antilipemic drug;
environmental contaminant;
geroprotector;
xenobiotic
sq-11725
Nadolol: A non-selective beta-adrenergic antagonist with a long half-life, used in cardiovascular disease to treat arrhythmias, angina pectoris, and hypertension. Nadolol is also used for MIGRAINE DISORDERS and for tremor.. nadolol : Nadolol is a diastereoisomeric mixture consisting of equimolar amounts of the four possible 2,3-cis-isomers of 5-[3-(tert-butylamino)-2-hydroxypropoxy]-1,2,3,4-tetrahydronaphthalene-2,3-diol.		2.0510
diltiazem
Diltiazem: A benzothiazepine derivative with vasodilating action due to its antagonism of the actions of CALCIUM ion on membrane functions.. diltiazem : A 5-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetate in which both stereocentres have S configuration. A calcium-channel blocker and vasodilator, it is used as the hydrochloride in the management of angina pectoris and hypertension.		2.45205-[2-(dimethylamino)ethyl]-2-(4-methoxyphenyl)-4-oxo-2,3,4,5-tetrahydro-1,5-benzothiazepin-3-yl acetateantihypertensive agent;
calcium channel blocker;
vasodilator agent
nimustine
Nimustine: Antineoplastic agent especially effective against malignant brain tumors. The resistance which brain tumor cells acquire to the initial effectiveness of this drug can be partially overcome by the simultaneous use of membrane-modifying agents such as reserpine, calcium antagonists such as nicardipine or verapamil, or the calmodulin inhibitor, trifluoperazine. The drug has also been used in combination with other antineoplastic agents or with radiotherapy for the treatment of various neoplasms.. nimustine : An organochlorine compound that is urea in which the two hydrogens on one of the amino groups are replaced by nitroso and 2-chloroethyl groups and one hydrogen from the other amino group is replaced by a 4-amino-2-methylpyrimidin-5-ylmethyl] group. An antineoplastic agent especially effective against malignant brain tumors.		2.0710aminopyrimidine;
N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
1-methyl-4-phenylpyridinium
1-Methyl-4-phenylpyridinium: An active neurotoxic metabolite of 1-METHYL-4-PHENYL-1,2,3,6-TETRAHYDROPYRIDINE. The compound reduces dopamine levels, inhibits the biosynthesis of catecholamines, depletes cardiac norepinephrine and inactivates tyrosine hydroxylase. These and other toxic effects lead to cessation of oxidative phosphorylation, ATP depletion, and cell death. The compound, which is related to PARAQUAT, has also been used as an herbicide.. N-methyl-4-phenylpyridinium : A pyridinium ion that is N-methylpyridinium having a phenyl substituent at the 4-position.		2.4920pyridinium ionapoptosis inducer;
herbicide;
human xenobiotic metabolite;
neurotoxin
ng-nitroarginine methyl ester
NG-Nitroarginine Methyl Ester: A non-selective inhibitor of nitric oxide synthase. It has been used experimentally to induce hypertension.		3.250alpha-amino acid ester;
L-arginine derivative;
methyl ester;
N-nitro compound		EC 1.14.13.39 (nitric oxide synthase) inhibitor
benoxaprofen
benoxaprofen: RN given refers to parent cpd; structure. benoxaprofen : A monocarboxylic acid that is propionic acid substituted at position 2 by a 2-(4-chlorophenyl)-1,3-benzoxazol-5-yl group. It was used as a non-steroidal anti-inflammatory drug until 1982 when it was withdrawn from the market due to adverse side-effects including liver necrosis, photosensitivity, and carcinogenicity in animals.		2.05101,3-benzoxazoles;
monocarboxylic acid;
monochlorobenzenes		antipsoriatic;
antipyretic;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
hepatotoxic agent;
nephrotoxin;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
protein kinase C agonist
permethrin
hemoglobin Atlanta-Coventry: Leu replaced by Pro at beta75 and Leu deleted at beta141		2.0510cyclopropanecarboxylate ester;
cyclopropanes		agrochemical;
ectoparasiticide;
pyrethroid ester acaricide;
pyrethroid ester insecticide;
scabicide
pirfenidone
pirfenidone : A pyridone that is 2-pyridone substituted at positions 1 and 5 by phenyl and methyl groups respectively. An anti-inflammatory drug used for the treatment of idiopathic pulmonary fibrosis.		5.9680pyridoneantipyretic;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
vindesine
Vindesine: Vinblastine derivative with antineoplastic activity against CANCER. Major side effects are myelosuppression and neurotoxicity. Vindesine is used extensively in chemotherapy protocols (ANTINEOPLASTIC COMBINED CHEMOTHERAPY PROTOCOLS).		2.7730methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
primary carboxamide;
tertiary alcohol;
tertiary amino compound;
vinca alkaloid		antineoplastic agent
desogestrel
Desogestrel: A synthetic progestational hormone used often as the progestogenic component of combined oral contraceptive agents (ORAL CONTRACEPTIVES, COMBINED).		2.051017beta-hydroxy steroid;
terminal acetylenic compound		contraceptive drug;
progestin;
synthetic oral contraceptive
muzolimine
Muzolimine: A pyrazole diuretic with long duration and high capacity of action. It was proposed for kidney failure and hypertension but was withdrawn worldwide because of severe neurological effects.		2.0510dichlorobenzene
nitazoxanide
nitazoxanide: a 5-nitrothiazolyl derivative used for a broad range of intestinal parasitic infections including CRYPTOSPORIDIUM and GIARDIA; it is a redox-active nitrothiazolyl-salicylamide prodrug		2.0810benzamides;
carboxylic ester
epirubicin
Epirubicin: An anthracycline which is the 4'-epi-isomer of doxorubicin. The compound exerts its antitumor effects by interference with the synthesis and function of DNA.		7.4420aminoglycoside;
anthracycline antibiotic;
anthracycline;
deoxy hexoside;
monosaccharide derivative;
p-quinones;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		antimicrobial agent;
antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
desflurane
Desflurane: A fluorinated ether that is used as a volatile anesthetic for maintenance of general anesthesia.		2.0510organofluorine compoundinhalation anaesthetic
idarubicin
Idarubicin: An orally administered anthracycline antineoplastic. The compound has shown activity against BREAST NEOPLASMS; LYMPHOMA; and LEUKEMIA.		5.91180anthracycline antibiotic;
deoxy hexoside;
monosaccharide derivative
propiconazole
Orbit: Bony cavity that holds the eyeball and its associated tissues and appendages.		4.5570conazole fungicide;
cyclic ketal;
dichlorobenzene;
triazole fungicide;
triazoles		antifungal agrochemical;
EC 1.14.13.70 (sterol 14alpha-demethylase) inhibitor;
environmental contaminant;
xenobiotic
piperacillin
Piperacillin: Semisynthetic, broad-spectrum, AMPICILLIN derived ureidopenicillin antibiotic proposed for PSEUDOMONAS infections. It is also used in combination with other antibiotics.. piperacillin : A penicillin in which the substituent at position 6 of the penam ring is a 2-[(4-ethyl-2,3-dioxopiperazin-1-yl)carboxamido]-2-phenylacetamido group.		2.0510penicillin allergen;
penicillin		antibacterial drug
paroxetine
Paroxetine: A serotonin uptake inhibitor that is effective in the treatment of depression.. paroxetine : A benzodioxole that consists of piperidine bearing 1,3-benzodioxol-5-yloxy)methyl and 4-fluorophenyl substituents at positions 3 and 4 respectively; the (3S,4R)-diastereomer. Highly potent and selective 5-HT uptake inhibitor that binds with high affinity to the serotonin transporter (Ki = 0.05 nM). Ki values are 1.1, 350 and 1100 nM for inhibition of [3H]-5-HT, [3H]-l-NA and [3H]-DA uptake respectively. Displays minimal affinity for alpha1-, alpha2- or beta-adrenoceptors, 5-HT2A, 5-HT1A, D2 or H1 receptors at concentrations below 1000 nM, however displays weak affinity for muscarinic ACh receptors (Ki = 42 nM). Antidepressant and anxiolytic in vivo.		2.4420aromatic ether;
benzodioxoles;
organofluorine compound;
piperidines		antidepressant;
anxiolytic drug;
hepatotoxic agent;
P450 inhibitor;
serotonin uptake inhibitor
captopril
Captopril: A potent and specific inhibitor of PEPTIDYL-DIPEPTIDASE A. It blocks the conversion of ANGIOTENSIN I to ANGIOTENSIN II, a vasoconstrictor and important regulator of arterial blood pressure. Captopril acts to suppress the RENIN-ANGIOTENSIN SYSTEM and inhibits pressure responses to exogenous angiotensin.. captopril : A L-proline derivative in which L-proline is substituted on nitrogen with a (2S)-2-methyl-3-sulfanylpropanoyl group. It is used as an anti-hypertensive ACE inhibitor drug.		2.7330alkanethiol;
L-proline derivative;
N-acylpyrrolidine;
pyrrolidinemonocarboxylic acid		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
cefoperazone
Cefoperazone: Semisynthetic broad-spectrum cephalosporin with a tetrazolyl moiety that is resistant to beta-lactamase. It may be used to treat Pseudomonas infections.. cefoperazone : A semi-synthetic parenteral cephalosporin with a tetrazolyl moiety that confers beta-lactamase resistance.		2.0510cephalosporinantibacterial drug
staurosporine
[no description available]		2.4820indolocarbazole alkaloid;
organic heterooctacyclic compound		apoptosis inducer;
bacterial metabolite;
EC 2.7.11.13 (protein kinase C) inhibitor;
geroprotector
foscarnet sodium
trisodium phosphonoformate : The trisodium salt of phosphonoformic acid. It is used as an antiviral agent in the treatment of cytomegalovirus retinitis (CMV retinitis, an inflamation of the retina that can lead to blindness) and as an alternative to ganciclovir for AIDS patients who require concurrent antiretroviral therapy but are unable to tolerate ganciclovir due to haematological toxicity.		2.0510one-carbon compound;
organic sodium salt		antiviral drug
moxalactam
Moxalactam: Broad- spectrum beta-lactam antibiotic similar in structure to the CEPHALOSPORINS except for the substitution of an oxaazabicyclo moiety for the thiaazabicyclo moiety of certain CEPHALOSPORINS. It has been proposed especially for the meningitides because it passes the blood-brain barrier and for anaerobic infections.. moxalactam : A broad-spectrum oxacephem antibiotic in which the oxazine ring is substituted with a tetrazolylthiomethyl group and the azetidinone ring carries methoxy and 2-carboxy-2-(4-hydroxyphenyl)acetamido substituents.		2.0510cephalosporin;
oxacephem		antibacterial drug
nicorandil
Nicorandil: A derivative of the NIACINAMIDE that is structurally combined with an organic nitrate. It is a potassium-channel opener that causes vasodilatation of arterioles and large coronary arteries. Its nitrate-like properties produce venous vasodilation through stimulation of guanylate cyclase.. nicorandil : A pyrimidinecarboxamide that is nicotinamide in which one of the hydrogens attached to the carboxamide nitrogen is replaced by a 2-(nitrooxy)ethyl group. It has both nitrate-like and ATP-sensitive potassium channel activator properties, and is used for the prevention and treatment of angina pectoris.		2.0510nitrate ester;
pyridinecarboxamide		potassium channel opener;
vasodilator agent
colforsin
Colforsin: Potent activator of the adenylate cyclase system and the biosynthesis of cyclic AMP. From the plant COLEUS FORSKOHLII. Has antihypertensive, positive inotropic, platelet aggregation inhibitory, and smooth muscle relaxant activities; also lowers intraocular pressure and promotes release of hormones from the pituitary gland.		2.830acetate ester;
cyclic ketone;
labdane diterpenoid;
organic heterotricyclic compound;
tertiary alpha-hydroxy ketone;
triol		adenylate cyclase agonist;
anti-HIV agent;
antihypertensive agent;
plant metabolite;
platelet aggregation inhibitor;
protein kinase A agonist
cefadroxil anhydrous
Cefadroxil: Long-acting, broad-spectrum, water-soluble, CEPHALEXIN derivative.. cefadroxil : A cephalosporin bearing methyl and (2R)-2-amino-2-(4-hydroxyphenyl)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		2.4520cephalosporinantibacterial drug
encainide
Encainide: One of the ANTI-ARRHYTHMIA AGENTS, it blocks VOLTAGE-GATED SODIUM CHANNELS and slows conduction within the His-Purkinje system and MYOCARDIUM.. encainide : 4-Methoxy-N-phenylbenzamide in which the hydrogen at the 2 position of the phenyl group is substituted by a 2-(1-methylpiperidin-2-yl)ethyl group. A class Ic antiarrhythmic, the hydrochloride was used for the treatment of severe or life-threatening ventricular arrhythmias, but it was associated with increased death rates in patients who had asymptomatic heart rhythm abnormalities after a recent heart attack and was withdrawn from the market.		2.0510benzamides;
piperidines		anti-arrhythmia drug;
sodium channel blocker
cefaclor anhydrous
Cefaclor: Semisynthetic, broad-spectrum antibiotic derivative of CEPHALEXIN.. cefaclor : A cephalosporin bearing chloro and (R)-2-amino-2-phenylacetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		2.0510cephalosporinantibacterial drug;
drug allergen
fomesafen
fomesafen: a protoporphyrinogen oxidase-inhibiting herbicide. fomesafen : An N-sulfonylcarboxamide that is N-(methylsulfonyl)benzamide in which the phenyl ring is substituted by a nitro group at position 2 and a 2-chloro-4-(trifluoromethyl)phenoxy group at position 5. A protoporphyrinogen oxidase inhibitor, it was specially developed for use (generally as the corresponding sodium salt, fomesafen-sodium) for post-emergence control of broad-leaf weeds in soya.		2.110aromatic ether;
C-nitro compound;
monochlorobenzenes;
N-sulfonylcarboxamide;
organofluorine compound;
phenols		agrochemical;
EC 1.3.3.4 (protoporphyrinogen oxidase) inhibitor;
herbicide
miglustat
miglustat: a glucosylceramide synthase inhibitor. miglustat : A hydroxypiperidine that is deoxynojirimycin in which the amino hydrogen is replaced by a butyl group.		2.0510piperidines;
tertiary amino compound		anti-HIV agent;
EC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
cefotetan
Cefotetan: A semisynthetic cephamycin antibiotic that is administered intravenously or intramuscularly. The drug is highly resistant to a broad spectrum of beta-lactamases and is active against a wide range of both aerobic and anaerobic gram-positive and gram-negative microorganisms.. cefotetan : A semi-synthetic second-generation cephamycin antibiotic with [(1-methyl-1H-tetrazol-5-yl)sulfanyl]methyl, methoxy and {[4-(2-amino-1-carboxy-2-oxoethylidene)-1,3-dithietan-2-yl]carbonyl}amino groups at the 3, 7alpha, and 7beta positions, respectively, of the cephem skeleton. It is resistant to a wide range of beta-lactamases and is active against a broad spectrum of aerobic and anaerobic Gram-positive and Gram-negative microorganisms.		2.0510
lovastatin
Lovastatin: A fungal metabolite isolated from cultures of Aspergillus terreus. The compound is a potent anticholesteremic agent. It inhibits 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It also stimulates the production of low-density lipoprotein receptors in the liver.. lovastatin : A fatty acid ester that is mevastatin carrying an additional methyl group on the carbobicyclic skeleton. It is used in as an anticholesteremic drug and has been found in fungal species such as Aspergillus terreus and Pleurotus ostreatus (oyster mushroom).		3.0140delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
polyketide;
statin (naturally occurring)		anticholesteremic drug;
antineoplastic agent;
Aspergillus metabolite;
prodrug
n-(4-nitrophenacyl)imidazole
N-(4-nitrophenacyl)imidazole: structure in first source		2.0810
enoximone
Enoximone: A selective phosphodiesterase inhibitor with vasodilating and positive inotropic activity that does not cause changes in myocardial oxygen consumption. It is used in patients with CONGESTIVE HEART FAILURE.		2.0510aromatic ketone
piritrexim
piritrexim: RN given refers to parent cpd; structure given in first source		2.0510
simvastatin
Simvastatin: A derivative of LOVASTATIN and potent competitive inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES), which is the rate-limiting enzyme in cholesterol biosynthesis. It may also interfere with steroid hormone production. Due to the induction of hepatic LDL RECEPTORS, it increases breakdown of LDL CHOLESTEROL.. simvastatin : A member of the class of hexahydronaphthalenes that is lovastatin in which the 2-methylbutyrate ester moiety has been replaced by a 2,2-dimethylbutyrate ester group. It is used as a cholesterol-lowering and anti-cardiovascular disease drug.		11.1691delta-lactone;
fatty acid ester;
hexahydronaphthalenes;
statin (semi-synthetic)		EC 1.1.1.34/EC 1.1.1.88 (hydroxymethylglutaryl-CoA reductase) inhibitor;
EC 3.4.24.83 (anthrax lethal factor endopeptidase) inhibitor;
ferroptosis inducer;
geroprotector;
prodrug
pravastatin
Pravastatin: An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (HYDROXYMETHYLGLUTARYL COA REDUCTASES).. pravastatin : A carboxylic ester resulting from the formal condensation of (S)-2-methylbutyric acid with the hydroxy group adjacent to the ring junction of (3R,5R)-7-[(1S,2S,6S,8S,8aR)-6,8-dihydroxy-2-methyl-1,2,6,7,8,8a-hexahydronaphthalen-1-yl]-3,5-dihydroxyheptanoic acid. Derived from microbial transformation of mevastatin, pravastatin is a reversible inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA). The sodium salt is used for lowering cholesterol and preventing cardiovascular disease. It is one of the lower potency statins, but has the advantage of fewer side effects compared with lovastatin and simvastatin.		2.45203-hydroxy carboxylic acid;
carbobicyclic compound;
carboxylic ester;
hydroxy monocarboxylic acid;
secondary alcohol;
statin (semi-synthetic)		anticholesteremic drug;
environmental contaminant;
metabolite;
xenobiotic
atomoxetine hydrochloride
Atomoxetine Hydrochloride: A propylamine derivative and selective ADRENERGIC UPTAKE INHIBITOR that is used in the treatment of ATTENTION DEFICIT HYPERACTIVITY DISORDER.. atomoxetine hydrochloride : The hydrochloride salt of atomoxetine.		2.0510hydrochlorideadrenergic uptake inhibitor;
antidepressant
atomoxetine
atomoxetine : A secondary amino compound having methyl and 3-(2-methylphenoxy)-3-phenylpropan-1-yl substituents.		2.0410aromatic ether;
secondary amino compound;
toluenes		adrenergic uptake inhibitor;
antidepressant;
environmental contaminant;
xenobiotic
quinapril
Quinapril: A tetrahydroisoquinoline derivative and ANGIOTENSIN CONVERTING ENZYME inhibitor that is used in the treatment of HYPERTENSION and HEART FAILURE.. quinapril : A member of the class of isoquinolines that is (3S)-2-L-alanyl-1,2,3,4-tetrahydroisoquinoline-3-carboxylic acid in which the alpha-amino group of the alanyl residue has been substituted by a 1-ethoxycarbonyl-4-phenylbutan-2-yl group (the all-S isomer). A prodrug for quinaprilat (by hydrolysis of the ethyl ester to the corresponding carboxylic acid), it is used as an angiotensin-converting enzyme inhibitor (ACE inhibitor) used (generally as the hydrochloride salt) for the treatment of hypertension and congestive heart failure.		2.0510dicarboxylic acid monoester;
ethyl ester;
isoquinolines;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
gepirone
gepirone: RN given refers to parent cpd; structure given in first source		2.0510N-arylpiperazine
mifepristone
Mifepristone: A progestational and glucocorticoid hormone antagonist. Its inhibition of progesterone induces bleeding during the luteal phase and in early pregnancy by releasing endogenous prostaglandins from the endometrium or decidua. As a glucocorticoid receptor antagonist, the drug has been used to treat hypercortisolism in patients with nonpituitary CUSHING SYNDROME.		2.45203-oxo-Delta(4) steroid;
acetylenic compound;
tertiary amino compound		abortifacient;
contraceptive drug;
hormone antagonist;
synthetic oral contraceptive
itraconazole
Itraconazole: A triazole antifungal agent that inhibits cytochrome P-450-dependent enzymes required for ERGOSTEROL synthesis.. itraconazole : An N-arylpiperazine that is cis-ketoconazole in which the imidazol-1-yl group is replaced by a 1,2,4-triazol-1-yl group and in which the actyl group attached to the piperazine moiety is replaced by a p-[(+-)1-sec-butyl-5-oxo-1,5-dihydro-4H-1,2,4-triazol-4-yl]phenyl group. A potent P-glycoprotein and CYP3A4 inhibitor, it is used as an antifungal drug for the treatment of various fungal infections, including aspergillosis, blastomycosis, candidiasis, chromoblastomycosis, coccidioidomycosis, cryptococcosis, histoplasmosis, and sporotrichosis.		2.7930aromatic ether;
conazole antifungal drug;
cyclic ketal;
dichlorobenzene;
dioxolane;
N-arylpiperazine;
triazole antifungal drug;
triazoles		EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor;
Hedgehog signaling pathway inhibitor;
P450 inhibitor
imiquimod
Imiquimod: A topically-applied aminoquinoline immune modulator that induces interferon production. It is used in the treatment of external genital and perianal warts, superficial CARCINOMA, BASAL CELL; and ACTINIC KERATOSIS.. imiquimod : An imidazoquinoline fused [4,5-c] carrying isobutyl and amino substituents at N-1 and C-4 respectively. A prescription medication, it acts as an immune response modifier and is used to treat genital warts, superficial basal cell carcinoma, and actinic keratosis.		10.3231imidazoquinolineantineoplastic agent;
interferon inducer
adefovir
adefovir: inhibitor of African swine fever virus. adefovir(1-) : A organophosphonate oxoanion obtained by removal of a proton from the phosphonate group of adefovir, a nucleoside reverse transcriptase inhibitor. It is the major microspecies at pH 7.3 (according to Marvin v 6.2.0.).. adefovir : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens has been replaced by a 2-(6-amino-9H-purin-9-yl)ethoxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(t-butoxycarbonyloxymethyl) ester (dipivoxil ester) prodrug is used to treat chronic hepatitis B viral infection.		2.04106-aminopurines;
ether;
phosphonic acids		antiviral drug;
DNA synthesis inhibitor;
drug metabolite;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent
aromasil
[no description available]		3.121017-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid		antineoplastic agent;
EC 1.14.14.14 (aromatase) inhibitor;
environmental contaminant;
xenobiotic
sparfloxacin
[no description available]		2.4520fluoroquinolone antibiotic;
N-arylpiperazine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone
zileuton
[no description available]		2.46201-benzothiophenes;
ureas		anti-asthmatic drug;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor;
ferroptosis inhibitor;
leukotriene antagonist;
non-steroidal anti-inflammatory drug
clopidogrel
Clopidogrel: A ticlopidine analog and platelet purinergic P2Y receptor antagonist that inhibits adenosine diphosphate-mediated PLATELET AGGREGATION. It is used to prevent THROMBOEMBOLISM in patients with ARTERIAL OCCLUSIVE DISEASES; MYOCARDIAL INFARCTION; STROKE; or ATRIAL FIBRILLATION.. clopidogrel : A thienopyridine that is 4,5,6,7-tetrahydrothieno[3,2-c]pyridine in which the hydrogen attached to the nitrogen is replaced by an o-chlorobenzyl group, the methylene hydrogen of which is replaced by a methoxycarbonyl group (the S enantiomer). A P2Y12 receptor antagonist, it is used to inhibit blood clots and prevent heart attacks.		2.830methyl ester;
monochlorobenzenes;
thienopyridine		anticoagulant;
P2Y12 receptor antagonist;
platelet aggregation inhibitor
cidofovir anhydrous
Cidofovir: An acyclic nucleoside phosphonate that acts as a competitive inhibitor of viral DNA polymerases. It is used in the treatment of RETINITIS caused by CYTOMEGALOVIRUS INFECTIONS and may also be useful for treating HERPESVIRUS INFECTIONS.. cidofovir anhydrous : Cytosine substituted at the 1 position by a 3-hydroxy-2-(phosphonomethoxy)propyl group (S configuration). A nucleoside analogue, it is an injectable antiviral used for the treatment of cytomegalovirus (CMV) retinitis in AIDS patients.		3.5620phosphonic acids;
pyrimidone		anti-HIV agent;
antineoplastic agent;
antiviral drug;
photosensitizing agent
topotecan
Topotecan: An antineoplastic agent used to treat ovarian cancer. It works by inhibiting DNA TOPOISOMERASES, TYPE I.. topotecan : A pyranoindolizinoquinoline used as an antineoplastic agent. It is a derivative of camptothecin and works by binding to the topoisomerase I-DNA complex and preventing religation of these 328 single strand breaks.		4.2250pyranoindolizinoquinolineantineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor
bromfenac
bromfenac: bromfenac sodium is the active cpd; structure in first source. bromfenac : Amfenac in which the the hydrogen at the 4 position of the benzoyl group is substituted by bromine. It is used for the management of ocular pain and treatment of postoperative inflammation in patients who have undergone cataract extraction. It was withdrawn from the US market in 1998, following concerns over off-label abuse and hepatic failure.		2.0510aromatic amino acid;
benzophenones;
organobromine compound;
substituted aniline		non-narcotic analgesic;
non-steroidal anti-inflammatory drug
pivalyloxymethyl butyrate
pivalyloxymethyl butyrate: structure given in first source		2.0310
gemcitabine
gemcitabine : A 2'-deoxycytidine having geminal fluoro substituents in the 2'-position. An inhibitor of ribonucleotide reductase, gemcitabine is used in the treatment of various carcinomas, particularly non-small cell lung cancer, pancreatic cancer, bladder cancer and breast cancer.		12.06246organofluorine compound;
pyrimidine 2'-deoxyribonucleoside		antimetabolite;
antineoplastic agent;
antiviral drug;
DNA synthesis inhibitor;
EC 1.17.4.1 (ribonucleoside-diphosphate reductase) inhibitor;
environmental contaminant;
immunosuppressive agent;
photosensitizing agent;
prodrug;
radiosensitizing agent;
xenobiotic
atorvastatin
[no description available]		3.5920aromatic amide;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrroles;
statin (synthetic)		environmental contaminant;
xenobiotic
lamivudine
[no description available]		2.4420monothioacetal;
nucleoside analogue;
oxacycle;
primary alcohol		allergen;
anti-HBV agent;
antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor;
HIV-1 reverse transcriptase inhibitor;
prodrug
duloxetine
[no description available]		2.0510duloxetine
irinotecan
[no description available]		14.85213carbamate ester;
delta-lactone;
N-acylpiperidine;
pyranoindolizinoquinoline;
ring assembly;
tertiary alcohol;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
valsartan
Valsartan: A tetrazole derivative and ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to treat HYPERTENSION.. valsartan : A monocarboxylic acid amide consisting of L-valine in which the amino hydrogens have been replaced by a pentanoyl and a [2'-(1H-tetrazol-5-yl)biphenyl]-4-yl]methyl group. It exhibits antihypertensive activity.		2.0510biphenylyltetrazole;
monocarboxylic acid amide;
monocarboxylic acid		angiotensin receptor antagonist;
antihypertensive agent;
environmental contaminant;
xenobiotic
adefovir dipivoxil
bis(pivaloyloxymethyl)-9-(2-phosphonylmethoxyethyl)adenine: structure given in first source. adefovir pivoxil : An organic phosphonate that is the dipivoxil ester of adefovir. A prodrug for adefovir, an HIV-1 reverse transcriptase inhibitor, adefovir pivoxil is used to treat chronic hepatitis B viral infection.		2.05106-aminopurines;
carbonate ester;
ether;
organic phosphonate		antiviral drug;
DNA synthesis inhibitor;
HIV-1 reverse transcriptase inhibitor;
nephrotoxic agent;
prodrug
azalanstat
azalanstat: inhibits lanosterol 14 alpha-demethylase, the enzyme which catalyzes the first step in conversion of lanosterol to cholesterol in mammals; structure given in first source		2.0810
capecitabine
Capecitabine: A deoxycytidine derivative and fluorouracil PRODRUG that is used as an ANTINEOPLASTIC ANTIMETABOLITE in the treatment of COLON CANCER; BREAST CANCER and GASTRIC CANCER.. capecitabine : A carbamate ester that is cytidine in which the hydrogen at position 5 is replaced by fluorine and in which the amino group attached to position 4 is converted into its N-(penyloxy)carbonyl derivative. Capecitabine is a antineoplastic agent used in the treatment of cancers.		9.91145carbamate ester;
cytidines;
organofluorine compound		antimetabolite;
antineoplastic agent;
prodrug
adenosine
quinquefolan B: isolated from roots of Panax quinquefolium L.; RN not in Chemline 10/87; RN from Toxlit		3.4670adenosines;
purines D-ribonucleoside		analgesic;
anti-arrhythmia drug;
fundamental metabolite;
human metabolite;
vasodilator agent
safranal
safranal: a monoterpene aldehyde; one of the main components responsible for the aroma of saffron; structure given in first source. safranal : A monoterpenoid formally derived from beta-cyclocitral by dehydrogenation.		2.110monoterpenoid
vanadates
Vanadates: Oxyvanadium ions in various states of oxidation. They act primarily as ion transport inhibitors due to their inhibition of Na(+)-, K(+)-, and Ca(+)-ATPase transport systems. They also have insulin-like action, positive inotropic action on cardiac ventricular muscle, and other metabolic effects.. vanadate(3-) : A vanadium oxoanion that is a trianion with formula VO4 in which the vanadium is in the +5 oxidation state and is attached to four oxygen atoms.		2.0310trivalent inorganic anion;
vanadium oxoanion		EC 3.1.3.1 (alkaline phosphatase) inhibitor;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
EC 3.1.3.41 (4-nitrophenylphosphatase) inhibitor;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor
acridine orange
Acridine Orange: A cationic cytochemical stain specific for cell nuclei, especially DNA. It is used as a supravital stain and in fluorescence cytochemistry. It may cause mutations in microorganisms.. acridine orange : Fluorescent dye useful for cell cycle determination. It is cell-permeable, and interacts with DNA and RNA by intercalation or electrostatic attractions respectively.. acridine orange free base : A member of the class of aminoacridines that is acridine carrying two dimethylamino substituents at positions 3 and 6. The hydrochloride salt is the fluorescent dye 'acridine orange', used for cell cycle determination.		2.520aminoacridines;
aromatic amine;
tertiary amino compound		fluorochrome;
histological dye
halofuginone
[no description available]		2.0510quinazolines
ortho-cept
ethinyl estradiol-desogestrel combination: Ethinyl Estradiol and Desogestrell given in fixed proportions; has proved to be an effective & well-tolerated oral contraceptive, which improves cycle control & has a beneficial effect on acne		2.0510
cefprozil
[no description available]		2.0510cephalosporin;
semisynthetic derivative		antibacterial drug
4-[1-[4-[2-(dimethylamino)ethoxy]phenyl]-2-phenylbut-1-enyl]phenol
[no description available]		2.0510stilbenoid
efavirenz
efavirenz: HIV-1 reverse transcriptase inhibitor. efavirenz : 1,4-Dihydro-2H-3,1-benzoxazin-2-one substituted at the 4 position by cyclopropylethynyl and trifluoromethyl groups (S configuration) and at the 6 position by chlorine. A non-nucleoside reverse transcriptase inhibitor with activity against HIV, it is used with other antiretrovirals for combination therapy of HIV infection.		2.4820acetylenic compound;
benzoxazine;
cyclopropanes;
organochlorine compound;
organofluorine compound		antiviral drug;
HIV-1 reverse transcriptase inhibitor
nelfinavir
Nelfinavir: A potent HIV protease inhibitor. It is used in combination with other antiviral drugs in the treatment of HIV in both adults and children.. nelfinavir : An aryl sulfide that is used (as its mesylate salt) for treatment of HIV and also exhibits some anticancer properties.		2.4520aryl sulfide;
benzamides;
organic heterobicyclic compound;
phenols;
secondary alcohol;
tertiary amino compound		antineoplastic agent;
HIV protease inhibitor
doxapram hydrochloride
[no description available]		2.0510hydrochloridecentral nervous system stimulant
chloroquine diphosphate
[no description available]		3.3510
ursolic acid
[no description available]		2.5920hydroxy monocarboxylic acid;
pentacyclic triterpenoid		geroprotector;
plant metabolite
n-methylnicotinamide
N-methylnicotinamide: structure. N-methylnicotinamide : A pyridinecarboxamide that is nicotinamide in which one of the amide hydrogens is substituted by a methyl group.		2.0410pyridinecarboxamidemetabolite
1,5-anhydroglucitol
1,5-anhydroglucitol: structure. 1,5-anhydro-D-glucitol : An anhydro sugar of D-glucitol.		2.0510anhydro sugarhuman metabolite
thiazolyl blue
thiazolyl blue: RN & II refers to bromide. 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide : The bromide salt of 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium.		4.4780organic bromide saltcolorimetric reagent;
dye
betulinic acid
[no description available]		2.5220hydroxy monocarboxylic acid;
pentacyclic triterpenoid		anti-HIV agent;
anti-inflammatory agent;
antimalarial;
antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
plant metabolite
arctigenin
arctigenin: precursor to catechols; in many plants		2.0310lignan
baicalin
[no description available]		4.9621dihydroxyflavone;
glucosiduronic acid;
glycosyloxyflavone;
monosaccharide derivative		antiatherosclerotic agent;
antibacterial agent;
anticoronaviral agent;
antineoplastic agent;
antioxidant;
cardioprotective agent;
EC 2.7.7.48 (RNA-directed RNA polymerase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
ferroptosis inhibitor;
neuroprotective agent;
non-steroidal anti-inflammatory drug;
plant metabolite;
prodrug
plerixafor
plerixafor: a bicyclam derivate, highly potent & selective inhibitor of HIV-1 & HIV-2. plerixafor : An azamacrocycle consisting of two cyclam rings connected by a 1,4-phenylenebis(methylene) linker. It is a CXCR4 chemokine receptor antagonist and a hematopoietic stem cell mobilizer. It is used in combination with grulocyte-colony stimulating factor (G-CSF) to mobilize hematopoietic stem cells to the perpheral blood for collection and subsequent autologous transplantation in patients with non-Hodgkin's lymphoma and multiple myeloma.		2.7530azacycloalkane;
azamacrocycle;
benzenes;
crown amine;
secondary amino compound;
tertiary amino compound		anti-HIV agent;
antineoplastic agent;
C-X-C chemokine receptor type 4 antagonist;
immunological adjuvant
amprenavir
[no description available]		2.0510carbamate ester;
sulfonamide;
tetrahydrofuryl ester		antiviral drug;
HIV protease inhibitor
5-methylcytosine
5-Methylcytosine: A methylated nucleotide base found in eukaryotic DNA. In ANIMALS, the DNA METHYLATION of CYTOSINE to form 5-methylcytosine is found primarily in the palindromic sequence CpG. In PLANTS, the methylated sequence is CpNpGp, where N can be any base.. 5-methylcytosine : A pyrimidine that is a derivative of cytosine, having a methyl group at the 5-position.		2.1510methylcytosine;
pyrimidines		human metabolite
diphenylcyclopropenone
diphenylcyclopropenone: strong contact sensitizer; a photosensitizing agent; RN given refers to parent cpd; structure given in first source. diphenylcyclopropenone : A cyclopropenone compound having phenyl substituents at the 2- and 3-positions.		3.2510cyclopropenonedrug allergen;
hapten;
photosensitizing agent
epigallocatechin gallate
epigallocatechin gallate: a steroid 5alpha-reductase inhibitor and antimutagen in green tea (Camellia sinensis). (-)-epigallocatechin 3-gallate : A gallate ester obtained by the formal condensation of gallic acid with the (3R)-hydroxy group of (-)-epigallocatechin.		2.4720flavans;
gallate ester;
polyphenol		antineoplastic agent;
antioxidant;
apoptosis inducer;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent;
plant metabolite
aica ribonucleotide
AICA ribonucleotide: purine precursor that has antineoplastic activity. AICA ribonucleotide : A 1-(phosphoribosyl)imidazolecarboxamide that is acadesine in which the hydroxy group at the 5' position has been converted to its monophosphate derivative.		2.25101-(phosphoribosyl)imidazolecarboxamide;
aminoimidazole		cardiovascular drug;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
lissamine rhodamine b
lissamine rhodamine B: RN given refers to parent cpd; Lissamine Rhodamine B refers to Na salt		2.4320
glutathione disulfide
Glutathione Disulfide: A GLUTATHIONE dimer formed by a disulfide bond between the cysteine sulfhydryl side chains during the course of being oxidized.		2.7430glutathione derivative;
organic disulfide		Escherichia coli metabolite;
mouse metabolite
hypusine
hypusine: N-terminal amino alcohol deriv of Lys occurring in bovine brain & in the urine of children with familial hyperlysinemia; minor descriptor (75-82); online & Index Medicus search LYSINE/AA (75-82). hypusine : An L-lysine derivative that is L-lysine bearing a (2R)-4-amino-2-hydroxybutyl substituent at position N(6).		2.0310
4-nitrobenzylthioinosine
4-nitrobenzylthioinosine: inhibitor of nucleoside transport; acts on ENT1		2.0410purine nucleoside
iopamidol
Iopamidol: A non-ionic, water-soluble contrast agent which is used in myelography, arthrography, nephroangiography, arteriography, and other radiological procedures.. iopamidol : A benzenedicarboxamide compound having N-substituted carbamoyl groups at the 1- and 3-positions, iodo substituents at the 2-, 4- and 6-positions and a (2S)-2-hydroxypropanamido group at the 5-position.		2.0310benzenedicarboxamide;
organoiodine compound;
pentol		environmental contaminant;
radioopaque medium;
xenobiotic
cephalosporin c
cephalosporin C: RN given refers to parent cpd; structure in Merck, 9th ed, #1937. cephalosporin C : A cephalosporin antibiotic carrying a 3-acetoxymethyl substituent and a 6-oxo-N(6)-L-lysino group at position 7.		2.0310cephalosporinfungal metabolite
bendamustine
[no description available]		2.0510benzimidazoles
erdosteine
[no description available]		2.0510N-acyl-amino acid
mizolastine
[no description available]		2.0510benzimidazoles
intoplicine
intoplicine: structure in first source		2.0510pyridoindole
telmisartan
Telmisartan: A biphenyl compound and benzimidazole derivative that acts as an angiotensin II type 1 receptor antagonist. It is used in the management of HYPERTENSION.. telmisartan : A member of the class of benzimidazoles used widely in the treatment of hypertension.		5.8771benzimidazoles;
biphenyls;
carboxybiphenyl		angiotensin receptor antagonist;
antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
environmental contaminant;
xenobiotic
dexfenfluramine
Dexfenfluramine: The S-isomer of FENFLURAMINE. It is a serotonin agonist and is used as an anorectic. Unlike fenfluramine, it does not possess any catecholamine agonist activity.. (S)-fenfluramine : The S-enantiomer of fenfluramine. It stimulates the release of serotonin and selectively inhibits its reuptake, but unlike fenfluramine it does not possess catecholamine agonist activity. It was formerly given by mouth as the hydrochloride in the treatment of obesity, but, like fenfluramine, was withdrawn wolrdwide following reports of valvular heart defects.		2.0510fenfluramineappetite depressant;
serotonergic agonist;
serotonin uptake inhibitor
iridium radioisotopes
Iridium Radioisotopes: Unstable isotopes of iridium that decay or disintegrate emitting radiation. Ir atoms with atomic weights 182-190, 192, and 194-198 are radioactive iridium isotopes.		2.0510
2-methoxyestradiol
2-methoxy-17beta-estradiol : A 17beta-hydroxy steroid, being 17beta-estradiol methoxylated at C-2.		2.442017beta-hydroxy steroid;
3-hydroxy steroid		angiogenesis modulating agent;
antimitotic;
antineoplastic agent;
human metabolite;
metabolite;
mouse metabolite
triazoles
Triazoles: Heterocyclic compounds containing a five-membered ring with two carbon atoms and three nitrogen atoms with the molecular formula C2H3N3.. triazoles : An azole in which the five-membered heterocyclic aromatic skeleton contains three N atoms and two C atoms.		7.052311,2,3-triazole
tangeretin
tangeretin: structure given in first source; from citrus plants; inhibits invasion of MO4 mouse cells into embryonic chick heart in vitro. tangeretin : A pentamethoxyflavone flavone with methoxy groups at positions 4', 5, 6 , 7 and 8.. pentamethoxyflavone : A methoxyflavone that is flavone substituted by a five methoxy groups.		2.0510pentamethoxyflavoneantineoplastic agent;
plant metabolite
delphinidin
Paraffin: A mixture of solid hydrocarbons obtained from petroleum. It has a wide range of uses including as a stiffening agent in ointments, as a lubricant, and as a topical anti-inflammatory. It is also commonly used as an embedding material in histology.. delphinidin chloride : An anthocyanidin chloride that has delphinidin as the cationic counterpart.		2.4110anthocyanidin chloride
medetomidine
Medetomidine: An agonist of RECEPTORS, ADRENERGIC ALPHA-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of DEXMEDETOMIDINE.		2.0510imidazoles
fluorodeoxyglucose f18
Fluorodeoxyglucose F18: The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)		15.156182-deoxy-2-((18)F)fluoro-D-glucose;
2-deoxy-2-fluoro-aldehydo-D-glucose
sertraline
Sertraline: A selective serotonin uptake inhibitor that is used in the treatment of depression.. sertraline : A member of the class of tetralins that is tetralin which is substituted at positions 1 and 4 by a methylamino and a 3,4-dichlorophenyl group, respectively (the S,S diastereoisomer). A selective serotonin-reuptake inhibitor (SSRI), it is administered orally as the hydrochloride salt as an antidepressant for the treatment of depression, obsessive-compulsive disorder, panic disorder and post-traumatic stress disorder.		2.0510dichlorobenzene;
secondary amino compound;
tetralins		antidepressant;
serotonin uptake inhibitor
sanguinarine chloride
[no description available]		2.0410
picosulfate sodium
picosulfate sodium: contains two active ingredients, sodium picosulfate and magnesium citrate, which are both laxatives; structure		2.0510aryl sulfate;
pyridines
zoledronic acid
Zoledronic Acid: An imidobisphosphonate inhibitor of BONE RESORPTION that is used for the treatment of malignancy-related HYPERCALCEMIA; OSTEITIS DEFORMANS; and OSTEOPOROSIS.. zoledronic acid : An imidazole compound having a 2,2-bis(phosphono)-2-hydroxyethane-1-yl substituent at the 1-position.		6.21231,1-bis(phosphonic acid);
imidazoles		bone density conservation agent
artemisinin
(+)-artemisinin : A sesquiterpene lactone obtained from sweet wormwood, Artemisia annua, which is used as an antimalarial for the treatment of multi-drug resistant strains of falciparum malaria.		2.5520organic peroxide;
sesquiterpene lactone		antimalarial;
plant metabolite
dienogest
[no description available]		2.051017beta-hydroxy steroid;
3-oxo-Delta(4) steroid;
aliphatic nitrile;
steroid hormone		progesterone receptor agonist;
progestin;
synthetic oral contraceptive
drospirenone
drospirenone: a progestational compound with antimineralocorticoid and antiandrogenic activity; structure given in first source		2.01103-oxo-Delta(4) steroid;
steroid lactone		aldosterone antagonist;
contraceptive drug;
progestin
morphazinamide
morphazinamide: RN given refers to parent cpd; RN in Chemline for mono-HCL: 1473-73-0; structure in Merck Index		2.0510morpholines;
pyrazines;
secondary carboxamide
2-hydroxychavicol
2-hydroxychavicol: antimutagen from betel leaf; structure given in first source		2.5220
dapoxetine
[no description available]		4.6111naphthalenes
dexrazoxane
Dexrazoxane: The (+)-enantiomorph of razoxane.		2.0510razoxaneantineoplastic agent;
cardiovascular drug;
chelator;
immunosuppressive agent
tocophersolan
tocophersolan: RN given refers to parent cpd		2.1710tocol
diflorasone
diflorasone: RN given refers to (6alpha,11beta,16beta)-isomer; structure. diflorasone : The 16beta-analogue of flumethasone. It is used as the 17,21-diacetate as a topical anti-inflammatory and antipruritic in the treatment of various skin disorders.		2.021011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
fluorinated steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		anti-inflammatory drug
voriconazole
Voriconazole: A triazole antifungal agent that specifically inhibits STEROL 14-ALPHA-DEMETHYLASE and CYTOCHROME P-450 CYP3A.. voriconazole : A triazole-based antifungal agent used for the treatment of esophageal candidiasis, invasive pulmonary aspergillosis, and serious fungal infections caused by Scedosporium apiospermum and Fusarium spp. It is an inhibitor of cytochrome P450 2C9 (CYP2C9) and CYP3A4.		5.9371conazole antifungal drug;
difluorobenzene;
pyrimidines;
tertiary alcohol;
triazole antifungal drug		P450 inhibitor
cyclobutyrol
cyclobutyrol: RN given refers to parent cpd; structure. cyclobutyrol : A hydroxy monocarboxylic acid in which the hydroxy group is geminal to a 1-carboxypropyl group on a cyclohexane ring.		2.0510hydroxy monocarboxylic acidbile therapy drug
terlipressin
terlivaz: first FDA approved injection to improve kidney function in adults with hepatorenal syndrome (HRS) with rapid reduction in kidney function.		2.0510polypeptide
ubenimex
ubenimex: growth inhibitor		2.0110
7-hydroxystaurosporine
[no description available]		3.2710
honokiol
[no description available]		2.0510biphenyls
isoflavone
[no description available]		2.0510isoflavones
chelerythrine chloride
[no description available]		2.4420
clevudine
[no description available]		2.0510
nobiletin
nobiletin : A methoxyflavone that is flavone substituted by methoxy groups at positions 5, 6, 7, 8, 3' and 4' respectively.		2.2510methoxyflavoneantineoplastic agent;
plant metabolite
mesoporphyrin ix
mesoporphyrin IX: RN given refers to parent cpd; mesoheme is the iron salt of mesoporphyrin IX. mesoporphyrin IX : A member of the class of mesoporphyrins obtained by formal hydrogenation of the two vinyl groups in protoporphyrin.		3.1210
alantolactone
alantolactone: allergenic sesquiterpene lactone; crystalline mixture of alantolactones from group of sesquiterpenes; structure. alantolactone : A sesquiterpene lactone that is 3a,5,6,7,8,8a,9,9a-octahydronaphtho[2,3-b]furan-2-one bearing two methyl substituents at positions 5 and 8a as well as a methylidene substituent at position 3.		2.0810naphthofuran;
olefinic compound;
sesquiterpene lactone		antineoplastic agent;
apoptosis inducer;
plant metabolite
tetrandrine
tetrandrine: a bisbenzylisoquinoline that exhibits antifibrogenic activity		2.9940bisbenzylisoquinoline alkaloid;
isoquinolines
tosyllysine chloromethyl ketone
Tosyllysine Chloromethyl Ketone: An inhibitor of SERINE ENDOPEPTIDASES. Acts as an alkylating agent and is known to interfere with the translation process.		2.0210sulfonic acid derivative
isoalantolactone
isoalantolactone: RN given refers to (3aR-(3aalpha,4aalpha,8abeta,9aalpha))-isomer; structure. isoalantolactone : A sesquiterpene lactone of the eudesmanolide group. It has been isolated from Inula helenium.		2.610eudesmane sesquiterpenoid;
sesquiterpene lactone		antifungal agent;
apoptosis inducer;
plant metabolite
fascaplysine
fascaplysine: from tropic sea sponges		2.0310
1,2,3,4,5,6-hexabromocyclohexane
[no description available]		2.4420bromoalkane;
bromohydrocarbon		EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
bendamustine hydrochloride
[no description available]		2.110
frovatriptan
[no description available]		2.0110carbazoles
rosiglitazone
[no description available]		2.4620aminopyridine;
thiazolidinediones		EC 6.2.1.3 (long-chain-fatty-acid--CoA ligase) inhibitor;
ferroptosis inhibitor;
insulin-sensitizing drug
2-(4-toluidino)-6-naphthalenesulfonic acid
2-(4-toluidino)-6-naphthalenesulfonic acid: RN given refers to parent cpd; structure		2.0310
4-nitrophenylglucuronide
4-nitrophenyl beta-D-glucuronide : A beta-D-glucosiduronic acid having a 4-nitrophenyl substituent at the anomeric position.		2.0410beta-D-glucosiduronic acid;
C-nitro compound		chromogenic compound
acetaminophen glucuronide
acetaminophen glucuronide: acetaminophen metabolite in rats. acetaminophen O-beta-D-glucosiduronic acid : A beta-D-glucosiduronic acid that is the O-glucuronide of paracetamol (acetaminophen).		2.0410beta-D-glucosiduronic aciddrug metabolite
clarithromycin
Clarithromycin: A semisynthetic macrolide antibiotic derived from ERYTHROMYCIN that is active against a variety of microorganisms. It can inhibit PROTEIN SYNTHESIS in BACTERIA by reversibly binding to the 50S ribosomal subunits. This inhibits the translocation of aminoacyl transfer-RNA and prevents peptide chain elongation.. clarithromycin : The 6-O-methyl ether of erythromycin A, clarithromycin is a macrolide antibiotic used in the treatment of respiratory-tract, skin and soft-tissue infections. It is also used to eradicate Helicobacter pylori in the treatment of peptic ulcer disease. It prevents bacteria from growing by interfering with their protein synthesis.		2.4520macrolide antibioticantibacterial drug;
environmental contaminant;
protein synthesis inhibitor;
xenobiotic
we 201
We 201: synthetic lysolecithin analog; RN given refers to hydroxide inner salt; structure		2.2110
coenzyme a
[no description available]		2.4110adenosine 3',5'-bisphosphatecoenzyme;
Escherichia coli metabolite;
mouse metabolite
nicotine
(S)-nicotine : A 3-(1-methylpyrrolidin-2-yl)pyridine in which the chiral centre has S-configuration. The naturally occurring and most active enantiomer of nicotine, isolated from Nicotiana tabacum.		5.24313-(1-methylpyrrolidin-2-yl)pyridineanxiolytic drug;
biomarker;
immunomodulator;
mitogen;
neurotoxin;
nicotinic acetylcholine receptor agonist;
peripheral nervous system drug;
phytogenic insecticide;
plant metabolite;
psychotropic drug;
teratogenic agent;
xenobiotic
nsc-172755
butocin: S-substituted analog of mercaptopurine which functions as a cytostatic agent; minor descriptor (75-85); on-line search 6-MERCAPTOPURINE/AA (75-84); Index Medicus search MERCAPTOPURINE/analogs (75-84)		2.4110
fibrinogen
Fibrinogen: Plasma glycoprotein clotted by thrombin, composed of a dimer of three non-identical pairs of polypeptide chains (alpha, beta, gamma) held together by disulfide bonds. Fibrinogen clotting is a sol-gel change involving complex molecular arrangements: whereas fibrinogen is cleaved by thrombin to form polypeptides A and B, the proteolytic action of other enzymes yields different fibrinogen degradation products.. D-iditol : The D-enantiomer of iditol.		2.1710iditolfungal metabolite
aucubin
[no description available]		2.1110organic molecular entitymetabolite
homocysteine
Homocysteine: A thiol-containing amino acid formed by a demethylation of METHIONINE.. homocysteine : A sulfur-containing amino acid consisting of a glycine core with a 2-mercaptoethyl side-chain.. L-homocysteine : A homocysteine that has L configuration.		2.1310amino acid zwitterion;
homocysteine;
serine family amino acid		fundamental metabolite;
mouse metabolite
9-hydroxyellipticine
9-hydroxyellipticine: RN given refers to parent cpd. 9-hydroxyellipticine : A organic heterotetracyclic compound that is ellipticine in which the hydrogen at position 9 has been replaced by a hydroxy group.		2.0510organic heterotetracyclic compound;
organonitrogen heterocyclic compound		antineoplastic agent
lopinavir
[no description available]		7.6361amphetamines;
dicarboxylic acid diamide		anticoronaviral agent;
antiviral drug;
HIV protease inhibitor
gypsogenin
gypsogenin: originally from Gypsophila species; structure in first source. gypsogenin : A sapogenin that is olean-12-en-28-oic acid substituted by a beta-hydroxy group at position 3 and an oxo group at position 23.		2.6620aldehyde;
monocarboxylic acid;
pentacyclic triterpenoid;
sapogenin
glucuronic acid
Glucuronic Acid: A sugar acid formed by the oxidation of the C-6 carbon of GLUCOSE. In addition to being a key intermediate metabolite of the uronic acid pathway, glucuronic acid also plays a role in the detoxification of certain drugs and toxins by conjugating with them to form GLUCURONIDES.. D-glucuronic acid : The D-enantiomer of glucuronic acid.. D-glucopyranuronic acid : A D-glucuronic acid in cyclic pyranose form.		2.1110D-glucuronic acidalgal metabolite
8-aminoadenosine
[no description available]		2.0710
5-iodotubercidin
7-iodotubercidin: inhibits Toxoplasma gondii adenosine kinase		2.0310organoiodine compound
1,3,4-oxadiazole
1,3,4-oxadiazole: structure in first source		2.5820
combretastatin
combretastatin: cytotoxic principle from South African tree COMBRETUM caffrum; structure given in first source; acts at COLCHICINE site of TUBULIN		3.1710
beta-hydroxyisovalerylshikonin
beta-hydroxyisovalerylshikonin: structure in first source		3.5220
bimolane
bimolane: structure given in first source		2.2510
n-methyladenosine
N-methyladenosine: is a inhibitor of cell differentiation. N(6)-methyladenosine : A methyladenosine compound with one methyl group attached to N(6) of the adenine nucleobase.		2.8220methyladenosine
cobalt
Cobalt: A trace element that is a component of vitamin B12. It has the atomic symbol Co, atomic number 27, and atomic weight 58.93. It is used in nuclear weapons, alloys, and pigments. Deficiency in animals leads to anemia; its excess in humans can lead to erythrocytosis.. cobalt(1+) : A monovalent inorganic cation obtained from cobalt.. cobalt atom : A cobalt group element atom that has atomic number 27.		2.0310cobalt group element atom;
metal allergen		micronutrient
fulvestrant
Fulvestrant: An estradiol derivative and estrogen receptor antagonist that is used for the treatment of estrogen receptor-positive, locally advanced or metastatic breast cancer.. fulvestrant : A 3-hydroxy steroid that is 17beta-estradiol in which the 7alpha hydrogen has been replaced by a nonyl group in which one of the hydrogens of the terminal methyl has been replaced by a (4,4,5,5,5-pentafluoropentyl)sulfinyl group. An estrogen receptor antagonist, it is used in the treatment of breast cancer.		4.14017beta-hydroxy steroid;
3-hydroxy steroid;
organofluorine compound;
sulfoxide		antineoplastic agent;
estrogen antagonist;
estrogen receptor antagonist
mafosfamide
mafosfamide: RN given refers to cis-(+-)-isomer		2.4620
yttrium radioisotopes
Yttrium Radioisotopes: Unstable isotopes of yttrium that decay or disintegrate emitting radiation. Y atoms with atomic weights 82-88 and 90-96 are radioactive yttrium isotopes.		2.0210
carbidopa, levodopa drug combination
[no description available]		2.1710
imipenem, anhydrous
Imipenem: Semisynthetic thienamycin that has a wide spectrum of antibacterial activity against gram-negative and gram-positive aerobic and anaerobic bacteria, including many multiresistant strains. It is stable to beta-lactamases. Clinical studies have demonstrated high efficacy in the treatment of infections of various body systems. Its effectiveness is enhanced when it is administered in combination with CILASTATIN, a renal dipeptidase inhibitor.. imipenem : A broad-spectrum, intravenous beta-lactam antibiotic of the carbapenem subgroup.		2.0510beta-lactam antibiotic allergen;
carbapenems;
zwitterion		antibacterial drug
sn 38
SN-38 : A member of the class of pyranoindolizinoquinolines that is (4S)-pyrano[3',4':6,7]indolizino[1,2-b]quinoline-3,14-dione bearing two additional ethyl substituents at positions 4 and 11 as well as two additional hydroxy substituents at positions 4 and 9. It is the active metabolite of irinotecan and is ~1000 times more active than irinotecan itself.		2.0210delta-lactone;
phenols;
pyranoindolizinoquinoline;
tertiary alcohol		antineoplastic agent;
apoptosis inducer;
drug metabolite;
EC 5.99.1.2 (DNA topoisomerase) inhibitor
sr141716
[no description available]		2.0510amidopiperidine;
carbohydrazide;
dichlorobenzene;
monochlorobenzenes;
pyrazoles		anti-obesity agent;
appetite depressant;
CB1 receptor antagonist
bosentan anhydrous
Bosentan: A sulfonamide and pyrimidine derivative that acts as a dual endothelin receptor antagonist used to manage PULMONARY HYPERTENSION and SYSTEMIC SCLEROSIS.		8.71131primary alcohol;
pyrimidines;
sulfonamide		antihypertensive agent;
endothelin receptor antagonist
fluo-3
Fluo-3: fluorescent Ca(2+) indicator; permits continuous monitoring of Ca without interference with use of UV-sensitive caged compounds		2.0410xanthene dyefluorochrome
1,n(6)-ethenoadenine
1,N(6)-ethenoadenine: biologically active fluorescent derivatives of this cpd potentially valuable in studies concerning interactions between adenine cpds & various enzymes for which they serve as substrates or co-factors; structure		4.6111imidazo[2,1-i]purinemutagen
paxilline
paxilline: structure given in first source; RN given refers to (2R-(2alpha,4bbeta,6aalpha,12bbeta,12calpha,14abeta))-isomer. paxilline : An indole diterpene alkaloid with formula C27H33NO4 isolated from Penicillium paxilli. It is a potent inhibitor of large conductance Ca2(+)- and voltage-activated K(+) (BK)-type channels.		3.3460diterpene alkaloid;
enone;
organic heterohexacyclic compound;
terpenoid indole alkaloid;
tertiary alcohol		anticonvulsant;
Aspergillus metabolite;
EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor;
genotoxin;
geroprotector;
mycotoxin;
Penicillium metabolite;
potassium channel blocker
selenomethionine
[no description available]		2.0510amino acid zwitterion;
selenomethionine		plant metabolite
artesunic acid
[no description available]		4.950
thiamethoxam
Thiamethoxam: A nitro-oxazine and thiazole derivative that is used as a broad spectrum neonicotinoid insecticide.. thiamethoxam : An oxadiazane that is tetrahydro-N-nitro-4H-1,3,5-oxadiazin-4-imine bearing (2-chloro-1,3-thiazol-5-yl)methyl and methyl substituents at positions 3 and 5 respectively.		4.61111,3-thiazoles;
2-nitroguanidine derivative;
organochlorine compound;
oxadiazane		antifeedant;
carcinogenic agent;
environmental contaminant;
neonicotinoid insectide;
xenobiotic
perindopril
Perindopril: An angiotensin-converting enzyme inhibitor. It is used in patients with hypertension and heart failure.. perindopril : An alpha-amino acid ester that is the ethyl ester of N-{(2S)-1-[(2S,3aS,7aS)-2-carboxyoctahydro-1H-indol-1-yl]-1-oxopropan-2-yl}-L-norvaline		2.4820alpha-amino acid ester;
dicarboxylic acid monoester;
ethyl ester;
organic heterobicyclic compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
fingolimod hydrochloride
Fingolimod Hydrochloride: A sphingosine-derivative and IMMUNOSUPPRESSIVE AGENT that blocks the migration and homing of LYMPHOCYTES to the CENTRAL NERVOUS SYSTEM through its action on SPHINGOSINE 1-PHOSPHATE RECEPTORS. It is used in the treatment of MULTIPLE SCLEROSIS.. fingolimod hydrochloride : The hydrochloride salt of 2-amino-2-[2-(4-octylphenyl) ethyl]-1,3-propanediol (fingolimod).		2.4620hydrochlorideimmunosuppressive agent;
prodrug;
sphingosine-1-phosphate receptor agonist
fingolimod
fingolimod : An aminodiol that consists of propane-1,3-diol having amino and 2-(4-octylphenyl)ethyl substituents at the 2-position. It is a sphingosine 1-phosphate receptor modulator used for the treatment of relapsing-remitting multiple sclerosis. A prodrug, fingolimod is phosphorylated by sphingosine kinase to active metabolite fingolimod-phosphate, a structural analogue of sphingosine 1-phosphate.		2.0510aminodiol;
primary amino compound		antineoplastic agent;
CB1 receptor antagonist;
immunosuppressive agent;
prodrug;
sphingosine-1-phosphate receptor agonist
triptolide
[no description available]		3.1650diterpenoid;
epoxide;
gamma-lactam;
organic heteroheptacyclic compound		antispermatogenic agent;
plant metabolite
tryptoquivaline
tryptoquivaline: tremor-producing metabolite from Aspergillus clavatus; tetrapeptide derived from tryptophan, anthranilic acid, valine, & methylalanine; structure & N1 names previously assigned to tryptoquivaline C & tryptoquivaline D found to be incorrect & are revised in third source; see also record for tryptoquivalone; structure in third source		2.9540
tamibarotene
tamibarotene: has retinoid-binding activity. tamibarotene : A dicarboxylic acid monoamide resulting from the condensation of one of the carboxy groups of terephthalic acid with the amino group of 5,5,8,8-tetramethyl-5,6,7,8-tetrahydronaphthalen-2-amine.		3.1310dicarboxylic acid monoamide;
retinoid;
tetralins		antineoplastic agent;
retinoic acid receptor alpha/beta agonist
carboxyamido-triazole
carboxyamido-triazole: structure given in first source; coccidiostat; U.S. patent No. 4,590,201		2.9740
ecteinascidin 743
[no description available]		4.8840acetate ester;
azaspiro compound;
bridged compound;
hemiaminal;
isoquinoline alkaloid;
lactone;
organic heteropolycyclic compound;
organic sulfide;
oxaspiro compound;
polyphenol;
tertiary amino compound		alkylating agent;
angiogenesis modulating agent;
anti-inflammatory agent;
antineoplastic agent;
marine metabolite
deoxyglucose
Deoxyglucose: 2-Deoxy-D-arabino-hexose. An antimetabolite of glucose with antiviral activity.. deoxyglucose : A deoxyhexose comprising glucose having at least one hydroxy group replaced by hydrogen.		4.0640
tadalafil
[no description available]		2.2510benzodioxoles;
pyrazinopyridoindole		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
1-phenyl-2-decanoylamino-3-morpholino-1-propanol
RV 538: noninactivating inhibitor of ceramide-UDPG glucosyltransferase; RN given for unspecified HCl; structure given in first source		2.0610
6-phenylhexyl isothiocyanate
[no description available]		2.0810
thromboxanes
thromboxane : A class of oxygenated oxane derivatives, originally derived from prostaglandin precursors in platelets, that stimulate aggregation of platelets and constriction of blood vessels.		2.4110
tanshinone
tanshinone: from root of Salvia miltiorrhiza Bunge; RN given refers to tanshinone I; cardioprotective agent and neuroprotective agent		2.5920abietane diterpenoidanticoronaviral agent
nitisinone
[no description available]		2.4320(trifluoromethyl)benzenes;
C-nitro compound;
cyclohexanones;
mesotrione		EC 1.13.11.27 (4-hydroxyphenylpyruvate dioxygenase) inhibitor
marimastat
marimastat: a matrix metalloproteinase inhibitor active in patients with advanced carcinoma of the pancreas, prostate, or ovary. marimastat : A secondary carboxamide resulting from the foraml condensation of the carboxy group of (2R)-2-[(1S)-1-hydroxy-2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the alpha-amino group of N,3-dimethyl-L-valinamide.		3.8721hydroxamic acid;
secondary carboxamide		antineoplastic agent;
matrix metalloproteinase inhibitor
clofarabine
[no description available]		4.7750adenosines;
organofluorine compound		antimetabolite;
antineoplastic agent
elacridar
Elacridar: inhibitor of MDR1 PROTEIN; structure given in first source		3.360
mitiglinide
mitiglinide: a rapid and short-acting hypoglycemic agent; acts on sulfonylurea receptor closing KATP channels; considered one of the glinides-an imprecise grouping; structure given in first source		2.0510benzenes;
monocarboxylic acid
piperaquine
piperaquine : An aminoquinoline that is 1,3-di(piperazin-1-yl)propane in which the nitrogen at position 4 of each of the piperazine moieties is replaced by a 7-chloroquinolin-4-yl group.		3.711aminoquinoline;
N-arylpiperazine;
organochlorine compound		antimalarial
celastrol
[no description available]		2.4620monocarboxylic acid;
pentacyclic triterpenoid		anti-inflammatory drug;
antineoplastic agent;
antioxidant;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
Hsp90 inhibitor;
metabolite
peroxynitrous acid
Peroxynitrous Acid: A potent oxidant synthesized by the cell during its normal metabolism. Peroxynitrite is formed from the reaction of two free radicals, NITRIC OXIDE and the superoxide anion (SUPEROXIDES).		521nitrogen oxoacid
fullerene c60
Fullerenes: A polyhedral CARBON structure composed of around 60-80 carbon atoms in pentagon and hexagon configuration. They are named after Buckminster Fuller because of structural resemblance to geodesic domes. Fullerenes can be made in high temperature such as arc discharge in an inert atmosphere.. fullerene : A compound composed solely of an even number of carbon atoms, which form a cage-like fused-ring polycyclic system with twelve five-membered rings and the rest six-membered rings. The term has been broadened to include any closed cage structure consisting entirely of three-coordinate carbon atoms.		2.4110fullerenegeroprotector
gefitinib
[no description available]		12.95802aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
morpholines;
quinazolines;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
epidermal growth factor receptor antagonist
n(6)-(3-iodobenzyl)-5'-n-methylcarboxamidoadenosine
N(6)-(3-iodobenzyl)-5'-N-methylcarboxamidoadenosine: structure given in first source; a selective A(3) adenosine receptor agonist. 3-iodobenzyl-5'-N-methylcarboxamidoadenosine : A derivative of adenosine in which the 5'-hydroxymethyl group is replaced by N-ethylcarboxamido and one of the hydrogens of the exocyclic amino function is substituted by a 3-iodobenzyl group.		2.0510adenosines;
monocarboxylic acid amide;
organoiodine compound		adenosine A3 receptor agonist
16-hydroxycleroda-3,13(14)-dien-15,16-olide
16-hydroxycleroda-3,13(14)-dien-15,16-olide: from Polyalthia longifolia; structure given in first source		2.0610
n-methylisoindigotin
N-methylisoindigotin: used in therapy of Lewis lung carcinoma; structure given in first source		2.0510
lestaurtinib
[no description available]		5.1550indolocarbazole
1-(7-(2-hydroxyethyl)dodecahydro-3a-methyl-1h-benz(e)inden-3-yl)ethanone
1-(7-(2-hydroxyethyl)dodecahydro-3a-methyl-1H-benz(e)inden-3-yl)ethanone: structure given in first source		2.0610
methotrexate
[no description available]		11.81443dicarboxylic acid;
monocarboxylic acid amide;
pteridines		abortifacient;
antimetabolite;
antineoplastic agent;
antirheumatic drug;
dermatologic drug;
DNA synthesis inhibitor;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
immunosuppressive agent
antiprimod
azaspirane: structure given in first source		2.0510
sulbactam
[no description available]		2.0510penicillanic acids
olmesartan medoxomil
Olmesartan Medoxomil: An ANGIOTENSIN II TYPE 1 RECEPTOR BLOCKER that is used to manage HYPERTENSION.		2.0510biphenyls
ilomastat
CS 610: matrix metalloproteinase inhibitor; structure in first source. ilomastat : An N-acyl-amino acid obtained by formal condensation of the carboxy group of (2R)-2-[2-(hydroxyamino)-2-oxoethyl]-4-methylpentanoic acid with the amino group of N-methyl-L-tryptophanamide. A cell permeable broad-spectrum matrix metalloproteinase (MMP) inhibitor		2.0510hydroxamic acid;
L-tryptophan derivative;
N-acyl-amino acid		anti-inflammatory agent;
antibacterial agent;
antineoplastic agent;
EC 3.4.24.24 (gelatinase A) inhibitor;
neuroprotective agent
5-carboxyfluorescein diacetate
[no description available]		2.0410
calcium borate
calcium borate: RN given refers to cpd with MF CaB4O7		4.6111
proline
Proline: A non-essential amino acid that is synthesized from GLUTAMIC ACID. It is an essential component of COLLAGEN and is important for proper functioning of joints and tendons.. proline : An alpha-amino acid that is pyrrolidine bearing a carboxy substituent at position 2.		2.7530amino acid zwitterion;
glutamine family amino acid;
L-alpha-amino acid;
proline;
proteinogenic amino acid		algal metabolite;
compatible osmolytes;
Escherichia coli metabolite;
micronutrient;
mouse metabolite;
nutraceutical;
Saccharomyces cerevisiae metabolite
docetaxel
[no description available]		2.0510hydrate;
secondary alpha-hydroxy ketone		antineoplastic agent
docetaxel anhydrous
Docetaxel: A semisynthetic analog of PACLITAXEL used in the treatment of locally advanced or metastatic BREAST NEOPLASMS and NON-SMALL CELL LUNG CANCER.. docetaxel anhydrous : A tetracyclic diterpenoid that is paclitaxel with the N-benzyloxycarbonyl group replaced by N-tert-butoxycarbonyl, and the acetoxy group at position 10 replaced by a hydroxy group.		13.083510secondary alpha-hydroxy ketone;
tetracyclic diterpenoid		antimalarial;
antineoplastic agent;
photosensitizing agent
perifosine
[no description available]		10.7431ammonium betaine;
phospholipid		EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
atazanavir
atazanavir : A heavily substituted carbohydrazide that is an antiretroviral drug of the protease inhibitor (PI) class used to treat infection of human immunodeficiency virus (HIV).		2.0510carbohydrazideantiviral drug;
HIV protease inhibitor
lonafarnib
lonafarnib: inhibitor of farnesyl protein transferase. lonafarnib : A 4-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamide that has R configuration. It is used as oral farnesyltransferase inhibitor.		7.371124-{2-[4-(3,10-dibromo-8-chloro-6,11-dihydro-5H-benzo[5,6]cyclohepta[1,2-b]pyridin-11-yl)piperidin-1-yl]-2-oxoethyl}piperidine-1-carboxamideantineoplastic agent;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
tariquidar
[no description available]		2.7530benzamides
levofloxacin
Levofloxacin: The L-isomer of Ofloxacin.. levofloxacin : An optically active form of ofloxacin having (S)-configuration; an inhibitor of bacterial topoisomerase IV and DNA gyrase.		2.05109-fluoro-3-methyl-10-(4-methylpiperazin-1-yl)-7-oxo-2,3-dihydro-7H-[1,4]oxazino[2,3,4-ij]quinoline-6-carboxylic acid;
fluoroquinolone antibiotic;
quinolone antibiotic		antibacterial drug;
DNA synthesis inhibitor;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
topoisomerase IV inhibitor
ezetimibe
Ezetimibe: An azetidine derivative and ANTICHOLESTEREMIC AGENT that inhibits intestinal STEROL absorption. It is used to reduce total CHOLESTEROL; LDL CHOLESTEROL, and APOLIPOPROTEINS B in the treatment of HYPERLIPIDEMIAS.. ezetimibe : A beta-lactam that is azetidin-2-one which is substituted at 1, 3, and 4 by p-fluorophenyl, 3-(p-fluorophenyl)-3-hydroxypropyl, and 4-hydroxyphenyl groups, respectively (the 3R,3'S,4S enantiomer).		2.0510azetidines;
beta-lactam;
organofluorine compound		anticholesteremic drug;
antilipemic drug;
antimetabolite
cariporide
cariporide: a selective sodium-hydrogen exchange subtype 1 inhibitor; structure in first source		3.8630
tezosentan
tezosentan: structure in first source		2.0510
vatalanib
[no description available]		10.39194monochlorobenzenes;
phthalazines;
pyridines;
secondary amino compound		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
vascular endothelial growth factor receptor antagonist
moxifloxacin
Moxifloxacin: A fluoroquinolone that acts as an inhibitor of DNA TOPOISOMERASE II and is used as a broad-spectrum antibacterial agent.. moxifloxacin : A quinolone that consists of 4-oxo-1,4-dihydroquinoline-3-carboxylic acid bearing a cyclopropyl substituent at position 1, a fluoro substitiuent at position 6, a (4aS,7aS)-octahydro-6H-pyrrolo[3,4-b]pyridin-6-yl group at position 7 and a methoxy substituent at position 8. A member of the fluoroquinolone class of antibacterial agents.		2.0510aromatic ether;
cyclopropanes;
fluoroquinolone antibiotic;
pyrrolidinopiperidine;
quinolinemonocarboxylic acid;
quinolone antibiotic;
quinolone		antibacterial drug
cyc 682
sapacitabine: structure in first source. sapacitabine : A nucleoside analogue resulting from the formal condensation of the carboxy group of hexadecanoic acid with the amino group of CNDAC. It is the prodrug of CNDAC and is currently in clinical development for the treatment of acute myeloid leukemia (AML).		3.1610nitrile;
nucleoside analogue;
secondary carboxamide		antimetabolite;
antineoplastic agent;
DNA synthesis inhibitor;
prodrug
ruboxistaurin
ruboxistaurin: inhibits protein kinase C beta; structure in first source		2.0310
jtt 501
JTT 501: an insulin sensitizer; structure in first source		2.0510
disopyramide, (s)-isomer
[no description available]		2.0410
naproxen
Naproxen: An anti-inflammatory agent with analgesic and antipyretic properties. Both the acid and its sodium salt are used in the treatment of rheumatoid arthritis and other rheumatic or musculoskeletal disorders, dysmenorrhea, and acute gout.. naproxen : A methoxynaphthalene that is 2-methoxynaphthalene substituted by a carboxy ethyl group at position 6. Naproxen is a non-steroidal anti-inflammatory drug commonly used for the reduction of pain, fever, inflammation and stiffness caused by conditions such as osteoarthritis, kidney stones, rheumatoid arthritis, psoriatic arthritis, gout, ankylosing spondylitis, menstrual cramps, tendinitis, bursitis, and for the treatment of primary dysmenorrhea. It works by inhibiting both the COX-1 and COX-2 enzymes.		2.7730methoxynaphthalene;
monocarboxylic acid		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
drug allergen;
environmental contaminant;
gout suppressant;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
canertinib
[no description available]		2.5820monochlorobenzenes;
morpholines;
organofluorine compound;
quinazolines		antineoplastic agent;
tyrosine kinase inhibitor
birb 796
[no description available]		3.1450aromatic ether;
morpholines;
naphthalenes;
pyrazoles;
ureas		EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
immunomodulator
naphthalenediimide
naphthalenediimide: structure in first source		2.1710
olmesartan
olmesartan: an active metabolite of CS 866		2.1710biphenylyltetrazoleangiotensin receptor antagonist;
antihypertensive agent
tipifarnib
[no description available]		7.9111imidazoles;
monochlorobenzenes;
primary amino compound;
quinolone		antineoplastic agent;
apoptosis inducer;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
atrasentan
Atrasentan: A pyrrolidine and benzodioxole derivative that acts a RECEPTOR, ENDOTHELIN A antagonist. It has therapeutic potential as an antineoplastic agent and for the treatment of DIABETIC NEPHROPATHIES.		3.8130pyrrolidines
cryptotanshinone
cryptotanshinone: from Salvia miltiorrhiza		3.0740abietane diterpenoidanticoronaviral agent
cyc 202
seliciclib : 2,6-Diaminopurine carrying benzylamino, (2R)-1-hydroxybutan-2-yl and isopropyl substituents at C-6, C-2-N and N-9 respectively. It is an experimental drug candidate in the family of pharmacological cyclin-dependent kinase (CDK) inhibitors.		4.27502,6-diaminopurinesantiviral drug;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
withanolide d
withanolide D: structure. withanolide D : A withanolide that is 5,6:22,26-diepoxyergosta-2,24-diene-1,26-dione substituted by hydroxy groups at positions 4 and 22 (the 4beta,5beta,6beta,22R stereoisomer). Isolated from Tubocapsicum anomalum and Withania somnifera, it exhibits cytotoxic activity.		2.051020-hydroxy steroid;
4-hydroxy steroid;
delta-lactone;
enone;
epoxy steroid;
ergostanoid;
secondary alcohol;
tertiary alcohol;
withanolide		antineoplastic agent
platycodin d
platycodin D: triterpenoid saponin from a root of Platycodon grandiflorum; RN refers to (2beta,3beta,16alpha)-isomer; structure given in first source		2.1710triterpenoid saponinmetabolite
paromomycin
Paromomycin: An aminoglycoside antibacterial and antiprotozoal agent produced by species of STREPTOMYCES.. paromomycin : An amino cyclitol glycoside that is the 1-O-(2-amino-2-deoxy-alpha-D-glucopyranoside) and the 3-O-(2,6-diamino-2,6-dideoxy-beta-L-idopyranosyl)-beta-D-ribofuranoside of 4,6-diamino-2,3-dihydroxycyclohexane (the 1R,2R,3S,4R,6S diastereoisomer). It is obtained from various Streptomyces species. A broad-spectrum antibiotic, it is used (generally as the sulfate salt) for the treatment of acute and chronic intestinal protozoal infections, but is not effective for extraintestinal protozoal infections. It is also used as a therapeutic against visceral leishmaniasis.		2.0510amino cyclitol glycoside;
aminoglycoside antibiotic		anthelminthic drug;
antibacterial drug;
antiparasitic agent;
antiprotozoal drug
avasimibe
[no description available]		2.4920monoterpenoid
boswellic acid
boswellic acid: ursane type; RN given refers to (3alpha,4beta)-isomer; active principle of salai guggal; see also record for salai guggal		2.110triterpenoid
2-nitrophenyl octyl ether
[no description available]		2.1510
biotin
vitamin B7 : Any member of a group of vitamers that belong to the chemical structural class called biotins that exhibit biological activity against vitamin B7 deficiency. Vitamin B7 deficiency is very rare in individuals who take a normal balanced diet. Foods rich in biotin are egg yolk, liver, cereals, vegetables (spinach, mushrooms) and rice. Symptoms associated with vitamin B7 deficiency include thinning hair, scaly skin rashes around eyes, nose and mouth, and brittle nails. The vitamers include biotin and its ionized and salt forms.		2.0510biotins;
vitamin B7		coenzyme;
cofactor;
Escherichia coli metabolite;
fundamental metabolite;
human metabolite;
mouse metabolite;
nutraceutical;
prosthetic group;
Saccharomyces cerevisiae metabolite
angiotensin ii
Giapreza: injectable form of angiotensin II used to increase blood pressure in adult patients with septic or other distributive shock. Ile(5)-angiotensin II : An angiotensin II that acts on the central nervous system (PDB entry: 1N9V).		3.3460amino acid zwitterion;
angiotensin II		human metabolite
atropine
tropan-3alpha-yl 3-hydroxy-2-phenylpropanoate : A tropane alkaloid that is (1R,5)-8-methyl-8-azabicyclo[3.2.1]octane substituted by a (3-hydroxy-2-phenylpropanoyl)oxy group at position 3.		2.7430
ropivacaine
Ropivacaine: An anilide used as a long-acting local anesthetic. It has a differential blocking effect on sensory and motor neurons.. ropivacaine : The piperidinecarboxamide obtained by the formal condensation of N-propylpipecolic acid and 2,6-dimethylaniline.. (S)-ropivacaine : A piperidinecarboxamide-based amide-type local anaesthetic (amide caine) in which (S)-N-propylpipecolic acid and 2,6-dimethylaniline are combined to form the amide bond.		2.1710piperidinecarboxamide;
ropivacaine		local anaesthetic
sb 203580
[no description available]		3.5780imidazoles;
monofluorobenzenes;
pyridines;
sulfoxide		EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector;
Hsp90 inhibitor;
neuroprotective agent
sb 216763
[no description available]		2.0710indoles;
maleimides
erlotinib
[no description available]		2.9840aromatic ether;
quinazolines;
secondary amino compound;
terminal acetylenic compound		antineoplastic agent;
epidermal growth factor receptor antagonist;
protein kinase inhibitor
erlotinib hydrochloride
[no description available]		12.24611hydrochloride;
terminal acetylenic compound		antineoplastic agent;
protein kinase inhibitor
organophosphonates
hydrogenphosphite : A divalent inorganic anion resulting from the removal of a proton from two of the hydroxy groups of phosphorous acid.		4.3730divalent inorganic anion;
phosphite ion
dexketoprofen trometamol
dexketoprofen trometamol: a water-soluble tromethamine salt of the racemic ketoprofen, rac(+-)-ketoprofen		2.5920
troleandomycin
Troleandomycin: A macrolide antibiotic that is similar to ERYTHROMYCIN.. troleandomycin : A semi-synthetic macrolide antibiotic obtained by acetylation of the three free hydroxy groups of oleandomycin. Troleandomycin is only found in individuals that have taken the drug.		2.0510acetate ester;
epoxide;
macrolide antibiotic;
monosaccharide derivative;
polyketide;
semisynthetic derivative		EC 1.14.13.97 (taurochenodeoxycholate 6alpha-hydroxylase) inhibitor;
xenobiotic
lapatinib
[no description available]		7.82180furans;
organochlorine compound;
organofluorine compound;
quinazolines		antineoplastic agent;
tyrosine kinase inhibitor
deferasirox
Deferasirox: A triazole and benzoate derivative that acts as a selective iron chelator. It is used in the management of chronic IRON OVERLOAD due to blood transfusion or non-transfusion dependent THALASSEMIA.. deferasirox : A member of the class of triazoles, deferasirox is 1,2,4-triazole substituted by a 4-carboxyphenyl group at position 1 and by 2-hydroxyphenyl groups at positions 3 and 5. An orally active iron chelator, it is used to manage chronic iron overload in patients receiving long-term blood transfusions.		2.4920benzoic acids;
monocarboxylic acid;
phenols;
triazoles		iron chelator
dabigatran
Dabigatran: A THROMBIN inhibitor which acts by binding and blocking thrombogenic activity and the prevention of thrombus formation. It is used to reduce the risk of stroke and systemic EMBOLISM in patients with nonvalvular atrial fibrillation.. dabigatran : An aromatic amide obtained by formal condensation of the carboxy group of 2-{[(4-carbamimidoylphenyl)amino]methyl}-1-methyl-1H-benzimidazole-5-carboxylic acid with the secondary amoino group of N-pyridin-2-yl-beta-alanine. The active metabolite of the prodrug dabigatran etexilate, it acts as an anticoagulant which is used for the prevention of stroke and systemic embolism.		2.6920aromatic amide;
benzimidazoles;
beta-alanine derivative;
carboxamidine;
pyridines		anticoagulant;
EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor;
EC 3.4.21.5 (thrombin) inhibitor
tbc-11251
sitaxsentan: endothelin A receptor antagonist; structure in first source		3.5420benzodioxoles
sorafenib
[no description available]		13.231001(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
phenylureas;
pyridinecarboxamide		angiogenesis inhibitor;
anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
ferroptosis inducer;
tyrosine kinase inhibitor
lenalidomide
[no description available]		7.3781aromatic amine;
dicarboximide;
isoindoles;
piperidones		angiogenesis inhibitor;
antineoplastic agent;
immunomodulator
cp 101,606
traxoprodil mesylate: a selective NMDA antagonist; structure given in first source		2.1510
cholic acid
Cholic Acid: A major primary bile acid produced in the liver and usually conjugated with glycine or taurine. It facilitates fat absorption and cholesterol excretion.. cholic acid : A bile acid that is 5beta-cholan-24-oic acid bearing three alpha-hydroxy substituents at position 3, 7 and 12.		2.041012alpha-hydroxy steroid;
3alpha-hydroxy steroid;
7alpha-hydroxy steroid;
bile acid;
C24-steroid;
trihydroxy-5beta-cholanic acid		human metabolite;
mouse metabolite
sitosterol, (3beta)-isomer
Sobatum: tradename; active fraction of Solanum trilobatum; reduces side-effects of radiation-induced toxicity. sitosterol : A member of the class of phytosterols that is stigmast-5-ene substituted by a beta-hydroxy group at position 3.		2.05103beta-hydroxy-Delta(5)-steroid;
3beta-sterol;
C29-steroid;
phytosterols;
stigmastane sterol		anticholesteremic drug;
antioxidant;
mouse metabolite;
plant metabolite;
sterol methyltransferase inhibitor
deoxycholic acid
Deoxycholic Acid: A bile acid formed by bacterial action from cholate. It is usually conjugated with glycine or taurine. Deoxycholic acid acts as a detergent to solubilize fats for intestinal absorption, is reabsorbed itself, and is used as a choleretic and detergent.. deoxycholic acid : A bile acid that is 5beta-cholan-24-oic acid substituted by hydroxy groups at positions 3 and 12 respectively.		2.2110bile acid;
C24-steroid;
dihydroxy-5beta-cholanic acid		human blood serum metabolite
cortisone
[no description available]		3.431111-oxo steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(4) steroid;
C21-steroid;
glucocorticoid;
primary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone		human metabolite;
mouse metabolite
pheophorbide a
pheophorbide a: split product of chlorophyll obtained by saponification of pheophytin		2.4520
anisomycin
Anisomycin: An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.. (-)-anisomycin : An antibiotic isolated from various Streptomyces species. It interferes with protein and DNA synthesis by inhibiting peptidyl transferase or the 80S ribosome system.		2.5120monohydroxypyrrolidine;
organonitrogen heterocyclic antibiotic		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
antiparasitic agent;
bacterial metabolite;
DNA synthesis inhibitor;
protein synthesis inhibitor
benzofurans
Benzofurans: Compounds that contain a BENZENE ring fused to a furan ring.		2.0810
benzarone
benzarone: antihemorrhagic agent; structure		2.05101-benzofurans
estramustine
Estramustine: A nitrogen mustard linked to estradiol, usually as phosphate; used to treat prostatic neoplasms; also has radiation protective properties.. estramustine : A carbamate ester obtained by the formal condensation of the hydroxy group of 17beta-estradiol with the carboxy group of bis(2-chloroethyl)carbamic acid.		4.113117beta-hydroxy steroid;
carbamate ester;
organochlorine compound		alkylating agent;
antineoplastic agent;
radiation protective agent
solanine
Solanine: A mixture of alpha-chaconine and alpha-solanine, found in SOLANACEAE plants.. solanine : A glycoalkaloid poison found in species of the nightshade family (Solanaceae), such as the potato (Solanum tuberosum). It is a trisccharide derivative of solanidine [(22beta)-solanid-5-en-3beta-ol].		2.610
noscapine
Noscapine: A naturally occurring opium alkaloid that is a centrally acting antitussive agent.. (-)-noscapine : A benzylisoquinoline alkaloid that is 1,2,3,4-tetrahydroisoquinoline which is substituted by a 4,5-dimethoxy-3-oxo-1,3-dihydro-2-benzofuran-1-yl group at position 1, a methylenedioxy group at positions 6-7 and a methoxy group at position 8. Obtained from plants of the Papaveraceae family, it lacks significant painkilling properties and is primarily used for its antitussive (cough-suppressing) effects.		2.4520aromatic ether;
benzylisoquinoline alkaloid;
cyclic acetal;
isobenzofuranone;
organic heterobicyclic compound;
organic heterotricyclic compound;
tertiary amino compound		antineoplastic agent;
antitussive;
apoptosis inducer;
plant metabolite
homoharringtonine
Homoharringtonine: Semisynthetic derivative of harringtonine that acts as a protein synthesis inhibitor and induces APOPTOSIS in tumor cells. It is used in the treatment of MYELOID LEUKEMIA, CHRONIC.. omacetaxine mepesuccinate : A cephalotaxine-derived alkaloid ester obtained from Cephalotaxus harringtonia; used for the treatment of chronic or accelerated phase chronic myeloid leukaemia.		11.49346alkaloid ester;
enol ether;
organic heteropentacyclic compound;
tertiary alcohol		anticoronaviral agent;
antineoplastic agent;
apoptosis inducer;
protein synthesis inhibitor
wortmannin
[no description available]		3.6690acetate ester;
cyclic ketone;
delta-lactone;
organic heteropentacyclic compound		anticoronaviral agent;
antineoplastic agent;
autophagy inhibitor;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
geroprotector;
Penicillium metabolite;
radiosensitizing agent
2-oxindole
2-oxindole: RN given refers to parent cpd; structure. indolin-2-one : An indolinone carrying an oxo group at position 2.		2.1110gamma-lactam;
indolinone
withanolides
Withanolides: Ergostane derivatives of 28 carbons with oxygens at C1, C22, and C26 positions and the side chain cyclized. They are found in WITHANIA plant genus and have cytotoxic and other effects.		2.0510
trimethoprim, sulfamethoxazole drug combination
Trimethoprim, Sulfamethoxazole Drug Combination: A drug combination with broad-spectrum antibacterial activity against both gram-positive and gram-negative organisms. It is effective in the treatment of many infections, including PNEUMOCYSTIS PNEUMONIA in AIDS.. co-trimoxazole : A two-component mixture comprising trimethoprim and sulfamethoxazole.		2.4420
o-(chloroacetylcarbamoyl)fumagillol
O-(Chloroacetylcarbamoyl)fumagillol: Semisynthetic analog of fumagillin (a cyclohexane-sesquiterpene antibiotic isolated from ASPERGILLUS FUMIGATUS) that inhibits angiogenesis.. O-(chloroacetylcarbamoyl)fumagillol : A carbamate ester that is fumagillol in which the hydroxy group has been converted to the corresponding N-(chloroacetyl)carbamate derivative.		2.0510carbamate ester;
organochlorine compound;
semisynthetic derivative;
sesquiterpenoid;
spiro-epoxide		angiogenesis inhibitor;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
methionine aminopeptidase 2 inhibitor;
retinoic acid receptor alpha antagonist
nsc 680410
NSC 680410: a bcr/abl kinase inhibitor; structure in first source		8.4170
bortezomib
[no description available]		8.82400amino acid amide;
L-phenylalanine derivative;
pyrazines		antineoplastic agent;
antiprotozoal drug;
protease inhibitor;
proteasome inhibitor
calcein am
calcein AM: a non-fluorescent compound cleaved to a fluorescent compound by non-specific intracellular esterases. calcein am : An organic heteropentacyclic compound that is calcein in which all four carboxy group hydrogens have been substituted by (acetyloxy)methoxy groups and the hyrodgens of the two hydroxy groups have been substituted by acetyl groups. It is a a non-fluorescent probe cleaved to a fluorescent probe by non-specific intracellular esterases.		2.01102-benzofurans;
acetate ester;
gamma-lactone;
organic heteropentacyclic compound;
oxaspiro compound;
xanthene dye		fluorochrome
ritonavir
Ritonavir: An HIV protease inhibitor that works by interfering with the reproductive cycle of HIV. It also inhibits CYTOCHROME P-450 CYP3A.. ritonavir : An L-valine derivative that is L-valinamide in which alpha-amino group has been acylated by a [(2-isopropyl-1,3-thiazol-4-yl)methyl]methylcarbamoyl group and in which a hydrogen of the carboxamide amino group has been replaced by a (2R,4S,5S)-4-hydroxy-1,6-diphenyl-5-{[(1,3-thiazol-5-ylmethoxy)carbonyl]amino}hexan-2-yl group. A CYP3A inhibitor and antiretroviral drug from the protease inhibitor class used to treat HIV infection and AIDS, it is often used as a fixed-dose combination with another protease inhibitor, lopinavir. Also used in combination with dasabuvir sodium hydrate, ombitasvir and paritaprevir (under the trade name Viekira Pak) for treatment of chronic hepatitis C virus genotype 1 infection as well as cirrhosis of the liver.		8.42821,3-thiazoles;
carbamate ester;
carboxamide;
L-valine derivative;
ureas		antiviral drug;
environmental contaminant;
HIV protease inhibitor;
xenobiotic
jib-04
JIB-04: structure in first source		2.2110
bardoxolone methyl
methyl 2-cyano-3,12-dioxooleana-1,9(11)-dien-28-oate: structure in first source		2.0410cyclohexenones
5-iodoindirubin-3'-monoxime
5-iodoindirubin-3'-monoxime: inhibits GSK-3beta		2.0310
nexavar
[no description available]		2.0510organosulfonate salt
permanganate
[no description available]		4.6111manganese oxoacid
leupeptins
Leupeptins: A group of acylated oligopeptides produced by Actinomycetes that function as protease inhibitors. They have been known to inhibit to varying degrees trypsin, plasmin, KALLIKREINS, papain and the cathepsins.		3.1650
carboplatin
[no description available]		8.54142
lithium chloride
Lithium Chloride: A salt of lithium that has been used experimentally as an immunomodulator.. lithium chloride : A metal chloride salt with a Li(+) counterion.		7.7530inorganic chloride;
lithium salt		antimanic drug;
geroprotector
leptomycin b
[no description available]		4.570
2H-pyrazolo[4,3-b]quinoxalin-3-amine
[no description available]		2.0310quinoxaline derivative
glycogen
glycogen : A polydisperse, highly branched glucan composed of chains of D-glucopyranose residues in alpha(1->4) glycosidic linkage, joined together by alpha(1->6) glycosidic linkages. A small number of alpha(1->3) glycosidic linkages and some cumulative alpha(1->6) links also may occur. The branches in glycogen typically contain 8 to 12 glucose residues.		2.610
bradykinin
[no description available]		3.5110oligopeptidehuman blood serum metabolite;
vasodilator agent
glucosamine
D-glucosamine : An amino sugar whose structure comprises D-glucose having an amino substituent at position 2.. 2-amino-2-deoxy-D-glucopyranose : A D-glucosamine whose structure comprises D-glucopyranose having an amino substituent at position 2.		2.0510D-glucosamineEscherichia coli metabolite;
geroprotector;
mouse metabolite
elastin
[no description available]		2.7530oligopeptide
naringenin
(S)-naringenin : The (S)-enantiomer of naringenin.		2.0410(2S)-flavan-4-one;
naringenin		expectorant;
plant metabolite
oxytocin
Oxytocin: A nonapeptide hormone released from the neurohypophysis (PITUITARY GLAND, POSTERIOR). It differs from VASOPRESSIN by two amino acids at residues 3 and 8. Oxytocin acts on SMOOTH MUSCLE CELLS, such as causing UTERINE CONTRACTIONS and MILK EJECTION.. oxytocin : A cyclic nonapeptide hormone with amino acid sequence CYIQNCPLG that also acts as a neurotransmitter in the brain; the principal uterine-contracting and milk-ejecting hormone of the posterior pituitary. Together with the neuropeptide vasopressin, it is believed to influence social cognition and behaviour.		2.0610heterodetic cyclic peptide;
peptide hormone		oxytocic;
vasodilator agent
taxifolin
(+)-taxifolin : A taxifolin that has (2R,3R)-configuration.		2.0410taxifolinmetabolite
tosylphenylalanyl chloromethyl ketone
Tosylphenylalanyl Chloromethyl Ketone: An inhibitor of Serine Endopeptidases. Acts as alkylating agent and is known to interfere with the translation process.. N-tosyl-L-phenylalanyl chloromethyl ketone : The N-tosyl derivative of L-phenylalanyl chloromethyl ketone.		2.0210alpha-chloroketone;
sulfonamide		alkylating agent;
serine proteinase inhibitor
taurolithocholic acid
Taurolithocholic Acid: A bile salt formed in the liver from lithocholic acid conjugation with taurine, usually as the sodium salt. It solubilizes fats for absorption and is itself absorbed. It is a cholagogue and choleretic.. taurolithocholic acid : The bile acid taurine conjugate of lithocholic acid.		2.0410bile acid taurine conjugate;
monocarboxylic acid amide		human metabolite
inositol 3-phosphate
inositol 3-phosphate: RN given refers to (myo)-isomer		2.0810
quinidine
Quinidine: An optical isomer of quinine, extracted from the bark of the CHINCHONA tree and similar plant species. This alkaloid dampens the excitability of cardiac and skeletal muscles by blocking sodium and potassium currents across cellular membranes. It prolongs cellular ACTION POTENTIALS, and decreases automaticity. Quinidine also blocks muscarinic and alpha-adrenergic neurotransmission.. quinidine : A cinchona alkaloid consisting of cinchonine with the hydrogen at the 6-position of the quinoline ring substituted by methoxy.		2.4520cinchona alkaloidalpha-adrenergic antagonist;
anti-arrhythmia drug;
antimalarial;
drug allergen;
EC 1.14.13.181 (13-deoxydaunorubicin hydroxylase) inhibitor;
EC 3.6.3.44 (xenobiotic-transporting ATPase) inhibitor;
muscarinic antagonist;
P450 inhibitor;
potassium channel blocker;
sodium channel blocker
meropenem
Meropenem: A thienamycin derivative antibacterial agent that is more stable to renal dehydropeptidase I than IMIPENEM, but does not need to be given with an enzyme inhibitor such as CILASTATIN. It is used in the treatment of bacterial infections, including infections in immunocompromised patients.. meropenem : A carbapenemcarboxylic acid in which the azetidine and pyrroline rings carry 1-hydroxymethyl and in which the azetidine and pyrroline rings carry 1-hydroxymethyl and 5-(dimethylcarbamoyl)pyrrolidin-3-ylthio substituents respectively.		2.0510alpha,beta-unsaturated monocarboxylic acid;
carbapenemcarboxylic acid;
organic sulfide;
pyrrolidinecarboxamide		antibacterial agent;
antibacterial drug;
drug allergen
griseofulvin
Griseofulvin: An antifungal agent used in the treatment of TINEA infections.. griseofulvin : An oxaspiro compound produced by Penicillium griseofulvum. It is used by mouth as an antifungal drug for infections involving the scalp, hair, nails and skin that do not respond to topical treatment.		2.05101-benzofurans;
antibiotic antifungal drug;
benzofuran antifungal drug;
organochlorine compound;
oxaspiro compound		antibacterial agent;
Penicillium metabolite
digitoxin
Digitoxin: A cardiac glycoside sometimes used in place of DIGOXIN. It has a longer half-life than digoxin; toxic effects, which are similar to those of digoxin, are longer lasting. (From Martindale, The Extra Pharmacopoeia, 30th ed, p665). digitoxin : A cardenolide glycoside in which the 3beta-hydroxy group of digitoxigenin carries a 2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl-(1->4)-2,6-dideoxy-beta-D-ribo-hexopyranosyl trisaccharide chain.		2.0510cardenolide glycosideEC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor
saquinavir
Saquinavir: An HIV protease inhibitor which acts as an analog of an HIV protease cleavage site. It is a highly specific inhibitor of HIV-1 and HIV-2 proteases, and also inhibits CYTOCHROME P-450 CYP3A.. saquinavir : An aspartic acid derivative obtained by formal condensation of the primary amino group of (2S,3R)-4-[(3S,4aS,8aS)-3-(tert-butylcarbamoyl)octahydroisoquinolin-2(1H)-yl]-3-hydroxy-1-phenylbutan-2-ylamine with the carboxy group of N(2)(-quinolin-2-ylcarbonyl)-L-asparagine. An inhibitor of HIV-1 protease.		2.9640L-asparagine derivative;
quinolines		antiviral drug;
HIV protease inhibitor
hyperforin
hyperforin: a prenylated acylphloroglucinol derivative; antibiotic component of novoimanine; psychoactive agent in St. John's wort; Russian; structure;. hyperforin : A cyclic terpene ketone that is a prenylated carbobicyclic acylphloroglucinol derivative produced by St. John's Wort, Hypericum perforatum.		2.2110
netilmicin
Netilmicin: Semisynthetic 1-N-ethyl derivative of SISOMYCIN, an aminoglycoside antibiotic with action similar to gentamicin, but less ear and kidney toxicity.		2.0510
trimethaphan camsylate
trimethaphan camsylate : The (S)-camphorsulfonate salt of trimethaphan.		2.0510
erythromycin estolate
Erythromycin Estolate: A macrolide antibiotic, produced by Streptomyces erythreus. It is the lauryl sulfate salt of the propionic ester of erythromycin. This erythromycin salt acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.		2.0510aminoglycoside sulfate salt;
erythromycin derivative		enzyme inhibitor
naringin
[no description available]		2.0610(2S)-flavan-4-one;
4'-hydroxyflavanones;
dihydroxyflavanone;
disaccharide derivative;
neohesperidoside		anti-inflammatory agent;
antineoplastic agent;
metabolite
cyclopamine
[no description available]		2.7930piperidinesglioma-associated oncogene inhibitor
lignans
Lignans: A class of dibenzylbutane derivatives which occurs in higher plants and in fluids (bile, serum, urine, etc.) in man and other animals. These compounds, which have a potential anti-cancer role, can be synthesized in vitro by human fecal flora. (From Singleton & Sainsbury, Dictionary of Microbiology and Molecular Biology, 2d ed)		2.0510
acetylleucyl-leucyl-norleucinal
acetylleucyl-leucyl-norleucinal: a proteasome inhibitor. acetylleucyl-leucyl-norleucinal : A tripeptide composed of N-acetylleucyl, leucyl and norleucinal residues joined in sequence.		2.0110aldehyde;
tripeptide		cysteine protease inhibitor
devazepide
Devazepide: A derivative of benzodiazepine that acts on the cholecystokinin A (CCKA) receptor to antagonize CCK-8's (SINCALIDE) physiological and behavioral effects, such as pancreatic stimulation and inhibition of feeding.. devazepide : An indolecarboxamide obtained by formal condensation of the carboxy group of indole-2-carboxylic acid with the exocyclic amino group of (3S)-3-amino-1-methyl-5-phenyl-1,3-dihydro-1,4-benzodiazepin-2-one. A cholecystokinin antagonist used for treatment of gastrointestinal disorders.		2.05101,4-benzodiazepinone;
indolecarboxamide		antineoplastic agent;
apoptosis inducer;
cholecystokinin antagonist;
gastrointestinal drug
actinonin
actinonin: natural hydroxamic acid, pseudopeptide antibiotic isolated from Streptomyces species; structure		2.0110
tolterodine
[no description available]		2.0510tertiary amineantispasmodic drug;
muscarinic antagonist;
muscle relaxant
difluprednate
difluprednate: RN given refers to (6alpha,11beta)-isomer		2.0210butyrate ester;
corticosteroid hormone
doxorubicin hydrochloride
[no description available]		2.0510anthracycline
dironyl
dironyl: pronounced antifertility agent in rats; lactation suppressor in other species; serotonin antagonist; RN given refers to parent cpd; structure		3.1710organic molecular entity
erythromycin ethylsuccinate
Erythromycin Ethylsuccinate: A macrolide antibiotic, produced by Streptomyces erythreus. This compound is an ester of erythromycin base and succinic acid. It acts primarily as a bacteriostatic agent. In sensitive organisms, it inhibits protein synthesis by binding to 50S ribosomal subunits. This binding process inhibits peptidyl transferase activity and interferes with translocation of amino acids during translation and assembly of proteins.. erythromycin ethylsuccinate : A erythromycin derivative that is erythromycin A in which the hydroxy group at position 3R is substituted by a (4-ethoxy-4-oxobutanoyl)oxy group. It is used for the treatment of a wide variety of bacterial infections.		2.0510cyclic ketone;
erythromycin derivative;
ethyl ester;
succinate ester
ao 128
AO 128: alpha-glucosidase inhibitor; structure given in first source		2.0510organic molecular entity
betadex
beta-Cyclodextrins: Cyclic GLUCANS consisting of seven (7) glucopyranose units linked by 1,4-glycosidic bonds.		3.3260cyclodextrin
acarbose
[no description available]		2.0510amino cyclitol;
glycoside
trichostatin a
trichostatin A: chelates zinc ion in the active site of histone deacetylases, resulting in preventing histone unpacking so DNA is less available for transcription; do not confuse with TRICHOSANTHIN which is a protein; found in STREPTOMYCES		3.1350antibiotic antifungal agent;
hydroxamic acid;
trichostatin		bacterial metabolite;
EC 3.5.1.98 (histone deacetylase) inhibitor;
geroprotector
tretinoin
Tretinoin: An important regulator of GENE EXPRESSION during growth and development, and in NEOPLASMS. Tretinoin, also known as retinoic acid and derived from maternal VITAMIN A, is essential for normal GROWTH; and EMBRYONIC DEVELOPMENT. An excess of tretinoin can be teratogenic. It is used in the treatment of PSORIASIS; ACNE VULGARIS; and several other SKIN DISEASES. It has also been approved for use in promyelocytic leukemia (LEUKEMIA, PROMYELOCYTIC, ACUTE).. retinoic acid : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraenoic acid substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).. all-trans-retinoic acid : A retinoic acid in which all four exocyclic double bonds have E- (trans-) geometry.		9.95361retinoic acid;
vitamin A		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
AP-1 antagonist;
human metabolite;
keratolytic drug;
retinoic acid receptor agonist;
retinoid X receptor agonist;
signalling molecule
arachidonic acid
icosa-5,8,11,14-tetraenoic acid : Any icosatetraenoic acid with the double bonds at positions 5, 8, 11 and 14.. arachidonate : A long-chain fatty acid anion resulting from the removal of a proton from the carboxy group of arachidonic acid.		2.4920icosa-5,8,11,14-tetraenoic acid;
long-chain fatty acid;
omega-6 fatty acid		Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
human metabolite;
mouse metabolite
resveratrol
trans-resveratrol : A resveratrol in which the double bond has E configuration.		3.5880resveratrolantioxidant;
phytoalexin;
plant metabolite;
quorum sensing inhibitor;
radical scavenger
retinol
Vitamin A: Retinol and derivatives of retinol that play an essential role in metabolic functioning of the retina, the growth of and differentiation of epithelial tissue, the growth of bone, reproduction, and the immune response. Dietary vitamin A is derived from a variety of CAROTENOIDS found in plants. It is enriched in the liver, egg yolks, and the fat component of dairy products.. vitamin A : Any member of a group of fat-soluble retinoids produced via metabolism of provitamin A carotenoids that exhibit biological activity against vitamin A deficiency. Vitamin A is involved in immune function, vision, reproduction, and cellular communication.. all-trans-retinol : A retinol in which all four exocyclic double bonds have E- (trans-) geometry.. retinol : A retinoid consisting of 3,7-dimethylnona-2,4,6,8-tetraen-1-ol substituted at position 9 by a 2,6,6-trimethylcyclohex-1-en-1-yl group (geometry of the four exocyclic double bonds is not specified).		5.7761retinol;
vitamin A		human metabolite;
mouse metabolite;
plant metabolite
latrunculin a
latrunculin A: 16-membered macrolide attached to 2-thiazolidinone moiety; from Red Sea sponge Latrunculia magnifica; see also latrunculin B; structure given in first source. latrunculin A : A bicyclic macrolide natural product consisting of a 16-membered bicyclic lactone attached to the rare 2-thiazolidinone moiety. It is obtained from the Red Sea sponge Latrunculia magnifica and from the Fiji Islands sponge Cacospongia mycofijiensis. Latrunculin A inhibits actin polymerisation, microfilament organsation and microfilament-mediated processes.		2.0210cyclic hemiketal;
macrolide;
oxabicycloalkane;
thiazolidinone		actin polymerisation inhibitor;
metabolite;
toxin
alpha-D-fructofuranose 1,6-bisphosphate
alpha-D-fructofuranose 1,6-bisphosphate : A D-fructofuranose 1,6-bisphosphate with an alpha-configuration at the anomeric position.		2.0510D-fructofuranose 1,6-bisphosphate
docosahexaenoate
efalex: a mixture of fish oil and primrose oil; used as a high-docosahexaenoic acid fatty acid supplement. docosahexaenoic acid : Any C22 polyunsaturated fatty acid containing six double bonds.. docosahexaenoate : A polyunsaturated fatty acid anion that is the conjugate base of docosahexaenoic acid, obtained by deprotonation of the carboxy group; major species at pH 7.3.. all-cis-docosa-4,7,10,13,16,19-hexaenoic acid : A docosahexaenoic acid having six cis-double bonds at positions 4, 7, 10, 13, 16 and 19.		2.0510docosahexaenoic acid;
omega-3 fatty acid		algal metabolite;
antineoplastic agent;
Daphnia tenebrosa metabolite;
human metabolite;
mouse metabolite;
nutraceutical
oleic acid
Oleic Acid: An unsaturated fatty acid that is the most widely distributed and abundant fatty acid in nature. It is used commercially in the preparation of oleates and lotions, and as a pharmaceutical solvent. (Stedman, 26th ed). oleic acid : An octadec-9-enoic acid in which the double bond at C-9 has Z (cis) stereochemistry.		2.0510octadec-9-enoic acidantioxidant;
Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
Escherichia coli metabolite;
mouse metabolite;
plant metabolite;
solvent
tacrolimus
Tacrolimus: A macrolide isolated from the culture broth of a strain of Streptomyces tsukubaensis that has strong immunosuppressive activity in vivo and prevents the activation of T-lymphocytes in response to antigenic or mitogenic stimulation in vitro.. tacrolimus (anhydrous) : A macrolide lactam containing a 23-membered lactone ring, originally isolated from the fermentation broth of a Japanese soil sample that contained the bacteria Streptomyces tsukubaensis.		6.7161macrolide lactambacterial metabolite;
immunosuppressive agent
farnesyl pyrophosphate
farnesyl pyrophosphate: a sesquiterpene that dimerizes to SQUALENE; RN given refers to cpd without isomeric designation. 2-trans,6-trans-farnesyl diphosphate : The trans,trans-stereoisomer of farnesyl diphosphate.		3.1110farnesyl diphosphateEscherichia coli metabolite;
mouse metabolite
cerivastatin
cerivastatin: cerivastatin is the ((E)-(+))-isomer; structure given in first source. cerivastatin : (3R,5S)-3,5-dihydroxyhept-6-enoic acid in which the (7E)-hydrogen is substituted by a 4-(4-fluorophenyl)-2,6-diisopropyl-5-(methoxymethyl)pyridin-3-yl group. Formerly used (as its sodium salt) to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.		2.4320dihydroxy monocarboxylic acid;
pyridines;
statin (synthetic)
rosuvastatin
rosuvastatin : A dihydroxy monocarboxylic acid that is (6E)-7-{4-(4-fluorophenyl)-2-[methyl(methylsulfonyl)amino]-6-(propan-2-yl)pyrimidin-5-yl} hept-6-enoic acid carrying two hydroxy substituents at positions 3 and 5 (the 3R,5S-diastereomer).		2.0510dihydroxy monocarboxylic acid;
monofluorobenzenes;
pyrimidines;
statin (synthetic);
sulfonamide		anti-inflammatory agent;
antilipemic drug;
cardioprotective agent;
CETP inhibitor;
environmental contaminant;
xenobiotic
cocaine
Cocaine: An alkaloid ester extracted from the leaves of plants including coca. It is a local anesthetic and vasoconstrictor and is clinically used for that purpose, particularly in the eye, ear, nose, and throat. It also has powerful central nervous system effects similar to the amphetamines and is a drug of abuse. Cocaine, like amphetamines, acts by multiple mechanisms on brain catecholaminergic neurons; the mechanism of its reinforcing effects is thought to involve inhibition of dopamine uptake.. cocaine : A tropane alkaloid obtained from leaves of the South American shrub Erythroxylon coca.		2.7630benzoate ester;
methyl ester;
tertiary amino compound;
tropane alkaloid		adrenergic uptake inhibitor;
central nervous system stimulant;
dopamine uptake inhibitor;
environmental contaminant;
local anaesthetic;
mouse metabolite;
plant metabolite;
serotonin uptake inhibitor;
sodium channel blocker;
sympathomimetic agent;
vasoconstrictor agent;
xenobiotic
eicosapentaenoic acid
icosapentaenoic acid : Any straight-chain, C20 polyunsaturated fatty acid having five C=C double bonds.. all-cis-5,8,11,14,17-icosapentaenoic acid : An icosapentaenoic acid having five cis-double bonds at positions 5, 8, 11, 14 and 17.		2.0510icosapentaenoic acid;
omega-3 fatty acid		anticholesteremic drug;
antidepressant;
antineoplastic agent;
Daphnia galeata metabolite;
fungal metabolite;
micronutrient;
mouse metabolite;
nutraceutical
thapsigargin
Thapsigargin: A sesquiterpene lactone found in roots of THAPSIA. It inhibits SARCOPLASMIC RETICULUM CALCIUM-TRANSPORTING ATPASES.. thapsigargin : An organic heterotricyclic compound that is a hexa-oxygenated 6,7-guaianolide isolated fron the roots of Thapsia garganica L., Apiaceae. A potent skin irritant, it is used in traditional medicine as a counter-irritant. Thapsigargin inhibits Ca(2+)-transporting ATPase mediated uptake of calcium ions into sarcoplasmic reticulum and is used in experimentation examining the impacts of increasing cytosolic calcium concentrations.		2.4820butyrate ester;
organic heterotricyclic compound;
sesquiterpene lactone		calcium channel blocker;
EC 3.6.3.8 (Ca(2+)-transporting ATPase) inhibitor
mycophenolic acid
Mycophenolic Acid: Compound derived from Penicillium stoloniferum and related species. It blocks de novo biosynthesis of purine nucleotides by inhibition of the enzyme inosine monophosphate dehydrogenase (IMP DEHYDROGENASE). Mycophenolic acid exerts selective effects on the immune system in which it prevents the proliferation of T-CELLS, LYMPHOCYTES, and the formation of antibodies from B-CELLS. It may also inhibit recruitment of LEUKOCYTES to sites of INFLAMMATION.. mycophenolate : A monocarboxylic acid anion resulting from the removal of a proton from the carboxy group of mycophenolic acid.. mycophenolic acid : A member of the class of 2-benzofurans that is 2-benzofuran-1(3H)-one which is substituted at positions 4, 5, 6, and 7 by methyl, methoxy, (2E)-5-carboxy-3-methylpent-2-en-1-yl, and hydroxy groups, respectively. It is an antibiotic produced by Penicillium brevi-compactum, P. stoloniferum, P. echinulatum and related species. An immunosuppressant, it is widely used (partiularly as its sodium salt and as the 2-(morpholin-4-yl)ethyl ester prodrug, mycophenolate mofetil) to prevent tissue rejection following organ transplants and for the treatment of certain autoimmune diseases.		7.63922-benzofurans;
gamma-lactone;
monocarboxylic acid;
phenols		anticoronaviral agent;
antimicrobial agent;
antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
environmental contaminant;
immunosuppressive agent;
mycotoxin;
Penicillium metabolite;
xenobiotic
mupirocin
Mupirocin: A topically used antibiotic from a strain of Pseudomonas fluorescens. It has shown excellent activity against gram-positive staphylococci and streptococci. The antibiotic is used primarily for the treatment of primary and secondary skin disorders, nasal infections, and wound healing.. mupirocin : An alpha,beta-unsaturated ester resulting from the formal condensation of the alcoholic hydroxy group of 9-hydroxynonanoic acid with the carboxy group of (2E)-4-[(2S)-tetrahydro-2H-pyran-2-yl]-3-methylbut-2-enoic acid in which the tetrahydropyranyl ring is substituted at positions 3 and 4 by hydroxy groups and at position 5 by a {(2S,3S)-3-[(2S,3S)-3-hydroxybutan-2-yl]oxiran-2-yl}methyl group. Originally isolated from the Gram-negative bacterium Pseudomonas fluorescens, it is used as a topical antibiotic for the treatment of Gram-positive bacterial infections.		2.0710alpha,beta-unsaturated carboxylic ester;
epoxide;
monocarboxylic acid;
oxanes;
secondary alcohol;
triol		antibacterial drug;
bacterial metabolite;
protein synthesis inhibitor
clindamycin
Clindamycin: An antibacterial agent that is a semisynthetic analog of LINCOMYCIN.. clindamycin : A carbohydrate-containing antibiotic that is the semisynthetic derivative of lincomycin, a natural antibiotic.		2.0510
fosfomycin
Fosfomycin: An antibiotic produced by Streptomyces fradiae.. fosfomycin : A phosphonic acid having an (R,S)-1,2-epoxypropyl group attached to phosphorus.		2.0510epoxide;
phosphonic acids		antimicrobial agent;
EC 2.5.1.7 (UDP-N-acetylglucosamine 1-carboxyvinyltransferase) inhibitor
zithromax
Azithromycin: A semi-synthetic macrolide antibiotic structurally related to ERYTHROMYCIN. It has been used in the treatment of Mycobacterium avium intracellulare infections, toxoplasmosis, and cryptosporidiosis.. azithromycin : A macrolide antibiotic useful for the treatment of bacterial infections.		2.5220macrolide antibioticantibacterial drug;
environmental contaminant;
xenobiotic
pd 173955
PD 173955: inhibits src family-selective tyrosine kinase; structure in first source		2.9440aryl sulfide;
dichlorobenzene;
methyl sulfide;
pyridopyrimidine		tyrosine kinase inhibitor
cefoxitin
Tn antigen: immediate precursor in biosynthesis of Thomsen-Friedenreich (T) antigen; present in about 90% of human carcinoma tissue; proposed as universal carcinoma marker. O-(N-acetyl-alpha-D-galactosaminyl)-L-serine : A non-proteinogenic L-amino acid that is N-acetyl-alpha-D-galactosamine linked via an alpha glycosidic bond to the O at position 3 of L-serine.		2.0810L-serine derivative;
non-proteinogenic L-alpha-amino acid		tumour antigen
drf 2725
ragaglitazar: a phenoxazine analogue of phenyl propanoic acid; Ragaglitazar is a coligand of PPARalpha and PPARgamma		2.0510
pd 166326
PD 166326: a pyrido(2,3-d)pyrimidine src tyrosine kinase inhibitor		5.92120
hts 466284
HTS 466284: a TGFbeta-RI inhibitor; structure in first source		2.0510pyrazoles;
pyridines;
quinolines		TGFbeta receptor antagonist
epothilone b
[no description available]		3.8540epothilone;
epoxide		antineoplastic agent;
apoptosis inducer;
microtubule-stabilising agent
n-(4-methoxybenzyl)-n'-(5-nitro-1,3-thiazol-2-yl)urea
N-(4-methoxybenzyl)-N'-(5-nitro-1,3-thiazol-2-yl)urea: structure in first source		2.0310
y 27632
Y 27632: RN given for di-HCl salt; inhibits Rho-associated protein kinase; inhibits calcium sensitization to affect smooth muscle relaxation; structure in first source. Y-27632 : A monocarboxylic acid amide that is trans-[(1R)-1-aminoethyl]cyclohexanecarboxamide in which one of the nitrogens of the aminocarbony group is substituted by a pyridine nucleus. It has been shown to exhibit inhibitory activity against Rho-associated protein kinase (ROCK) enzyme.		3.1450aromatic amide
h 1152
(S)-2-methyl-1-(4-methylisoquinoline-5-sulfonyl)-1,4-diazepane : A member of the class of isoquinolines that is the sulfonamide formed by the formal condensation of the sulfo group of 4-methylisoquinoline-5-sulfonic acid with the 1-amino group of (S)-2-methyl-1,4-diazepane.		2.0310isoquinolines;
N-sulfonyldiazepane		EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
diethylstilbestrol
Diethylstilbestrol: A synthetic nonsteroidal estrogen used in the treatment of menopausal and postmenopausal disorders. It was also used formerly as a growth promoter in animals. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), diethylstilbestrol has been listed as a known carcinogen. (Merck, 11th ed). diethylstilbestrol : An olefinic compound that is trans-hex-3-ene in which the hydrogens at positions 3 and 4 have been replaced by p-hydroxyphenyl groups.		2.4520olefinic compound;
polyphenol		antifungal agent;
antineoplastic agent;
autophagy inducer;
calcium channel blocker;
carcinogenic agent;
EC 1.1.1.146 (11beta-hydroxysteroid dehydrogenase) inhibitor;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
endocrine disruptor;
xenoestrogen
bms 214662
7-cyano-2,3,4,5-tetrahydro-1-(1H-imidazol-4-ylmethyl)-3-(phenylmethyl)-4-(2-thienylsulfonyl)-1H-1,4-benzodiazepine: a farnesyltransferase inhibitor; structure in first source. BMS-214662 : A member of the class of benzodiazepines that is 2,3,4,5-tetrahydro-1H-1,4-benzodiazepine substituted by (1H-imidazol-5-yl)methyl, benzyl, (thiophen-2-yl)sulfonyl, and cyano groups at positions 1, 3R, 4 and 7, respectively. It is a potent inhibitor of farnesyltransferase (IC50 = 1.35nM) which was under clinical development for the treatment of solid tumors.		4.8840benzenes;
benzodiazepine;
imidazoles;
nitrile;
sulfonamide;
thiophenes		antineoplastic agent;
apoptosis inducer;
EC 2.5.1.58 (protein farnesyltransferase) inhibitor
epothilone a
Epothilones: A group of 16-member MACROLIDES which stabilize MICROTUBULES in a manner similar to PACLITAXEL. They were originally found in the myxobacterium Sorangium cellulosum, now renamed to Polyangium (MYXOCOCCALES).		5.860epothilone;
epoxide		antineoplastic agent;
metabolite;
microtubule-stabilising agent;
tubulin modulator
7-n-butyl-6-(4'-hydroxyphenyl)-5h-pyrrolo(2,3b)pyrazine
[no description available]		2.0310
6-bromoindirubin-3'-oxime
6-bromoindirubin-3'-oxime: structure in first source. 6-bromoindirubin-3'-oxime : A member of the class of biindoles that is indirubin substituted at position 6 by a bromo group and in which the keto group at position 3' has undergone condensation with hydroxylamine to form the corresponding oxime.		2.0310
alitretinoin
Alitretinoin: A retinoid that is used for the treatment of chronic hand ECZEMA unresponsive to topical CORTICOSTEROIDS. It is also used to treat cutaneous lesions associated with AIDS-related KAPOSI SARCOMA.		2.0510retinoic acidantineoplastic agent;
keratolytic drug;
metabolite;
retinoid X receptor agonist
h 89
N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide: structure given in first source. N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A member of the class of isoquinolines that is the sulfonamide obtained by formal condensation of the sulfo group of isoquinoline-5-sulfonic acid with the primary amino group of N(1)-[3-(4-bromophenyl)prop-2-en-1-yl]ethane-1,2-diamine. It is a protein kinase A inhibitor.. (E)-N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide : A N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide in which the double bond adopts a trans-configuration.		2.0310N-[2-(4-bromocinnamylamino)ethyl]isoquinoline-5-sulfonamide
aclarubicin
Aclarubicin: An anthracycline produced by Streptomyces galilaeus. It has potent antineoplastic activity.. aclacinomycin A : An anthracycline antibiotic that is produced by Streptomyces galilaeus and also has potent antineoplastic activity.		2.0810aminoglycoside;
anthracycline;
methyl ester;
phenols;
polyketide;
tetracenequinones;
trisaccharide derivative;
zwitterion		antimicrobial agent;
antineoplastic agent;
apoptosis inducer;
bacterial metabolite;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
decitabine
[no description available]		9.91922'-deoxyribonucleoside
teniposide
[no description available]		2.0510aromatic ether;
beta-D-glucoside;
cyclic acetal;
furonaphthodioxole;
gamma-lactone;
monosaccharide derivative;
phenols;
thiophenes		antineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor
troxacitabine
troxacitabine: shows good anti-HIV activity without cytotoxicity		6.1231carbohydrate derivative;
nucleobase-containing molecular entity
purvalanol a
6-((3-chloro)anilino)-2-(isopropyl-2-hydroxyethylamino)-9-isopropylpurine: purvalanol A is the (1R)-isomer;		2.5120purvalanol
cefamandole
Cefamandole: Semisynthetic wide-spectrum cephalosporin with prolonged action, probably due to beta-lactamase resistance. It is used also as the nafate.. cefamandole : A cephalosporin compound having (R)-mandelamido and N-methylthiotetrazole side-groups.		2.0410cephalosporin;
semisynthetic derivative		antibacterial drug
dactinomycin
Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)		3.1750actinomycinmutagen
tiazofurin
tiazofurin: RN given refers to (beta-D)-isomer; structure given in first source. tiazofurine : A C-glycosyl compound that is 1,3-thiazole-4-carboxamide in which the hydrogen at position 2 has been replaced by a beta-D-ribofuranosyl group. It is metabolised to thiazole-4-carboxamide adenine dinucleotide (TAD), a selective inhibitor of inosine monophosphate dehydrogenase (IMP dehydrogenase).		2.05101,3-thiazoles;
C-glycosyl compound;
monocarboxylic acid amide		antineoplastic agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
prodrug
melphalan
Melphalan: An alkylating nitrogen mustard that is used as an antineoplastic in the form of the levo isomer - MELPHALAN, the racemic mixture - MERPHALAN, and the dextro isomer - MEDPHALAN; toxic to bone marrow, but little vesicant action; potential carcinogen.. melphalan : A phenylalanine derivative comprising L-phenylalanine having [bis(2-chloroethyl)amino group at the 4-position on the phenyl ring.		3.2960L-phenylalanine derivative;
nitrogen mustard;
non-proteinogenic L-alpha-amino acid;
organochlorine compound		alkylating agent;
antineoplastic agent;
carcinogenic agent;
drug allergen;
immunosuppressive agent
benzyloxycarbonylleucyl-leucyl-leucine aldehyde
benzyloxycarbonylleucyl-leucyl-leucine aldehyde: proteasome inhibitor. N-benzyloxycarbonyl-L-leucyl-L-leucyl-L-leucinal : A tripeptide that is L-leucyl-L-leucyl-L-leucine in which the C-terminal carboxy group has been reduced to the corresponding aldehyde and the N-terminal amino group is protected as its benzyloxycarbonyl derivative.		2.9940amino aldehyde;
carbamate ester;
tripeptide		proteasome inhibitor
tenofovir
tenofovir (anhydrous) : A member of the class of phosphonic acids that is methylphosphonic acid in which one of the methyl hydrogens is replaced by a [(2R)-1-(6-amino-9H-purin-9-yl)propan-2-yl]oxy group. An inhibitor of HIV-1 reverse transcriptase, the bis(isopropyloxycarbonyloxymethyl) ester (disoproxil ester) prodrug is used as the fumaric acid salt in combination therapy for the treatment of HIV infection.		3.5620nucleoside analogue;
phosphonic acids		antiviral drug;
drug metabolite;
HIV-1 reverse transcriptase inhibitor
posaconazole
[no description available]		2.0310aromatic ether;
conazole antifungal drug;
N-arylpiperazine;
organofluorine compound;
oxolanes;
triazole antifungal drug;
triazoles		trypanocidal drug
l 743,872
[no description available]		2.4820
rubitecan
rubitecan: RN refers to (+-)-isomer; anti-HIV agent; DNA Topoisomerases, Type I inhibitor. rubitecan : A pyranoindolizinoquinoline that is camptothecin in which the hydrogen at position 9 has been replaced by a nitro group. It is a prodrug for 9-aminocamptothecin.		2.0510C-nitro compound;
delta-lactone;
pyranoindolizinoquinoline;
semisynthetic derivative;
tertiary alcohol		antineoplastic agent;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
prodrug
micafungin
Micafungin: A cyclic lipo-hexapeptide echinocandin antifungal agent that is used for the treatment and prevention of CANDIDIASIS.. micafungin : A cyclic hexapeptide echinocandin antibiotic which exerts its effect by inhibiting the synthesis of 1,3-beta-D-glucan, an integral component of the fungal cell wall. It is used as the sodium salt for the treatment of invasive candidiasis, and of aspergillosis in patients who are intolerant of other therapy.		2.0510antibiotic antifungal drug;
echinocandin		antiinfective agent
2-methyl-5-(4-methylanilino)-1,3-benzothiazole-4,7-dione
[no description available]		2.0310aminotoluene
cmx 001
[no description available]		2.1110
favipiravir
favipiravir : A member of the class of pyrazines that is pyrazine substituted by aminocarbonyl, hydroxy and fluoro groups at positions 2, 3 and 6, respectively. It is an anti-viral agent that inhibits RNA-dependent RNA polymerase of several RNA viruses and is approved for the treatment of influenza in Japan.		5.3431hydroxypyrazine;
organofluorine compound;
primary carboxamide		anticoronaviral agent;
antiviral drug;
EC 2.7.7.48 (RNA-directed RNA polymerase) inhibitor
riboflavin
vitamin B2 : Any member of a group of vitamers that belong to the chemical structural class called flavins that exhibit biological activity against vitamin B2 deficiency. Symptoms associated with vitamin B2 deficiency include glossitis, seborrhea, angular stomaitis, cheilosis and photophobia. The vitamers include riboflavin and its phosphate derivatives (and includes their salt, ionised and hydrate forms).		2.0510flavin;
vitamin B2		anti-inflammatory agent;
antioxidant;
cofactor;
Escherichia coli metabolite;
food colouring;
fundamental metabolite;
human urinary metabolite;
mouse metabolite;
photosensitizing agent;
plant metabolite
2,3-bis(bromomethyl)quinoxaline-1,4-dioxide
conoidin A: inhibits the peroxiredoxin TgPrx11; structure in first source		4.6111
sodium bicarbonate
Sodium Bicarbonate: A white, crystalline powder that is commonly used as a pH buffering agent, an electrolyte replenisher, systemic alkalizer and in topical cleansing solutions.		2.4820one-carbon compound;
organic sodium salt		antacid;
food anticaking agent
sodium acetate, anhydrous
Sodium Acetate: The trihydrate sodium salt of acetic acid, which is used as a source of sodium ions in solutions for dialysis and as a systemic and urinary alkalizer, diuretic, and expectorant.		2.0510organic sodium saltNMR chemical shift reference compound
sodium benzoate
Sodium Benzoate: The sodium salt of BENZOIC ACID. It is used as an antifungal preservative in pharmaceutical preparations and foods. It may also be used as a test for liver function.. sodium benzoate : An organic sodium salt resulting from the replacement of the proton from the carboxy group of benzoic acid by a sodium ion.		2.0510organic sodium saltalgal metabolite;
antimicrobial food preservative;
drug allergen;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor;
human xenobiotic metabolite;
plant metabolite
dipyrone
Dipyrone: A drug that has analgesic, anti-inflammatory, and antipyretic properties. It is the sodium sulfonate of AMINOPYRINE.. metamizole sodium : An organic sodium salt of antipyrine substituted at C-4 by a methyl(sulfonatomethyl)amino group, commonly used as a powerful analgesic and antipyretic.		2.0510organic sodium saltanti-inflammatory agent;
antipyretic;
antirheumatic drug;
cyclooxygenase 3 inhibitor;
non-narcotic analgesic;
peripheral nervous system drug;
prodrug
ditiocarb sodium
[no description available]		2.0510organic molecular entity
bromochloroacetic acid
Keratins: A class of fibrous proteins or scleroproteins that represents the principal constituent of EPIDERMIS; HAIR; NAILS; horny tissues, and the organic matrix of tooth ENAMEL. Two major conformational groups have been characterized, alpha-keratin, whose peptide backbone forms a coiled-coil alpha helical structure consisting of TYPE I KERATIN and a TYPE II KERATIN, and beta-keratin, whose backbone forms a zigzag or pleated sheet structure. alpha-Keratins have been classified into at least 20 subtypes. In addition multiple isoforms of subtypes have been found which may be due to GENE DUPLICATION.. bromochloroacetic acid : A monocarboxylic acid that is acetic acid in which one of the methyl hydrogens is replaced by bromine while a second is replaced by chlorine. A low-melting (27.5-31.5degreeC), hygroscopic crystalline solid, it can be formed during the disinfection (by chlorination) of water that contains bromide ions and organic matter, so can occur in drinking water as a byproduct of the disinfection process.		2.74302-bromocarboxylic acid;
monocarboxylic acid;
organochlorine compound
sch 22219
alclometasone dipropionate : A prednisolone compound having an alpha-chloro substituent at the 7-position, an alpha-methyl substituent at the 16-position and O-propanoyl groups at the 17- and 21-positions.		2.021011beta-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid;
chlorinated steroid;
glucocorticoid;
propanoate ester;
steroid ester		anti-inflammatory drug
carbenoxolone
[no description available]		2.0510
isomethyleugenol
Methylation: Addition of methyl groups. In histo-chemistry methylation is used to esterify carboxyl groups and remove sulfate groups by treating tissue sections with hot methanol in the presence of hydrochloric acid. (From Stedman, 25th ed)		2.830isomethyleugenol
piplartine
piplartine: Antineoplastic Agent, Phytogenic; alkaloid from Piper; structure in first source		2.610cinnamamides;
dicarboximide
stilbenes
Stilbenes: Organic compounds that contain 1,2-diphenylethylene as a functional group.. trans-stilbene : The trans-isomer of stilbene.		4.7690stilbene
xanthohumol
xanthohumol: from hop plant, Humulus lupulus. xanthohumol : A member of the class of chalcones that is trans-chalcone substituted by hydroxy groups at positions 4, 2' and 4', a methoxy group at position 6' and a prenyl group at position 3'. Isolated from Humulus lupulus, it induces apoptosis in human malignant glioblastoma cells.		2.0410aromatic ether;
chalcones;
polyphenol		anti-HIV-1 agent;
antineoplastic agent;
antiviral agent;
apoptosis inducer;
EC 2.3.1.20 (diacylglycerol O-acyltransferase) inhibitor;
metabolite
discodermolide
[no description available]		2.0510diterpenoid
cannabidiol
Cannabidiol: Compound isolated from Cannabis sativa extract.. cannabidiol : An cannabinoid that is cyclohexene which is substituted by a methyl group at position 1, a 2,6-dihydroxy-4-pentylphenyl group at position 3, and a prop-1-en-2-yl group at position 4.		2.5320olefinic compound;
phytocannabinoid;
resorcinols		antimicrobial agent;
plant metabolite
s 1033
[no description available]		24.1673491(trifluoromethyl)benzenes;
imidazoles;
pyridines;
pyrimidines;
secondary amino compound;
secondary carboxamide		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
leuprolide
Leuprolide: A potent synthetic long-acting agonist of GONADOTROPIN-RELEASING HORMONE that regulates the synthesis and release of pituitary gonadotropins, LUTEINIZING HORMONE and FOLLICLE STIMULATING HORMONE.. leuprolide : An oligopeptide comprising pyroglutamyl, histidyl, tryptophyl, seryl, tyrosyl, D-leucyl, leucyl, arginyl, and N-ethylprolinamide residues joined in sequence. It is a synthetic nonapeptide analogue of gonadotropin-releasing hormone, and is used as a subcutaneous hydrogel implant (particularly as the acetate salt) for the treatment of prostate cancer and for the suppression of gonadal sex hormone production in children with central precocious puberty.		4.4520oligopeptideanti-estrogen;
antineoplastic agent;
gonadotropin releasing hormone agonist
fludarabine
[no description available]		9.35182purine nucleoside
propylthiouracil
Propylthiouracil: A thiourea antithyroid agent. Propythiouracil inhibits the synthesis of thyroxine and inhibits the peripheral conversion of throxine to tri-iodothyronine. It is used in the treatment of hyperthyroidism. (From Martindale, The Extra Pharmacopeoia, 30th ed, p534). 6-propyl-2-thiouracil : A pyrimidinethione consisting of uracil in which the 2-oxo group is substituted by a thio group and the hydrogen at position 6 is substituted by a propyl group.		2.0510pyrimidinethioneantidote to paracetamol poisoning;
antimetabolite;
antioxidant;
antithyroid drug;
carcinogenic agent;
EC 1.14.13.39 (nitric oxide synthase) inhibitor;
hormone antagonist
r 59949
R 59949: diacylglycerol kinase inhibitor		2.0310diarylmethane
prothionamide
Prothionamide: Antitubercular agent similar in action and side effects to ETHIONAMIDE. It is used mostly in combination with other agents.		2.0510pyridines
sesquiterpenes
[no description available]		5.3970
chlorprothixene
Chlorprothixene: A thioxanthine with effects similar to the phenothiazine antipsychotics.. (Z)-chlorprothixene : A chlorprothixene in which the double bond adopts a (Z)-configuration.		2.0410chlorprothixene
etomidate
Etomidate: Imidazole derivative anesthetic and hypnotic with little effect on blood gases, ventilation, or the cardiovascular system. It has been proposed as an induction anesthetic.. etomidate : The ethyl ester of 1-[(1R)-1-phenylethyl]-1H-imidazole-5-carboxylic acid. It is an intravenous general anaesthetic with no analgesic activity.		2.0510ethyl ester;
imidazoles		intravenous anaesthetic;
sedative
mercaptopurine
Mercaptopurine: An antimetabolite antineoplastic agent with immunosuppressant properties. It interferes with nucleic acid synthesis by inhibiting purine metabolism and is used, usually in combination with other drugs, in the treatment of or in remission maintenance programs for leukemia.. purine-6-thiol : A thiol that is the tautomer of mercaptopurine.. mercaptopurine : A member of the class of purines that is 6,7-dihydro-1H-purine carrying a thione group at position 6. An adenine analogue, it is used in the treatment of acute lymphocytic leukemia (ALL), chronic myeloid leukemia (CML), Crohn's disease, and ulcerative colitis.		6.6591aryl thiol;
purines;
thiocarbonyl compound		anticoronaviral agent;
antimetabolite;
antineoplastic agent
3,3',4,5'-tetrahydroxystilbene
3,3',4,5'-tetrahydroxystilbene: demethyl derivative of isorhapontigenin; structure in first source; a Syk kinase inhibitor; found in heartwood of FABACEAE; inhibitor of photosynthesis in spinach chloroplasts; may be inhibitor of plant growth; RN given refers to (E)-isomer. piceatannol : A stilbenol that is trans-stilbene in which one of the phenyl groups is substituted by hydroxy groups at positions 3 and 4, while the other phenyl group is substituted by hydroxy groups at positions 3 and 5.		2.4320catechols;
polyphenol;
resorcinols;
stilbenol		antineoplastic agent;
apoptosis inducer;
geroprotector;
hypoglycemic agent;
plant metabolite;
protein kinase inhibitor;
tyrosine kinase inhibitor
thioinosine
Thioinosine: Sulfhydryl analog of INOSINE that inhibits nucleoside transport across erythrocyte plasma membranes, and has immunosuppressive properties. It has been used similarly to MERCAPTOPURINE in the treatment of leukemia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p503)		2.0410
caffeic acid
trans-caffeic acid : The trans-isomer of caffeic acid.		2.5720caffeic acidgeroprotector;
mouse metabolite
4-(4-(4-chloro-phenyl)thiazol-2-ylamino)phenol
[no description available]		2.4110substituted aniline
eszopiclone
Eszopiclone: A pyridine, pyrazine, and piperazine derivative that is used as a HYPNOTIC AND SEDATIVE in the treatment of INSOMNIA.. eszopiclone : The (5S)- (active) enantiomer of zopiclone. Unlike almost all other hypnotic sedatives, which are approved only for the relief of short-term (6-8 weeks) insomnia, eszopiclone is approved by the U.S. Food and Drug Administration for long-term use.		2.0610zopiclonecentral nervous system depressant;
sedative
curcumin
Curcumin: A yellow-orange dye obtained from tumeric, the powdered root of CURCUMA longa. It is used in the preparation of curcuma paper and the detection of boron. Curcumin appears to possess a spectrum of pharmacological properties, due primarily to its inhibitory effects on metabolic enzymes.. curcumin : A beta-diketone that is methane in which two of the hydrogens are substituted by feruloyl groups. A natural dyestuff found in the root of Curcuma longa.		5.2101aromatic ether;
beta-diketone;
diarylheptanoid;
enone;
polyphenol		anti-inflammatory agent;
antifungal agent;
antineoplastic agent;
biological pigment;
contraceptive drug;
dye;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
EC 1.1.1.21 (aldehyde reductase) inhibitor;
EC 1.1.1.25 (shikimate dehydrogenase) inhibitor;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor;
EC 1.8.1.9 (thioredoxin reductase) inhibitor;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
EC 3.5.1.98 (histone deacetylase) inhibitor;
flavouring agent;
food colouring;
geroprotector;
hepatoprotective agent;
immunomodulator;
iron chelator;
ligand;
lipoxygenase inhibitor;
metabolite;
neuroprotective agent;
nutraceutical;
radical scavenger
rhodanine
2-mercaptothiazolinone: metabolite in urine from persons exposed to CS2; structure		2.3110thiazolidinone
thiohydantoins
Thiohydantoins: Sulfur analogs of hydantoins with one or both carbonyl groups replaced by thiocarbonyl groups.		3.4110
methimazole
Methimazole: A thioureylene antithyroid agent that inhibits the formation of thyroid hormones by interfering with the incorporation of iodine into tyrosyl residues of thyroglobulin. This is done by interfering with the oxidation of iodide ion and iodotyrosyl groups through inhibition of the peroxidase enzyme.. methimazole : A member of the class of imidazoles that it imidazole-2-thione in which a methyl group replaces the hydrogen which is attached to a nitrogen.		2.05101,3-dihydroimidazole-2-thionesantithyroid drug
sulindac
Sulindac: A sulfinylindene derivative prodrug whose sulfinyl moiety is converted in vivo to an active NSAID analgesic. Specifically, the prodrug is converted by liver enzymes to a sulfide which is excreted in the bile and then reabsorbed from the intestine. This helps to maintain constant blood levels with reduced gastrointestinal side effects.. sulindac : A monocarboxylic acid that is 1-benzylidene-1H-indene which is substituted at positions 2, 3, and 5 by methyl, carboxymethyl, and fluorine respectively, and in which the phenyl group of the benzylidene moiety is substituted at the para position by a methylsulfinyl group. It is a prodrug for the corresponding sulfide, a non-steroidal anti-inflammatory drug, used particularly in the treatment of acute and chronic inflammatory conditions.		2.4520monocarboxylic acid;
organofluorine compound;
sulfoxide		analgesic;
antineoplastic agent;
antipyretic;
apoptosis inducer;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
prodrug;
tocolytic agent
capsaicin
ALGRX-4975: an injectable capsaicin (TRPV1 receptor agonist) formulation for longlasting pain relief. capsaicinoid : A family of aromatic fatty amides produced as secondary metabolites by chilli peppers.		2.0510capsaicinoidnon-narcotic analgesic;
TRPV1 agonist;
voltage-gated sodium channel blocker
terbinafine
[no description available]		2.0510acetylenic compound;
allylamine antifungal drug;
enyne;
naphthalenes;
tertiary amine		EC 1.14.13.132 (squalene monooxygenase) inhibitor;
P450 inhibitor;
sterol biosynthesis inhibitor
epalrestat
epalrestat : A monocarboxylic acid that is 1,3-thiazolidine which is substituted on the nitrogen by a carboxymethyl group, at positions 2 and 4 by thioxo and oxo groups, respectively, and at position 5 by a 2-methyl-3-phenylprop-2-en-1-ylidene group. It is an inhibitor of aldose reductase (which catalyses the conversion of glucose to sorbitol) and is used for the treatment of some diabetic complications, including neuropathy.		2.3110monocarboxylic acid;
thiazolidines		EC 1.1.1.21 (aldehyde reductase) inhibitor
tg 003
TG 003: a Clk inhibitor; structure in first source		2.0310
thioguanine anhydrous
Thioguanine: An antineoplastic compound which also has antimetabolite action. The drug is used in the therapy of acute leukemia.. tioguanine : A 2-aminopurine that is the 6-thiono derivative of 2-amino-1,9-dihydro-6H-purine. Incorporates into DNA and inhibits synthesis. Used in the treatment of leukaemia.		3.57202-aminopurinesanticoronaviral agent;
antimetabolite;
antineoplastic agent
tacrine hydrochloride
[no description available]		2.0510
thiourea
Thiourea: A photographic fixative used also in the manufacture of resins. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), this substance may reasonably be anticipated to be a carcinogen (Merck Index, 9th ed). Many of its derivatives are ANTITHYROID AGENTS and/or FREE RADICAL SCAVENGERS.. thiourea : The simplest member of the thiourea class, consisting of urea with the oxygen atom substituted by sulfur.		2.9940one-carbon compound;
thioureas;
ureas		antioxidant;
chromophore
sodium propionate
sodium propionate: was term of propionic acid (1986-2006). sodium propionate : An organic sodium salt comprising equal numbers of sodium and propionate ions.		2.0510organic sodium saltantifungal drug;
food preservative
thioacetamide
Thioacetamide: A crystalline compound used as a laboratory reagent in place of HYDROGEN SULFIDE. It is a potent hepatocarcinogen.. thioacetamide : A thiocarboxamide consiting of acetamide having the oxygen replaced by sulfur.		340thiocarboxamidehepatotoxic agent
digoxin
Digoxin: A cardiotonic glycoside obtained mainly from Digitalis lanata; it consists of three sugars and the aglycone DIGOXIGENIN. Digoxin has positive inotropic and negative chronotropic activity. It is used to control ventricular rate in ATRIAL FIBRILLATION and in the management of congestive heart failure with atrial fibrillation. Its use in congestive heart failure and sinus rhythm is less certain. The margin between toxic and therapeutic doses is small. (From Martindale, The Extra Pharmacopoeia, 30th ed, p666). digoxin : A cardenolide glycoside that is digitoxin beta-hydroxylated at C-12. A cardiac glycoside extracted from the foxglove plant, Digitalis lanata, it is used to control ventricular rate in atrial fibrillation and in the management of congestive heart failure with atrial fibrillation, but the margin between toxic and therapeutic doses is small.		2.9840cardenolide glycoside;
steroid saponin		anti-arrhythmia drug;
cardiotonic drug;
EC 3.6.3.9 (Na(+)/K(+)-transporting ATPase) inhibitor;
epitope
streptozocin
[no description available]		2.0510
tamoxifen
[no description available]		5.93180stilbenoid;
tertiary amino compound		angiogenesis inhibitor;
antineoplastic agent;
bone density conservation agent;
EC 1.2.3.1 (aldehyde oxidase) inhibitor;
EC 2.7.11.13 (protein kinase C) inhibitor;
estrogen antagonist;
estrogen receptor antagonist;
estrogen receptor modulator
buclizine
1-octyl-3-methylimidazolium: structure in first source. 3-methyl-1-octylimidazolium : A 1-alkyl-3-methylimidazolium in which the alkyl substituent at C-1 is octyl.		2.15101-alkyl-3-methylimidazolium
nadp
[no description available]		2.7630
ethionamide
Ethionamide: A second-line antitubercular agent that inhibits mycolic acid synthesis.. ethionamide : A thiocarboxamide that is pyridine-4-carbothioamide substituted by an ethyl group at position 2. A prodrug that undergoes metabolic activation by conversion to the corresponding S-oxide.		2.0510pyridines;
thiocarboxamide		antilipemic drug;
antitubercular agent;
fatty acid synthesis inhibitor;
leprostatic drug;
prodrug
stattic
[no description available]		2.11101-benzothiophenes;
C-nitro compound;
sulfone		antineoplastic agent;
radiosensitizing agent;
STAT3 inhibitor
krn 7000
KRN 7000: has an alpha-galactosylceramide structure; structure given in first source. alpha-galactosylceramide : A galactosylceramide in which the galactosyl residue has alpha anomeric conofiguration.. 1-O-(alpha-D-galactosyl)-N-hexacosanoylphytosphingosine : A glycophytoceramide having an alpha-D-galactosyl residue at the O-1 position and a hexacosanoyl group attached to the nitrogen.		2.0310glycophytoceramide;
N-acyl-beta-D-galactosylphytosphingosine		allergen;
antigen;
antineoplastic agent;
epitope;
immunological adjuvant
fusidic acid
Fusidic Acid: An antibiotic isolated from the fermentation broth of Fusidium coccineum. (From Merck Index, 11th ed). It acts by inhibiting translocation during protein synthesis.. fusidic acid : A steroid antibiotic that is isolated from the fermentation broth of Fusidium coccineum.		2.452011alpha-hydroxy steroid;
3alpha-hydroxy steroid;
alpha,beta-unsaturated monocarboxylic acid;
steroid acid;
steroid antibiotic;
sterol ester		EC 2.7.1.33 (pantothenate kinase) inhibitor;
Escherichia coli metabolite;
protein synthesis inhibitor
estrone sulfate
estrone sulfate: sulfoconjugated estrone; RN given refers to parent cpd		2.452017-oxo steroid;
steroid sulfate		human metabolite;
mouse metabolite
hmr 3647
[no description available]		2.0510
toremifene
Toremifene: A first generation selective estrogen receptor modulator (SERM). Like TAMOXIFEN, it is an estrogen agonist for bone tissue and cholesterol metabolism but is antagonistic on mammary and uterine tissue.		2.5120aromatic ether;
organochlorine compound;
tertiary amine		antineoplastic agent;
bone density conservation agent;
estrogen antagonist;
estrogen receptor modulator
u 0126
U 0126: protein kinase kinase inhibitor; structure in first source		5.15101aryl sulfide;
dinitrile;
enamine;
substituted aniline		antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
osteogenesis regulator;
vasoconstrictor agent
telaprevir
[no description available]		2.0510cyclopentapyrrole;
cyclopropanes;
oligopeptide;
pyrazines		antiviral drug;
hepatitis C protease inhibitor;
peptidomimetic
nitrogen dioxide
Nitrogen Dioxide: Nitrogen oxide (NO2). A highly poisonous gas. Exposure produces inflammation of lungs that may only cause slight pain or pass unnoticed, but resulting edema several days later may cause death. (From Merck, 11th ed) It is a major atmospheric pollutant that is able to absorb UV light that does not reach the earth's surface.		4.6111nitrogen oxide
droloxifene
[no description available]		2.0510stilbenoid
or 1259
[no description available]		2.0510hydrazone;
nitrile;
pyridazinone		anti-arrhythmia drug;
cardiotonic drug;
EC 3.1.4.17 (3',5'-cyclic-nucleotide phosphodiesterase) inhibitor;
vasodilator agent
gestodene
Gestodene: synthetic steroid with progestational activity; RN given refers to (17alpha)-isomer		2.0510steroidestrogen
orlistat
Orlistat: A lactone derivative of LEUCINE that acts as a pancreatic lipase inhibitor to limit the absorption of dietary fat; it is used in the management of obesity.. orlistat : A carboxylic ester resulting from the formal condensation of the carboxy group of N-formyl-L-leucine with the hydroxy group of (3S,4S)-3-hexyl-4-[(2S)-2-hydroxytridecyl]oxetan-2-one. A pancreatic lipase inhibitor, it is used as an anti-obesity drug.		2.0510beta-lactone;
carboxylic ester;
formamides;
L-leucine derivative		anti-obesity agent;
bacterial metabolite;
EC 2.3.1.85 (fatty acid synthase) inhibitor;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor
idoxifene
idoxifene: structure given in first source		2.0510stilbenoid
quinine
[no description available]		2.0410cinchona alkaloidantimalarial;
muscle relaxant;
non-narcotic analgesic
1,2-bis(2-aminophenoxy)ethane n,n,n',n'-tetraacetic acid acetoxymethyl ester
[no description available]		2.0810
amrubicin
amrubicin: structure in first source; a 9-amino-anthracycline antibiotic. amrubicin : A synthetic anthracycline antibiotic with molecular formula C25H25NO9. A specific inhibitor of topoisomerase II, it is used (particularly as the hydrochloride salt) in the treatment of cancer, especially lung cancer, where it is a prodrug for the active metabolite, ambrucinol.		8.5320anthracycline antibiotic;
methyl ketone;
primary amino compound;
quinone;
tetracenes		antineoplastic agent;
prodrug;
topoisomerase II inhibitor
rtki cpd
RTKI cpd: preferentially inhibits human glioma cells expressing truncated rather than wild-type epidermal growth factor receptors		2.0710
brassinin
[no description available]		2.2110dithiocarbamic ester;
indole phytoalexin
cystine
[no description available]		2.5220
ly335979
[no description available]		2.7430carbopolycyclic compound
tandutinib
[no description available]		2.0410aromatic ether;
N-arylpiperazine;
N-carbamoylpiperazine;
phenylureas;
piperidines;
quinazolines;
tertiary amino compound		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
dasatinib
N-(2-chloro-6-methylphenyl)-2-((6-(4-(2-hydroxyethyl)piperazin-1-yl)-2-methylpyrimidin-4-yl)amino)-1,3-thiazole-5-carboxamide: a dasatinib prodrug; structure in first source. dasatinib (anhydrous) : An aminopyrimidine that is 2-methylpyrimidine which is substituted at position 4 by the primary amino group of 2-amino-1,3-thiazole-5-carboxylic acid and at position 6 by a 4-(2-hydroxyethyl)piperazin-1-yl group, and in which the carboxylic acid group has been formally condensed with 2-chloro-6-methylaniline to afford the corresponding amide. A multi-targeted kinase inhibitor, it is used, particularly as the monohydrate, for the treatment of chronic, accelerated, or myeloid or lymphoid blast phase chronic myeloid leukemia. Note that the name 'dasatinib' is used to refer to the monohydrate (USAN) as well as to anhydrous dasatinib (INN).		24.788541031,3-thiazoles;
aminopyrimidine;
monocarboxylic acid amide;
N-(2-hydroxyethyl)piperazine;
N-arylpiperazine;
organochlorine compound;
secondary amino compound;
tertiary amino compound		anticoronaviral agent;
antineoplastic agent;
tyrosine kinase inhibitor
laromustine
laromustine: has antineoplastic activity		3.1610
zd 6474
CH 331: structure in first source		6.34100aromatic ether;
organobromine compound;
organofluorine compound;
piperidines;
quinazolines;
secondary amine		antineoplastic agent;
tyrosine kinase inhibitor
2-fluoro-2-deoxyglucose-6-phosphate
2-fluoro-2-deoxyglucose-6-phosphate: metabolite of 2-fluoro-2-deoxyglucose; RN given refers to D-Glu cpd; RN for parent cpd not avail 10/90		2.0210
salinomycin
salinomycin: from Streptomyces albus; RN given refers to parent cpd; structure		2.0510polyketide;
spiroketal		animal growth promotant;
potassium ionophore
silybin
[no description available]		2.0510
ovalbumin
Ovalbumin: An albumin obtained from the white of eggs. It is a member of the serpin superfamily.		3.3260
gtp 14564
[no description available]		2.0310pyrazoles;
ring assembly
sb 218078
[no description available]		2.0310indolocarbazole
fh535
FH535: inhibits Wnt signaling		2.1510sulfonamide
crocin
crocin: a free radical scavenger		2.110
galactomannan
galactomannan: a galectin inhibitor. galactomannan : A heteroglycan consisting of a mannan backbone with galactose side groups.		2.2110oligosaccharide
mtt formazan
MTT formazan: a blue MEM-insoluble mitochondrial byproduct; used to determine viability of cells with active mitochondrial dehydrogenase enzymes		2.0510
chloramine-t
chloramine-T: RN given refers to unlabeled parent cpd. chloramine T : An organic sodium salt derivative of toluene-4-sulfonamide with a chloro substituent in place of an amino hydrogen.		2.0510organic sodium saltallergen;
antifouling biocide;
disinfectant
zinc protoporphyrin ix
[no description available]		2.0510
sb 225002
[no description available]		2.3110nitrophenol
naphthoquinones
Naphthoquinones: Naphthalene rings which contain two ketone moieties in any position. They can be substituted in any position except at the ketone groups.		4.2850
d 609
[no description available]		2.0810
osteoprotegerin
Osteoprotegerin: A secreted member of the TNF receptor superfamily that negatively regulates osteoclastogenesis. It is a soluble decoy receptor of RANK LIGAND that inhibits both CELL DIFFERENTIATION and function of OSTEOCLASTS by inhibiting the interaction between RANK LIGAND and RECEPTOR ACTIVATOR OF NUCLEAR FACTOR-KAPPA B.		4.0740long-chain fatty acid
flosequinan
[no description available]		2.0510quinolines
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1h-imidazol-2-yl)benzamide
4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide: a TGF-beta type I receptor kinase activity inhibitor		2.4420benzamides;
benzodioxoles;
imidazoles;
pyridines		EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
rhodamine 123
Rhodamine 123: A fluorescent probe with low toxicity which is a potent substrate for ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 and the bacterial multidrug efflux transporter. It is used to assess mitochondrial bioenergetics in living cells and to measure the efflux activity of ATP BINDING CASSETTE TRANSPORTER, SUBFAMILY B, MEMBER 1 in both normal and malignant cells. (Leukemia 1997;11(7):1124-30). rhodamine 123(1+) : A cationic fluorescent dye derived from 9-phenylxanthene.		2.7230organic cation;
xanthene dye		fluorochrome
tolcapone
Tolcapone: A benzophenone and nitrophenol compound that acts as an inhibitor of CATECHOL O-METHYLTRANSFERASE, an enzyme involved in the metabolism of DOPAMINE and LEVODOPA. It is used in the treatment of PARKINSON DISEASE in patients for whom levodopa is ineffective or contraindicated.. tolcapone : Benzophenone substituted on one of the phenyl rings at C-3 and C-4 by hydroxy groups and at C-5 by a nitro group, and on the other phenyl ring by a methyl group at C-4. It is an inhibitor of catechol O-methyltransferase.		2.05102-nitrophenols;
benzophenones;
catechols		antiparkinson drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
alsterpaullone
alsterpaullone: structure in first source. alsterpaullone : An organic heterotetracyclic compound that is 1,3-dihydro-2H-1-benzazepin-2-one which shares its 4-5 bond with the 3-2 bond of 5-nitro-1H-indole.		2.5120C-nitro compound;
caprolactams;
organic heterotetracyclic compound		anti-HIV-1 agent;
antineoplastic agent;
apoptosis inducer;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor;
EC 2.7.11.26 (tau-protein kinase) inhibitor
diethyl maleate
diethyl maleate : A maleate ester resulting from the formal condensation of both carboxy groups of maleic acid with ethanol. A colourless liquid at room temperature (m.p. -10degreeC) with boiling point 220degreeC at 1 atm., it is commonly used as a dienophile for Diels-Alder-type cycloaddition reactions in organic synthesis.		2.0310ethyl ester;
maleate ester		glutathione depleting agent
ku 55933
2-morpholin-4-yl-6-thianthren-1-yl-pyran-4-one: specific inhibitor of the ataxia-telangiectasia mutated kinase ATM; structure in first source		2.0710
sphingosine
sphing-4-enine : A sphingenine in which the C=C double bond is located at the 4-position.. sphingenine : A 2-aminooctadecene-1,3-diol having (2S,3R)-configuration.. sphingoid : Sphinganine, its homologs and stereoisomers, and the hydroxy and unsaturated derivatives of these compounds.. 2-aminooctadec-4-ene-1,3-diol : A 2-aminooctadecene-1,3-diol having its double bond at position 4.		3.3160sphing-4-eninehuman metabolite;
mouse metabolite
quercetin
[no description available]		2.97407-hydroxyflavonol;
pentahydroxyflavone		antibacterial agent;
antineoplastic agent;
antioxidant;
Aurora kinase inhibitor;
chelator;
EC 1.10.99.2 [ribosyldihydronicotinamide dehydrogenase (quinone)] inhibitor;
geroprotector;
phytoestrogen;
plant metabolite;
protein kinase inhibitor;
radical scavenger
bilirubin
[no description available]		5.0952biladienes;
dicarboxylic acid		antioxidant;
human metabolite;
mouse metabolite
dinoprostone
prostaglandin E2 : Prostaglandin F2alpha in which the hydroxy group at position 9 has been oxidised to the corresponding ketone. Prostaglandin E2 is the most common and most biologically potent of mammalian prostaglandins.		3.1650prostaglandins Ehuman metabolite;
mouse metabolite;
oxytocic
dinoprost
Dinoprost: A naturally occurring prostaglandin that has oxytocic, luteolytic, and abortifacient activities. Due to its vasocontractile properties, the compound has a variety of other biological actions.. prostaglandin F2alpha : A prostaglandins Falpha that is prosta-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15. It is a naturally occurring prostaglandin used to induce labor.		2.0510monocarboxylic acid;
prostaglandins Falpha		human metabolite;
mouse metabolite
biochanin a
[no description available]		2.04104'-methoxyisoflavones;
7-hydroxyisoflavones		antineoplastic agent;
EC 3.5.1.99 (fatty acid amide hydrolase) inhibitor;
phytoestrogen;
plant metabolite;
tyrosine kinase inhibitor
apigenin
Chamomile: Common name for several daisy-like plants (MATRICARIA; TRIPLEUROSPERMUM; ANTHEMIS; CHAMAEMELUM) native to Europe and Western Asia, now naturalized in the United States and Australia.		2.9740trihydroxyflavoneantineoplastic agent;
metabolite
calcitriol
dihydroxy-vitamin D3: as a major in vitro metabolite of 1alpha,25-dihydroxyvitamin D3, produced in primary cultures of neonatal human keratinocytes		7.34121D3 vitamins;
hydroxycalciol;
triol		antineoplastic agent;
antipsoriatic;
bone density conservation agent;
calcium channel agonist;
calcium channel modulator;
hormone;
human metabolite;
immunomodulator;
metabolite;
mouse metabolite;
nutraceutical
beta carotene
beta Carotene: A carotenoid that is a precursor of VITAMIN A. Beta carotene is administered to reduce the severity of photosensitivity reactions in patients with erythropoietic protoporphyria (PORPHYRIA, ERYTHROPOIETIC).. provitamin A : A provitamin that can be converted into vitamin A by enzymes from animal tissues.		2.0510carotenoid beta-end derivative;
cyclic carotene		antioxidant;
biological pigment;
cofactor;
ferroptosis inhibitor;
human metabolite;
mouse metabolite;
plant metabolite;
provitamin A
leukotriene c4
Leukotriene C4: The conjugation product of LEUKOTRIENE A4 and glutathione. It is the major arachidonic acid metabolite in macrophages and human mast cells as well as in antigen-sensitized lung tissue. It stimulates mucus secretion in the lung, and produces contractions of nonvascular and some VASCULAR SMOOTH MUSCLE. (From Dictionary of Prostaglandins and Related Compounds, 1990). leukotriene C4 : A leukotriene that is (5S,7E,9E,11Z,14Z)-5-hydroxyicosa-7,9,11,14-tetraenoic acid in which a glutathionyl group is attached at position 6 via a sulfide linkage.		2.0510leukotrienebronchoconstrictor agent;
human metabolite;
mouse metabolite
thromboxane a2
Thromboxane A2: An unstable intermediate between the prostaglandin endoperoxides and thromboxane B2. The compound has a bicyclic oxaneoxetane structure. It is a potent inducer of platelet aggregation and causes vasoconstriction. It is the principal component of rabbit aorta contracting substance (RCS).. thromboxane A2 : A thromboxane which is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.		2.2110epoxy monocarboxylic acid;
thromboxanes A		mouse metabolite
hymecromone
Hymecromone: A coumarin derivative possessing properties as a spasmolytic, choleretic and light-protective agent. It is also used in ANALYTICAL CHEMISTRY TECHNIQUES for the determination of NITRIC ACID.		2.5820hydroxycoumarinantineoplastic agent;
hyaluronic acid synthesis inhibitor
daphnetin
[no description available]		2.0310hydroxycoumarin
alprostadil
[no description available]		2.4920prostaglandins Eanticoagulant;
human metabolite;
platelet aggregation inhibitor;
vasodilator agent
vitamin d 2
Ergocalciferols: Derivatives of ERGOSTEROL formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. They differ from CHOLECALCIFEROL in having a double bond between C22 and C23 and a methyl group at C24.. vitamin D2 : A vitamin D supplement and has been isolated from alfalfa.		2.0310hydroxy seco-steroid;
seco-ergostane;
vitamin D		bone density conservation agent;
nutraceutical;
plant metabolite;
rodenticide
cholecalciferol
Cholecalciferol: Derivative of 7-dehydroxycholesterol formed by ULTRAVIOLET RAYS breaking of the C9-C10 bond. It differs from ERGOCALCIFEROL in having a single bond between C22 and C23 and lacking a methyl group at C24.. calciol : A hydroxy seco-steroid that is (5Z,7E)-9,10-secocholesta-5,7,10(19)-triene in which the pro-S hydrogen at position 3 has been replaced by a hydroxy group. It is the inactive form of vitamin D3, being hydroxylated in the liver to calcidiol (25-hydroxyvitamin D3), which is then further hydroxylated in the kidney to give calcitriol (1,25-dihydroxyvitamin D3), the active hormone.		6.782D3 vitamins;
hydroxy seco-steroid;
seco-cholestane;
secondary alcohol;
steroid hormone		geroprotector;
human metabolite
genistein
[no description available]		3.841107-hydroxyisoflavonesantineoplastic agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
geroprotector;
human urinary metabolite;
phytoestrogen;
plant metabolite;
tyrosine kinase inhibitor
amphotericin b
Amphotericin B: Macrolide antifungal antibiotic produced by Streptomyces nodosus obtained from soil of the Orinoco river region of Venezuela.. amphotericin B : A macrolide antibiotic used to treat potentially life-threatening fungal infections.		2.7330antibiotic antifungal drug;
macrolide antibiotic;
polyene antibiotic		antiamoebic agent;
antiprotozoal drug;
bacterial metabolite
clavulanic acid
Clavulanic Acid: A beta-lactam antibiotic produced by the actinobacterium Streptomyces clavuligerus. It is a suicide inhibitor of bacterial beta-lactamase enzymes. Administered alone, it has only weak antibacterial activity against most organisms, but given in combination with other beta-lactam antibiotics it prevents antibiotic inactivation by microbial lactamase.. clavulanate : The conjugate base of clavulanic acid.. clavulanic acid : Antibiotic isolated from Streptomyces clavuligerus. It acts as a suicide inhibitor of bacterial beta-lactamase enzymes.		2.0510oxapenamantibacterial drug;
anxiolytic drug;
bacterial metabolite;
EC 3.5.2.6 (beta-lactamase) inhibitor
pulmicort
Budesonide: A glucocorticoid used in the management of ASTHMA, the treatment of various skin disorders, and allergic RHINITIS.. budesonide : A glucocorticoid steroid having a highly oxygenated pregna-1,4-diene structure. It is used mainly in the treatment of asthma and non-infectious rhinitis and for treatment and prevention of nasal polyposis.		2.452011beta-hydroxy steroid;
20-oxo steroid;
21-hydroxy steroid;
3-oxo-Delta(1),Delta(4)-steroid;
cyclic acetal;
glucocorticoid;
primary alpha-hydroxy ketone		anti-inflammatory drug;
bronchodilator agent;
drug allergen
oxymetholone
Oxymetholone: A synthetic hormone with anabolic and androgenic properties. It is used mainly in the treatment of anemias. According to the Fourth Annual Report on Carcinogens (NTP 85-002), this compound may reasonably be anticipated to be a carcinogen. (From Merck Index, 11th ed). oxymetholone : A 3-oxo-5alpha- steroid that is 4,5alpha-dihydrotestosterone which is substituted by a hydroxymethylidene group at position 2 and by a methyl group at the 17alpha position. A synthetic androgen, it was mainly used for the treatment of anaemias until being replaced by treatments with fewer side effects.		2.0510
montelukast
montelukast: a leukotriene D4 receptor antagonist		2.520aliphatic sulfide;
monocarboxylic acid;
quinolines		anti-arrhythmia drug;
anti-asthmatic drug;
leukotriene antagonist
mycophenolate mofetil
mycophenolate mofetil : A carboxylic ester resulting from the formal condensation between the carboxylic acid group of mycophenolic acid and the hydroxy group of 2-(morpholin-4-yl)ethanol. In the liver, it is metabolised to mycophenolic acid, an immunosuppressant for which it is a prodrug. It is widely used to prevent tissue rejection following organ transplants as well as for the treatment of certain autoimmune diseases.		2.0510carboxylic ester;
ether;
gamma-lactone;
phenols;
tertiary amino compound		anticoronaviral agent;
EC 1.1.1.205 (IMP dehydrogenase) inhibitor;
immunosuppressive agent;
prodrug
entacapone
entacapone: structure given in first source. entacapone : A monocarboxylic acid amide that is N,N-diethylprop-2-enamide in which the hydrogen at position 2 is substituted by a cyano group and the hydrogen at the 3E position is substituted by a 3,4-dihydroxy-5-nitrophenyl group.		2.05102-nitrophenols;
catechols;
monocarboxylic acid amide;
nitrile		antidyskinesia agent;
antiparkinson drug;
central nervous system drug;
EC 2.1.1.6 (catechol O-methyltransferase) inhibitor
astaxanthine
astaxanthine: a keto form of carotene; pigment in flesh of Scottish salmon (Salmo salar) crustacoa-lobster (Homarus gammarus, flamingo feathers; structure; a carotenoid without vitamin A activity, has shown anti-oxidant and anti-inflammatory activities. astaxanthin : A carotenone that consists of beta,beta-carotene-4,4'-dione bearing two hydroxy substituents at positions 3 and 3' (the 3S,3'S diastereomer). A carotenoid pigment found mainly in animals (crustaceans, echinoderms) but also occurring in plants. It can occur free (as a red pigment), as an ester, or as a blue, brown or green chromoprotein.		2.0510carotenol;
carotenone		animal metabolite;
anticoagulant;
antioxidant;
food colouring;
plant metabolite
fucoxanthin
fucoxanthin: RN given refers to (3S,3'S,5R,5'R,6S,6'R)-isomer. fucoxanthin : An epoxycarotenol that is found in brown seaweed and which exhibits anti-cancer, anti-diabetic, anti-oxidative and neuroprotective properties.		2.1710
cucurbitacin b
[no description available]		7.1310cucurbitacin;
secondary alpha-hydroxy ketone;
tertiary alpha-hydroxy ketone
zearalenone
Zearalenone: (S-(E))-3,4,5,6,8,10-Hexahydro-14,16-dihydroxy-3-methyl-1H-2-benzoxacyclotetradecin-1,7(8H)-dione. One of a group of compounds known under the general designation of resorcylic acid lactones. Cis, trans, dextro and levo forms have been isolated from the fungus Gibberella zeae (formerly Fusarium graminearum). They have estrogenic activity, cause toxicity in livestock as feed contaminant, and have been used as anabolic or estrogen substitutes.. zearalenone : A macrolide comprising a fourteen-membered lactone fused to 1,3-dihydroxybenzene; a potent estrogenic metabolite produced by some Giberella species.		2.0410macrolide;
resorcinols		fungal metabolite;
mycoestrogen
baicalein
[no description available]		4.6111trihydroxyflavoneangiogenesis inhibitor;
anti-inflammatory agent;
antibacterial agent;
anticoronaviral agent;
antifungal agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
EC 1.13.11.31 (arachidonate 12-lipoxygenase) inhibitor;
EC 1.13.11.33 (arachidonate 15-lipoxygenase) inhibitor;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
EC 3.4.22.69 (SARS coronavirus main proteinase) inhibitor;
EC 4.1.1.17 (ornithine decarboxylase) inhibitor;
ferroptosis inhibitor;
geroprotector;
hormone antagonist;
plant metabolite;
prostaglandin antagonist;
radical scavenger
chrysin
chrysin : A dihydroxyflavone in which the two hydroxy groups are located at positions 5 and 7.		2.04107-hydroxyflavonol;
dihydroxyflavone		anti-inflammatory agent;
antineoplastic agent;
antioxidant;
EC 2.7.11.18 (myosin-light-chain kinase) inhibitor;
hepatoprotective agent;
plant metabolite
diosmetin
[no description available]		2.25103'-hydroxyflavonoid;
monomethoxyflavone;
trihydroxyflavone		angiogenesis inhibitor;
anti-inflammatory agent;
antineoplastic agent;
antioxidant;
apoptosis inducer;
bone density conservation agent;
cardioprotective agent;
plant metabolite;
tropomyosin-related kinase B receptor agonist;
vasodilator agent
diosmin
[no description available]		2.0510dihydroxyflavanone;
disaccharide derivative;
glycosyloxyflavone;
monomethoxyflavone;
rutinoside		anti-inflammatory agent;
antioxidant
galangin
5,7-dihydroxyflavonol: antimicrobial from the twigs of Populus nigra x Populus deltoides; structure in first source. galangin : A 7-hydroxyflavonol with additional hydroxy groups at positions 3 and 5 respectively; a growth inhibitor of breast tumor cells.		7.04107-hydroxyflavonol;
trihydroxyflavone		antimicrobial agent;
EC 3.1.1.3 (triacylglycerol lipase) inhibitor;
plant metabolite
morin
morin: a light yellowish pigment found in the wood of old fustic (Chlorophora tinctoria). morin : A pentahydroxyflavone that is 7-hydroxyflavonol bearing three additional hydroxy substituents at positions 2' 4' and 5.		2.04107-hydroxyflavonol;
pentahydroxyflavone		angiogenesis modulating agent;
anti-inflammatory agent;
antibacterial agent;
antihypertensive agent;
antineoplastic agent;
antioxidant;
EC 5.99.1.2 (DNA topoisomerase) inhibitor;
hepatoprotective agent;
metabolite;
neuroprotective agent
myricetin
[no description available]		2.6107-hydroxyflavonol;
hexahydroxyflavone		antineoplastic agent;
antioxidant;
cyclooxygenase 1 inhibitor;
food component;
geroprotector;
hypoglycemic agent;
plant metabolite
wogonin
wogonin: structure in first source. wogonin : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-8.		2.5220dihydroxyflavone;
monomethoxyflavone		angiogenesis inhibitor;
antineoplastic agent;
cyclooxygenase 2 inhibitor;
plant metabolite
cynarine
cynarine: active principle of the artichoke; functions primarily as a cholagogue and choleretic and also as antilipemic agent		2.0510alkyl caffeate ester;
quinic acid		plant metabolite
rosmarinic acid
rosmarinic acid: RN given refers to parent cpd; promote OT project. (R)-rosmarinic acid : A stereoisomer of rosmarinic acid having (R)-configuration.. rosmarinic acid : The 1-carboxy-2-(2,4-dihydroxyphenyl)ethyl ester of trans-caffeic acid.		2.110rosmarinic acidgeroprotector;
plant metabolite
shogaol
shogaol: from ginger, ZINGIBER OFFICINALE; less mutagenic than GINGEROL; structure given in first source		2.3110enone;
monomethoxybenzene;
phenols
wedelolactone
wedelolactone: antihepatotoxic coumestan from Eclipta prostrata and Wedelia calendulacea (both Asteraceae); structure given in first source. wedelolactone : A member of the class of coumestans that is coumestan with hydroxy substituents as positions 1, 8 and 9 and a methoxy substituent at position 3.		2.0310aromatic ether;
coumestans;
delta-lactone;
polyphenol		antineoplastic agent;
apoptosis inducer;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
hepatoprotective agent;
metabolite
maytansine
Maytansine: An ansa macrolide isolated from the MAYTENUS genus of East African shrubs.. maytansine : An organic heterotetracyclic compound and 19-membered macrocyclic lactam antibiotic originally isolated from the Ethiopian shrub Maytenus serrata but also found in other Maytenus species. It exhibits cytotoxicity against many tumour cell lines.		2.4110alpha-amino acid ester;
carbamate ester;
epoxide;
maytansinoid;
organic heterotetracyclic compound;
organochlorine compound		antimicrobial agent;
antimitotic;
antineoplastic agent;
plant metabolite;
tubulin modulator
rottlerin
rottlerin: an angiogenesis inhibitor; an inhibitor of protein kinase Cdelta (PKCdelta) and calmodulin kinase III; RN refers to (E)-isomer; do not confuse this chalcone with an anthraquinone that is also called rottlerin (RN 481-72-1);. rottlerin : A chromenol that is 2,2-dimethyl-2H-chromene substituted by hydroxy groups at positions 5 and 7, a 3-acetyl-2,4,6-trihydroxy-5-methylbenzyl group at position 6 and a (1E)-3-oxo-1-phenylprop-1-en-3-yl group at position 8. A potassium channel opener, it is isolated from Mallotus philippensis.		2.9840aromatic ketone;
benzenetriol;
chromenol;
enone;
methyl ketone		anti-allergic agent;
antihypertensive agent;
antineoplastic agent;
apoptosis inducer;
K-ATP channel agonist;
metabolite
flupenthixol
cis-flupenthixol : A flupenthixol in which the double bond adopts a cis-configuration.		2.0410flupenthixoldopaminergic antagonist
sdz psc 833
valspodar: nonimmunosuppressive cyclosporin analog which is a potent multidrug resistance modifier; 7-10 fold more potent than cyclosporin A; a potent P glycoprotein inhibitor; MW 1215		4.2160homodetic cyclic peptide
l 660,711
[no description available]		2.0410quinolines
coenzyme q10
coenzyme Q10: Ubiquinone ring with a chain of 10 isoprene units; redox equilibrium with ubiqunol serving in mitochondrial inner membrane to transfer electrons; presence during reconstitution of acetylcholine receptor into phospholipid vesicles yields vesicles active in catalyzing carbamylcholine-sensitive Na+ flux; coenzyme Q10 depletion has been noted with use of statins. coenzyme Q10 : A ubiquinone having a side chain of 10 isoprenoid units. In the naturally occurring isomer, all isoprenyl double bonds are in the E- configuration.		2.0510ubiquinonesantioxidant;
ferroptosis inhibitor;
human metabolite
tranilast
tranilast: antiallergic drug; potent inhibitor of homologous passive cutaneous anaphylaxis. tranilast : An amidobenzoic acid that is anthranilic acid in which one of the anilino hydrogens is replaced by a 3,4-dimethoxycinnamoyl group.		2.4520amidobenzoic acid;
cinnamamides;
dimethoxybenzene;
secondary carboxamide		anti-allergic agent;
anti-asthmatic drug;
antineoplastic agent;
aryl hydrocarbon receptor agonist;
calcium channel blocker;
hepatoprotective agent;
nephroprotective agent
etretinate
retinoid : Oxygenated derivatives of 3,7-dimethyl-1-(2,6,6-trimethylcyclohex-1-enyl)nona-1,3,5,7-tetraene and derivatives thereof.		2.0510enoate ester;
ethyl ester;
retinoid		keratolytic drug
isotretinoin
Isotretinoin: A topical dermatologic agent that is used in the treatment of ACNE VULGARIS and several other skin diseases. The drug has teratogenic and other adverse effects.. isotretinoin : A retinoic acid that is all-trans-retinoic acid in which the double bond which is alpha,beta- to the carboxy group is isomerised to Z configuration. A synthetic retinoid, it is used for the treatment of severe cases of acne and other skin diseases.		2.0510retinoic acidantineoplastic agent;
keratolytic drug;
teratogenic agent
misoprostol
Misoprostol: A synthetic analog of natural prostaglandin E1. It produces a dose-related inhibition of gastric acid and pepsin secretion, and enhances mucosal resistance to injury. It is an effective anti-ulcer agent and also has oxytocic properties.. misoprostol : A diastereoisomeric mixture composed of approximately equal amounts of a double racemate of four of the sixteen possible diastereoisomers of methyl (13E)-11,16-dihydroxy-16-methyl-9-oxoprost-13-en-1-oate that is racemic prostaglandin E1 which is lacking the hydroxy group at position 15, but which has an additional hydroxy group at position 16. It is a synthetic prostaglandin E1 analogue, used in the treatment of gastric and duodenal ulcers. A weak abortifacient, it is also used for cervical ripening prior to surgical termination of pregnancy. The (11R,16S)-diastereoisomer is the pharmacologically active form.		2.4920
indocyanine green
[no description available]		2.04101,1-diunsubstituted alkanesulfonate;
benzoindole;
cyanine dye
ozagrel
ozagrel: RN refers to (E)-isomer		2.0510cinnamic acids
pitavastatin
pitavastatin : A dihydroxy monocarboxylic acid that is (6E)-7-[2-cyclopropyl-4-(4-fluorophenyl)quinolin-3-yl]hept-6-enoic acid in which the two hydroxy groups are located at positions 3 and 5 (the 3R,5S-stereoisomer). Used as its calcium salt for treatment of hypercholesterolemia (elevated levels of cholesterol in the blood) on patients unable to sufficiently lower their cholesterol levels by diet and exercise.		3.6120cyclopropanes;
dihydroxy monocarboxylic acid;
monofluorobenzenes;
quinolines;
statin (synthetic)		antioxidant
alatrofloxacin mesylate
[no description available]		2.0510
4-hydroxy-2-nonenal
4-hydroxy-2-nonenal: cytotoxic product from peroxidation of liver microsomal lipids; RN given refers to cpd without isomeric designation. 4-hydroxynon-2-enal : An enal consisting of non-2-ene having an oxo group at the 1-position and a hydroxy group at the 4-position.. 4-hydroxynonenal : A monounsaturated fatty aldehyde that is nonanal that has undergone dehydrogenation to introduce a double bond at any position in the aliphatic chain and in which a hydrogen at position 4 has been replaced by a hydroxy group.		2.15104-hydroxynon-2-enal;
4-hydroxynonenal
menaquinone 6
menaquinone 6: RN given refers to (all-E)-isomer		4.9521
sphingosine 1-phosphate
sphingosine 1-phosphate: RN given refers to (R-(R*,S*-(E)))-isomer; RN for cpd without isomeric designation not available 8/89. sphingosine 1-phosphate : A phosphosphingolipid that consists of sphingosine having a phospho group attached at position 1		2.9840sphingoid 1-phosphatemouse metabolite;
signalling molecule;
sphingosine-1-phosphate receptor agonist;
T-cell proliferation inhibitor;
vasodilator agent
codeine
[no description available]		2.0510morphinane alkaloid;
organic heteropentacyclic compound		antitussive;
drug allergen;
environmental contaminant;
opioid analgesic;
opioid receptor agonist;
prodrug;
xenobiotic
cyclosporine
ramihyphin A: one of the metabolites produced by Fusarium sp. S-435; RN given refers to cpd with unknown MF		2.7330homodetic cyclic peptideanti-asthmatic drug;
anticoronaviral agent;
antifungal agent;
antirheumatic drug;
carcinogenic agent;
dermatologic drug;
EC 3.1.3.16 (phosphoprotein phosphatase) inhibitor;
geroprotector;
immunosuppressive agent;
metabolite
phenylephrine hydrochloride
Nose: A part of the upper respiratory tract. It contains the organ of SMELL. The term includes the external nose, the nasal cavity, and the PARANASAL SINUSES.. phenylephrine hydrochloride : A hydrochloride that is the monohydrochloride salt of phenylephrine.		2.2110hydrochloride
natamycin
[no description available]		2.0510antibiotic antifungal drug;
dicarboxylic acid monoester;
epoxide;
macrolide antibiotic;
monosaccharide derivative;
polyene antibiotic		antifungal agrochemical;
antimicrobial food preservative;
apoptosis inducer;
bacterial metabolite;
ophthalmology drug
acitretin
Acitretin: An oral retinoid effective in the treatment of psoriasis. It is the major metabolite of ETRETINATE with the advantage of a much shorter half-life when compared with etretinate.. acitretin : A retinoid that consists of 3,7-dimethylnona-2,4,6,8-tetraenoic acid having a 4-methoxy-2,3,6-trimethylphenyl group attached at position 9.		2.4420acitretin;
alpha,beta-unsaturated monocarboxylic acid;
retinoid		keratolytic drug
dothiepin
[no description available]		2.0510dothiepin
levetiracetam
Levetiracetam: A pyrrolidinone and acetamide derivative that is used primarily for the treatment of SEIZURES and some movement disorders, and as a nootropic agent.. levetiracetam : A pyrrolidinone and carboxamide that is N-methylpyrrolidin-2-one in which one of the methyl hydrogens is replaced by an aminocarbonyl group, while another is replaced by an ethyl group (the S enantiomer). An anticonvulsant, it is used for the treatment of epilepsy in both human and veterinary medicine.		2.0510pyrrolidin-2-onesanticonvulsant;
environmental contaminant;
xenobiotic
nalorphine
Nalorphine: A narcotic antagonist with some agonist properties. It is an antagonist at mu opioid receptors and an agonist at kappa opioid receptors. Given alone it produces a broad spectrum of unpleasant effects and it is considered to be clinically obsolete.		2.0510morphinane alkaloid
naloxone
Naloxone: A specific opiate antagonist that has no agonist activity. It is a competitive antagonist at mu, delta, and kappa opioid receptors.. naloxone : A synthetic morphinane alkaloid that is morphinone in which the enone double bond has been reduced to a single bond, the hydrogen at position 14 has been replaced by a hydroxy group, and the methyl group attached to the nitrogen has been replaced by an allyl group. A specific opioid antagonist, it is used (commonly as its hydrochloride salt) to reverse the effects of opioids, both following their use of opioids during surgery and in cases of known or suspected opioid overdose.		2.4920morphinane alkaloid;
organic heteropentacyclic compound;
tertiary alcohol		antidote to opioid poisoning;
central nervous system depressant;
mu-opioid receptor antagonist
oxymorphone
Oxymorphone: An opioid analgesic with actions and uses similar to those of MORPHINE, apart from an absence of cough suppressant activity. It is used in the treatment of moderate to severe pain, including pain in obstetrics. It may also be used as an adjunct to anesthesia. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1092)		2.0510morphinane alkaloid
sirolimus
Sirolimus: A macrolide compound obtained from Streptomyces hygroscopicus that acts by selectively blocking the transcriptional activation of cytokines thereby inhibiting cytokine production. It is bioactive only when bound to IMMUNOPHILINS. Sirolimus is a potent immunosuppressant and possesses both antifungal and antineoplastic properties.. sirolimus : A macrolide lactam isolated from Streptomyces hygroscopicus consisting of a 29-membered ring containing 4 trans double bonds, three of which are conjugated. It is an antibiotic, immunosupressive and antineoplastic agent.		13.33745antibiotic antifungal drug;
cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
organic heterotricyclic compound;
secondary alcohol		antibacterial drug;
anticoronaviral agent;
antineoplastic agent;
bacterial metabolite;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
topiramate
Topiramate: A sulfamate-substituted fructose analog that was originally identified as a hypoglycemic agent. It is used for the treatment of EPILEPSY and MIGRAINE DISORDERS, and may also promote weight loss.. topiramate : A hexose derivative that is 2,3:4,5-di-O-isopropylidene-beta-D-fructopyranose in which the hydroxy group has been converted to the corresponding sulfamate ester. It blocks voltage-dependent sodium channels and is used as an antiepileptic and for the prevention of migraine.		2.0510cyclic ketal;
ketohexose derivative;
sulfamate ester		anticonvulsant;
sodium channel blocker
gamma-cyclodextrin
gamma-cyclodextrin : A cycloamylose composed of eight alpha-(1->4) linked D-glucopyranose units.		2.1110cyclodextrin
menaquinone 7
menaquinone-7 : A menaquinone whose side-chain contains seven isoprene units in an all-trans-configutation.		4.6111menaquinonebone density conservation agent;
cofactor;
Escherichia coli metabolite;
human blood serum metabolite;
Mycoplasma genitalium metabolite
brefeldin a
[no description available]		2.7430macrolide antibioticPenicillium metabolite
alvocidib
alvocidib: structure given in first source. alvocidib : A synthetic dihydroxyflavone that is 5,7-dihydroxyflavone which is substituted by a 3-hydroxy-1-methylpiperidin-4-yl group at position 8 and by a chlorine at the 2' position (the (-)-3S,4R stereoisomer). A cyclin-dependent kinase 9 (CDK9) inhibitor, it has been studied for the treatment of acute myeloid leukaemia, arthritis and atherosclerotic plaque formation.		6.4121dihydroxyflavone;
hydroxypiperidine;
monochlorobenzenes;
tertiary amino compound		antineoplastic agent;
antirheumatic drug;
apoptosis inducer;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
seocalcitol
seocalcitol: structure given in first source		2.0510
fenretinide
Fenretinide: A synthetic retinoid that is used orally as a chemopreventive against prostate cancer and in women at risk of developing contralateral breast cancer. It is also effective as an antineoplastic agent.. 4-hydroxyphenyl retinamide : A retinoid obtained by formal condensation of the carboxy group of all-trans retinoic acid and the anilino group of 4-hydroxyaniline. Synthetic retinoid agonist. Antiproliferative, antioxidant and anticancer agent with a long half-life in vivo. Apoptotic effects appear to be mediated by a mechanism distinct from that of 'classical' retinoids.		2.4820monocarboxylic acid amide;
retinoid		antineoplastic agent;
antioxidant
geldanamycin
[no description available]		2.45201,4-benzoquinones;
ansamycin;
carbamate ester;
organic heterobicyclic compound		antimicrobial agent;
antineoplastic agent;
antiviral agent;
cysteine protease inhibitor;
Hsp90 inhibitor
17-(dimethylaminoethylamino)-17-demethoxygeldanamycin
17-(dimethylaminoethylamino)-17-demethoxygeldanamycin: structure in first source. alvespimycin : A 19-membered macrocyle that is geldanamycin in which the methoxy group attached to the benzoquinone moiety has been replaced by a 2-(N,N-dimethylamino)ethylamino group.		2.44201,4-benzoquinones;
ansamycin;
carbamate ester;
secondary amino compound;
tertiary amino compound		Hsp90 inhibitor
morphine
Meconium: The thick green-to-black mucilaginous material found in the intestines of a full-term fetus. It consists of secretions of the INTESTINAL GLANDS; BILE PIGMENTS; FATTY ACIDS; AMNIOTIC FLUID; and intrauterine debris. It constitutes the first stools passed by a newborn.		3.2250morphinane alkaloid;
organic heteropentacyclic compound;
tertiary amino compound		anaesthetic;
drug allergen;
environmental contaminant;
geroprotector;
mu-opioid receptor agonist;
opioid analgesic;
plant metabolite;
vasodilator agent;
xenobiotic
demycarosylturimycin h
[no description available]		2.0510
su 5402
SU 5402: structure given in first source. SU5402 : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is substituted by a 3-(2-carboxyethyl)-4-methyl-1H-pyrrol-2-yl group. It is an ATP-competitive inhibitor of the tyrosine kinase activity of fibroblast growth factor receptor 1.		2.0210
su 9516
[no description available]		2.0310
clobetasol
Clobetasol: A derivative of PREDNISOLONE with high glucocorticoid activity and low mineralocorticoid activity. Absorbed through the skin faster than FLUOCINONIDE, it is used topically in treatment of PSORIASIS but may cause marked adrenocortical suppression.. clobetasol : A 3-oxo-Delta(1),Delta(4)-steroid that is 16beta-methylpregna-1,4-diene-3,20-dione bearing hydroxy groups at the 11beta and 17alpha positions, fluorine at position 9, and a chlorine substituent at position 21. It is used as its 17alpha-propionate ester to treat various skin disorders, including exzema and psoriasis.		3.141011beta-hydroxy steroid;
17alpha-hydroxy steroid;
20-oxo steroid;
3-oxo-Delta(1),Delta(4)-steroid;
chlorinated steroid;
fluorinated steroid;
glucocorticoid;
tertiary alpha-hydroxy ketone		anti-inflammatory drug;
SMO receptor agonist
herbimycin
herbimycin: herbicidal antibiotic produced by Streptomyces sp.; see also herbimycin B; structure for herbimycin A in second source. herbimycin : A 19-membered macrocyle incorporating a benzoquinone ring and a lactam functionality. It is an ansamycin antibiotic that induces apoptosis and displays antitumour effects.		3.27601,4-benzoquinones;
lactam;
macrocycle		antimicrobial agent;
apoptosis inducer;
herbicide;
Hsp90 inhibitor;
tyrosine kinase inhibitor
pd 180970
PD 180970: inhibits p210(Bcr-Abl) tyrosine kinase; structure in first source		5.2960
iloprost
Iloprost: An eicosanoid, derived from the cyclooxygenase pathway of arachidonic acid metabolism. It is a stable and synthetic analog of EPOPROSTENOL, but with a longer half-life than the parent compound. Its actions are similar to prostacyclin. Iloprost produces vasodilation and inhibits platelet aggregation.. iloprost : A carbobicyclic compound that is prostaglandin I2 in which the endocyclic oxygen is replaced by a methylene group and in which the (1E,3S)-3-hydroxyoct-1-en-1-yl side chain is replaced by a (3R)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl group. A synthetic analogue of prostacyclin, it is used as the trometamol salt (generally by intravenous infusion) for the treatment of peripheral vascular disease and pulmonary hypertension.		3.8330carbobicyclic compound;
monocarboxylic acid;
secondary alcohol		platelet aggregation inhibitor;
vasodilator agent
lysophosphatidylcholines
lysophosphatidylcholine : An acylglycerophosphocholine resulting from partial hydrolysis of a phosphatidylcholine, which removes one of the fatty acyl groups. The structure is depicted in the image where R1 = acyl, R2 = H or where R1 = H, R2 = acyl.		2.21101-O-acyl-sn-glycero-3-phosphocholine
n-(n-(3,5-difluorophenacetyl)alanyl)phenylglycine tert-butyl ester
DAPT : A dipeptide consisting of alanylphenylglycine derivatised as a 3,5-difluorophenylacetamide at the amino terminal and a tert-butyl ester at the carboxy terminal. A gamma-secretase inhibitor.		2.2110carboxylic ester;
difluorobenzene;
dipeptide;
tert-butyl ester		EC 3.4.23.46 (memapsin 2) inhibitor
nalbuphine
Nalbuphine: A narcotic used as a pain medication. It appears to be an agonist at KAPPA RECEPTORS and an antagonist or partial agonist at MU RECEPTORS.		2.1710organic heteropentacyclic compoundmu-opioid receptor antagonist;
opioid analgesic
seglitide
seglitide: more potent than somatostatin for inhibition of insulin, glucagon & growth hormone release; used experimentally in treatment of Alzheimer's disease; somatostatin receptor antagonist		2.0410
vinorelbine
[no description available]		2.0510acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
ring assembly;
vinca alkaloid		antineoplastic agent;
photosensitizing agent
3-[6-[4-(trifluoromethoxy)anilino]-4-pyrimidinyl]benzamide
[no description available]		2.4110pyrimidines
kn 93
KN 93: reduces dopamine content in PC12h cells. KN-93 : A sulfonamide resulting from the formal condensation of p-methoxybenzenesulfonic acid with the anilino nitrogen of 2-(aminomethyl)-N-(2-hydroxyethyl)aniline in which the hydrogens of the primary amino group have been replaced by methyl and p-chlorocinnamyl groups. KN-93 is a selective inhibitor of Ca(2+)/calmodulin-dependent protein kinase II.		2.0310monochlorobenzenes;
monomethoxybenzene;
primary alcohol;
sulfonamide;
tertiary amino compound		EC 2.7.11.17 (Ca(2+)/calmodulin-dependent protein kinase) inhibitor;
geroprotector
su 6656
SU 6656: a c-Src kinase inhibitor; used to probe growth signaling; structure in first source. SU6656 : A member of the class of oxindoles that is 3-methyleneoxindole in which the hydrogeh at position 5 has been replaced by a dimethylaminosulfonyl group and in which one of the hydrogens of the methylene group has been replaced by a 4,5,6,7-tetrahydro-indol-2-yl group. It is a specific inhibitor of Src family kinase.		4.0740
biliverdine
[no description available]		2.0210
andrographolide
[no description available]		2.2110carbobicyclic compound;
gamma-lactone;
labdane diterpenoid;
primary alcohol;
secondary alcohol		anti-HIV agent;
anti-inflammatory drug;
antineoplastic agent;
metabolite
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one
5,7-dihydroxy-6-methoxy-2-phenylchromen-4-one: isolated from the Chinese herb Scutellariae radix. oroxylin A : A dihydroxy- and monomethoxy-flavone in which the hydroxy groups are positioned at C-5 and C-7 and the methoxy group is at C-6.		2.5320dihydroxyflavone;
monomethoxyflavone		antineoplastic agent;
EC 1.14.13.39 (nitric oxide synthase) inhibitor
furazolidone
[no description available]		2.0510
fluvoxamine
Fluvoxamine: A selective serotonin reuptake inhibitor that is used in the treatment of DEPRESSION and a variety of ANXIETY DISORDERS.. fluvoxamine : An oxime O-ether that is benzene substituted by a (1E)-N-(2-aminoethoxy)-5-methoxypentanimidoyl group at position 1 and a trifluoromethyl group at position 4. It is a selective serotonin reuptake inhibitor that is used for the treatment of obsessive-compulsive disorder.		2.0510(trifluoromethyl)benzenes;
5-methoxyvalerophenone O-(2-aminoethyl)oxime		antidepressant;
anxiolytic drug;
serotonin uptake inhibitor
casein kinase ii
Casein Kinase II: A ubiquitous casein kinase that is comprised of two distinct catalytic subunits and dimeric regulatory subunit. Casein kinase II has been shown to phosphorylate a large number of substrates, many of which are proteins involved in the regulation of gene expression.		3.5670
tyrphostin ag-494
AG 494: tyrphostin that blocks Cdk2 activation; structure in first source		2.0310
ag-490
[no description available]		3.82110catechols;
enamide;
monocarboxylic acid amide;
nitrile;
secondary carboxamide		anti-inflammatory agent;
antioxidant;
apoptosis inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
geroprotector;
STAT3 inhibitor
bosutinib
4-((2,4-dichloro-5-methoxyphenyl)amino)-6-methoxy-7-(3-(4-methyl-1-piperazinyl)propoxy)-3-quinolinecarbonitrile: a Src kinase inhibitor; structure in first source		22.8810523aminoquinoline;
aromatic ether;
dichlorobenzene;
N-methylpiperazine;
nitrile;
tertiary amino compound		antineoplastic agent;
tyrosine kinase inhibitor
semaxinib
semaxanib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is replaced by a 3,5-dimethylpyrrol-2-yl group.		11.2870olefinic compound;
oxindoles;
pyrroles		angiogenesis modulating agent;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
vascular endothelial growth factor receptor antagonist
orantinib
orantinib: an antiangiogenic agent. orantinib : An oxindole that is 3-methyleneoxindole in which one of the hydrogens of the methylene group is substituted by a 2-(2-carboxyethyl)-3,5-dimethylpyrrol-3-yl group. It is an ATP-competitive inhibitor of the tyrosine kinase activity of fibroblast growth factor receptor 1.		5.2430
su 11248
[no description available]		22.1535551monocarboxylic acid amide;
pyrroles		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
immunomodulator;
neuroprotective agent;
vascular endothelial growth factor receptor antagonist
su 11652
SU 11652: a tyrosine kinase inhibitor; amino acid sequence in first source. SU11652 : A member of the class of pyrrolecarboxamides obtained by formal condensation of the carboxy group of 5-[(Z)-(5-chloro-2-oxo-1,2-dihydroindol-3-ylidene)methyl]-2,4-dimethylpyrrole-3-carboxylic acid with the primary amino group of N(1),N(1)-diethylethane-1,2-diamine.		2.0310olefinic compound;
organochlorine compound;
oxindoles;
pyrrolecarboxamide;
tertiary amino compound		EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
EC 3.1.4.12 (sphingomyelin phosphodiesterase) inhibitor
palbociclib
[no description available]		5.5451aminopyridine;
aromatic ketone;
cyclopentanes;
piperidines;
pyridopyrimidine;
secondary amino compound;
tertiary amino compound		antineoplastic agent;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
fosbretabulin
[no description available]		2.3110stilbenoid
fosbretabulin
fosbretabulin: a microtubule destabilizing agent isolated from Combretum caffrum; structure in first source		3.110
stellettin b
stellettin B: from the marine sponge Rhabdastrella globostellata; structure in first source		2.1510
lead
Lead: A soft, grayish metal with poisonous salts; atomic number 82, atomic weight 207.2, symbol Pb.		4.9521carbon group element atom;
elemental lead;
metal atom		neurotoxin
bay 11-7082
(E)-3-tosylacrylonitrile : A nitrile that is acrylonitrile in which the hydrogen located beta,trans to the cyano group is replaced by a tosyl group. It is an inhibitor of cytokine-induced IkappaB-alpha phosphorylation in cells.		2.0510nitrile;
sulfone		apoptosis inducer;
EC 2.7.11.10 (IkappaB kinase) inhibitor;
EC 3.1.3.48 (protein-tyrosine-phosphatase) inhibitor;
non-steroidal anti-inflammatory drug;
platelet aggregation inhibitor
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid
(6E)-7-[3-(4-fluorophenyl)-1-(propan-2-yl)-1H-indol-2-yl]-3,5-dihydroxyhept-6-enoic acid : A dihydroxy monocarboxylic acid that is N-isopropylindole which is substituted at position 3 by a p-fluorophenyl group and at position 2 by a 6-carboxy-3,5-dihydroxyhex-1-en-1-yl group. It has four possible diastereoisomers.		2.0510dihydroxy monocarboxylic acid;
indoles;
organofluorine compound
molsidomine
[no description available]		2.0510ethyl ester;
morpholines;
oxadiazole;
zwitterion		antioxidant;
apoptosis inhibitor;
cardioprotective agent;
nitric oxide donor;
vasodilator agent
arsenic
Arsenic: A shiny gray element with atomic symbol As, atomic number 33, and atomic weight 75. It occurs throughout the universe, mostly in the form of metallic arsenides. Most forms are toxic. According to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985), arsenic and certain arsenic compounds have been listed as known carcinogens. (From Merck Index, 11th ed)		10.72431metalloid atom;
pnictogen		micronutrient
naltrexone
Naltrexone: Derivative of noroxymorphone that is the N-cyclopropylmethyl congener of NALOXONE. It is a narcotic antagonist that is effective orally, longer lasting and more potent than naloxone, and has been proposed for the treatment of heroin addiction. The FDA has approved naltrexone for the treatment of alcohol dependence.. naltrexone : An organic heteropentacyclic compound that is naloxone substituted in which the allyl group attached to the nitrogen is replaced by a cyclopropylmethyl group. A mu-opioid receptor antagonist, it is used to treat alcohol dependence.		2.5220cyclopropanes;
morphinane-like compound;
organic heteropentacyclic compound		antidote to opioid poisoning;
central nervous system depressant;
environmental contaminant;
mu-opioid receptor antagonist;
xenobiotic
dextromethorphan
Dextromethorphan: Methyl analog of DEXTRORPHAN that shows high affinity binding to several regions of the brain, including the medullary cough center. This compound is an NMDA receptor antagonist (RECEPTORS, N-METHYL-D-ASPARTATE) and acts as a non-competitive channel blocker. It is one of the widely used ANTITUSSIVES, and is also used to study the involvement of glutamate receptors in neurotoxicity.. dextromethorphan : A 6-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthrene in which the sterocenters at positions 4a, 10 and 10a have S-configuration. It is a prodrug of dextrorphan and used as an antitussive drug for suppressing cough.		2.45206-methoxy-11-methyl-1,3,4,9,10,10a-hexahydro-2H-10,4a-(epiminoethano)phenanthreneantitussive;
environmental contaminant;
neurotoxin;
NMDA receptor antagonist;
oneirogen;
prodrug;
xenobiotic
cefixime
[no description available]		2.0510cephalosporinantibacterial drug;
drug allergen
lisinopril
Lisinopril: One of the ANGIOTENSIN-CONVERTING ENZYME INHIBITORS (ACE inhibitors), orally active, that has been used in the treatment of hypertension and congestive heart failure.		2.4520dipeptideEC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
ramipril
Ramipril: A long-acting angiotensin-converting enzyme inhibitor. It is a prodrug that is transformed in the liver to its active metabolite ramiprilat.. ramipril : A dipeptide that is the prodrug for ramiprilat, the active metabolite obtained by hydrolysis of the ethyl ester group. An angiotensin-converting enzyme (ACE) inhibitor, used to treat high blood pressure and congestive heart failure.. quark : Quarks comprise one of two classes of the fundamental particles. Quarks possess fractional electric charges and are not observed in free state. The word "quark" first appears in James Joyce's Finnegans Wake and has been chosen by Murray Gell-Mann as a name for fundamental building blocks of particles.		2.0510azabicycloalkane;
cyclopentapyrrole;
dicarboxylic acid monoester;
dipeptide;
ethyl ester		bradykinin receptor B2 agonist;
cardioprotective agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
matrix metalloproteinase inhibitor;
prodrug
indinavir sulfate
Indinavir: A potent and specific HIV protease inhibitor that appears to have good oral bioavailability.		2.7630dicarboxylic acid diamide;
N-(2-hydroxyethyl)piperazine;
piperazinecarboxamide		HIV protease inhibitor
sulfur
Sulfur: An element that is a member of the chalcogen family. It has an atomic symbol S, atomic number 16, and atomic weight [32.059; 32.076]. It is found in the amino acids cysteine and methionine.		3.0840chalcogen;
nonmetal atom		macronutrient
geldanamycin
[no description available]		3.2960
costunolide
[no description available]		2.1710
plastoquinone
[no description available]		2.2510plastoquinone
7-hydroxymethotrexate
[no description available]		2.1510folic acids
enalapril
Enalapril: An angiotensin-converting enzyme inhibitor that is used to treat HYPERTENSION and HEART FAILURE.. enalapril : A dicarboxylic acid monoester that is ethyl 4-phenylbutanoate in which a hydrogen alpha to the carboxy group is substituted by the amino group of L-alanyl-L-proline (S-configuration).		2.0510dicarboxylic acid monoester;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
geroprotector;
prodrug
nitrofurazone
Nitrofurazone: A topical anti-infective agent effective against gram-negative and gram-positive bacteria. It is used for superficial WOUNDS AND INJURIES and skin infections. Nitrofurazone has also been administered orally in the treatment of TRYPANOSOMIASIS.. nitrofurazone : A semicarbazone resulting from the formal condensation of semicarbazide with 5-nitrofuraldehyde. A broad spectrum antibacterial drug, although with little activity against Pseudomonas species, it is used as a local application for burns, ulcers, wounds and skin infections.		2.0510
cotylenin a
cotylenin A: induces differentiation in murine and human myeloid leukemia cells; structure in first source		2.1710
bleomycin
[no description available]		2.0510bleomycinantineoplastic agent;
metabolite
cysteine
Cysteine: A thiol-containing non-essential amino acid that is oxidized to form CYSTINE.. L-cysteinium : The L-enantiomer of cysteinium.. cysteine : A sulfur-containing amino acid that is propanoic acid with an amino group at position 2 and a sulfanyl group at position 3.		3.1750cysteiniumfundamental metabolite
phosphorus
Phosphorus: A non-metal element that has the atomic symbol P, atomic number 15, and atomic weight 31. It is an essential element that takes part in a broad variety of biochemical reactions.		4.9721monoatomic phosphorus;
nonmetal atom;
pnictogen		macronutrient
enalaprilat anhydrous
Enalaprilat: The active metabolite of ENALAPRIL and one of the potent, intravenously administered, ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. It is an effective agent for the treatment of essential hypertension and has beneficial hemodynamic effects in heart failure. The drug produces renal vasodilation with an increase in sodium excretion.. enalaprilat dihydrate : The dihydrate form of enalaprilat, an angiotensin-converting enzyme (ACE) inhibitor that is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is administered by intravenous injection.. enalaprilat (anhydrous) : Enalapril in which the ethyl ester group has been hydrolysed to the corresponding carboxylic acid. Enalaprilat is an angiotensin-converting enzyme (ACE) inhibitor and is used (often in the form of its prodrug, enalapril) in the treatment of hypertension and heart failure, for reduction of proteinuria and renal disease in patients with nephropathies, and for the prevention of stroke, myocardial infarction, and cardiac death in high-risk patients. Unlike enalapril, enalaprilat is not absorbed by mouth but is given by intravenous injection, usually as the dihydrate.		2.0510dicarboxylic acid;
dipeptide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor
imidapril
imidapril: structure given in first source. imidapril : A member of the class of imidazolidines that is (4S)-1-methyl-2-oxoimidazolidine-4-carboxylic acid in which the hydrogen of the imidazolidine nitrogen has been substituted by (1S)-1-{[(2S)-1-ethoxy-1-oxo-4-phenylbutan-2-yl]amino}ethyl group. It is the prodrug for imidaprilat, an ACE inhibitor used for the treatment of chronic heart failure.		2.0510dicarboxylic acid monoester;
dipeptide;
ethyl ester;
imidazolidines;
N-acylurea;
secondary amino compound		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
sulindac sulfone
sulindac sulfone: inhibits K-ras-dependent cyclooxygenase-2; sulfated analog of indomethacin;; CP248 is an antineoplastic agent that fosters microtubule depolymerization; structure in first source. sulindac sulfone : A sulfone metabolite of sulindac that inhibits cell growth by inducing apoptosis independently of cyclooxygenase inhibition. It inhibits the development and induces regression of premalignant adenomatous polyps. Lipoxygenase and Cox-2 inhibitor.		2.4520monocarboxylic acid;
organofluorine compound;
sulfone		apoptosis inducer;
cyclooxygenase 2 inhibitor;
EC 1.13.11.34 (arachidonate 5-lipoxygenase) inhibitor
ximelagatran
ximelagatran: prodrug (via hydroxylation) of melagatran & a direct thrombin inhibitor; liver toxicity concerns so AZD0837 being developed to replace this. ximelagatran : A member of the class of azetidines that is melagatran in which the carboxylic acid group has been converted to the corresponding ethyl ester and in which the amidine group has been converted into the corresponding amidoxime. A prodrug for melagatran, ximelagatran was the first orally available direct thrombin inhibitor to be brought to market as an anticoagulant, but was withdrawn in 2006 following reports of it causing liver damage.		2.0510amidoxime;
azetidines;
carboxamide;
ethyl ester;
hydroxylamines;
secondary amino compound;
secondary carboxamide;
tertiary carboxamide		anticoagulant;
EC 3.4.21.5 (thrombin) inhibitor;
prodrug;
serine protease inhibitor
ceftriaxone
[no description available]		2.05101,2,4-triazines;
1,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen;
EC 3.5.2.6 (beta-lactamase) inhibitor
cefepime
Cefepime: A fourth-generation cephalosporin antibacterial agent that is used in the treatment of infections, including those of the abdomen, urinary tract, respiratory tract, and skin. It is effective against PSEUDOMONAS AERUGINOSA and may also be used in the empiric treatment of FEBRILE NEUTROPENIA.. cefepime : A cephalosporin bearing (1-methylpyrrolidinium-1-yl)methyl and (2Z)-2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetamido groups at positions 3 and 7, respectively, of the cephem skeleton.		2.0310cephalosporin;
oxime O-ether		antibacterial drug
l 685458
L 685458: a gamma-secretase inhibitor; structure in first source. L-685,458 : A peptide and carboxamide that is L-leucyl-L-phenylalaninamide, L-Leu-L-Phe-NH2, which has been acylated on the N-terminus by a Phe-Phe hydroxyethylene dipeptide isotere, 2R-benzyl-5S-tert-butoxycarbonylamino-4R-hydroxy-6-phenylhexanoic acid. Compounds based on the structure of L-685,458 are potent inhibitors of gamma-secretase, which mediates the final catalytic step that generates the amyloid beta-peptide (Abeta), which assembles into the neurotoxic aggregates in the brains of sufferers of Alzheimer's disease.		2.0410carbamate ester;
monocarboxylic acid amide;
peptide;
secondary alcohol		EC 3.4.23.46 (memapsin 2) inhibitor;
peptidomimetic
trandolapril
trandolapril : A heterobicylic compound that is (2S,3aR,7aS)-1-[(2S)-2-aminopropanoyl]octahydro-1H-indole-2-carboxylic acid in which the hydrogen of the amino group is substituted by a (2R)-1-ethoxy-1-oxo-4-phenylbutan-2-yl group. It is a angiotensin-converting enzyme inhibitor and a prodrug used for the treatment of hypertension.		2.0510dicarboxylic acid monoester;
dipeptide;
ethyl ester;
organic heterobicyclic compound;
secondary amino compound;
tertiary carboxamide		antihypertensive agent;
EC 3.4.15.1 (peptidyl-dipeptidase A) inhibitor;
prodrug
2-tert-butyl-9-fluoro-3,6-dihydro-7h-benz(h)imidazo(4,5-f)isoquinoline-7-one
2-tert-butyl-9-fluoro-3,6-dihydro-7H-benz(h)imidazo(4,5-f)isoquinoline-7-one: a janus-activated kinase inhibitor. 2-tert-butyl-9-fluoro-1,6-dihydrobenzo[h]imidazo[4,5-f]isoquinolin-7-one : An organic heterotetracyclic compound that is 1,6-dihydrobenzo[h]imidazo[4,5-f]isoquinolin-7-one bearing additional tert-butyl and fluoro substituents at positions 2 and 9 respectively.		2.0310organic heterotetracyclic compound;
organofluorine compound		EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
vx680
[no description available]		6.38160N-arylpiperazine
arglabin
arglabin: a sesquiterpene lactone from the Chinese herb Artemisia myriantha; structure given in first source. arglabin : An organic heterotetracyclic compound and guaianolide sesquiterpene lactone that is acrylic acid which is substituted at position 2 by a 4-hydroxy-3,8-dimethyl-1,3a,4,5,6,7-hexahydroazulen-5-yl group in which the double bond in the 7-membered ring has been epoxidised and in which the hydroxy group and the carboxy group have undergone formal condensation to give the corresponding gamma-lactone. It is found in Artemisia glabella. Arglabin-DMA HCl, the hydrochloride salt of the adduct resulting from the conjugate addition of dimethylamine to the ene-lactone moiety, has been successfully used in Khazakhstan for the treatment of breast, colon, ovarian and lung cancers.		3.1210epoxide;
gamma-lactone;
organic heterotetracyclic compound;
sesquiterpene lactone		antineoplastic agent;
metabolite
guanabenz acetate
[no description available]		2.0510dichlorobenzenegeroprotector
famotidine
[no description available]		2.05101,3-thiazoles;
guanidines;
sulfonamide		anti-ulcer drug;
H2-receptor antagonist;
P450 inhibitor
bafilomycin a
[no description available]		3.5110
carbocyanines
Carbocyanines: Compounds that contain three methine groups. They are frequently used as cationic dyes used for differential staining of biological materials.		2.0810cyanine dye;
organic iodide salt		fluorochrome
cefotaxime
Cefotaxime: Semisynthetic broad-spectrum cephalosporin.. cefotaxime : A cephalosporin compound having acetoxymethyl and [2-(2-amino-1,3-thiazol-4-yl)-2-(methoxyimino)acetyl]amino side groups.		2.05101,3-thiazoles;
cephalosporin;
oxime O-ether		antibacterial drug;
drug allergen
aztreonam
[no description available]		2.0510beta-lactam antibiotic allergen;
monobactam		antibacterial drug;
drug allergen;
EC 2.4.1.129 (peptidoglycan glycosyltransferase) inhibitor
viroxime
[no description available]		2.4110
cinidon-ethyl
Lotus: A genus of the PEA FAMILY. The genus Lotus, formerly known as Tetragonolobus, is unrelated to other plants with the common name of lotus (NELUMBO and NYMPHAEA).. cinidon ethyl : A carboxylic ester and organochlorine compound that is the ethyl ester of cinidon.		2.2110ethyl ester;
isoindoles;
monochlorobenzenes		herbicide
st 638
[no description available]		2.0310
su 1498
SU 1498: structure in first source. SU1498 : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of (2E)-2-cyano-3-[4-hydroxy-3,5-di(propan-2-yl)phenyl]prop-2-enoic acid with the amino group of 3-phenylpropylamine.		2.0310enamide;
monocarboxylic acid amide;
nitrile;
phenols;
secondary carboxamide		vascular endothelial growth factor receptor antagonist
bisabolol
bisabolol: monocyclic sesquiterpene alcohol with strong bacteriocidal effects, especilly against M. Tuberc.; isolated from seed plant Populus tacamacaha; RN given refers to cpd without isomeric desigation		2.4720
proguanil
Proguanil: A biguanide compound which metabolizes in the body to form cycloguanil, an anti-malaria agent.. proguanil : A biguanide compound which has isopropyl and p-chlorophenyl substituents on the terminal N atoms. A prophylactic antimalarial drug, it works by inhibiting the enzyme dihydrofolate reductase, which is involved in the reproduction of the malaria parasites Plasmodium falciparum and P. vivax within the red blood cells.		2.0510biguanides;
monochlorobenzenes		antimalarial;
antiprotozoal drug;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor
monorden
monorden: inhibits HSP90 Heat-Shock Proteins, DNA topoisomerase VI and human Topoisomerase II		2.0310cyclic ketone;
enone;
epoxide;
macrolide antibiotic;
monochlorobenzenes;
phenols		antifungal agent;
metabolite;
tyrosine kinase inhibitor
rifamycin sv
rifamycin SV: RN given refers to parent cpd; structure in Merck Index, 9th ed, #8009. rifamycin SV : A member of the class of rifamycins that exhibits antibiotic and antitubercular properties.		2.0510acetate ester;
cyclic ketal;
lactam;
macrocycle;
organic heterotetracyclic compound;
polyphenol;
rifamycins		antimicrobial agent;
antitubercular agent;
bacterial metabolite
selenium
Selenium: An element with the atomic symbol Se, atomic number 34, and atomic weight 78.97. It is an essential micronutrient for mammals and other animals but is toxic in large amounts. Selenium protects intracellular structures against oxidative damage. It is an essential component of GLUTATHIONE PEROXIDASE.		3.1710chalcogen;
nonmetal atom		micronutrient
epoprostenol sodium
[no description available]		2.0510prostanoid
vlx600
VLX600: has antineoplastic activity; structure in first source		2.1710
9,13-retinoic acid
[no description available]		2.0110retinoid
ml 3403
[no description available]		2.0310
d 4476
[no description available]		2.0310imidazoles
GSK3-XIII
GSK3-XIII : A member of the class of aromatic amines that is ammonia with two of the hydrogens replaced by 5-methylpyrazol-3-yl and 2-phenylquinazolin-4-yl groups.		2.0310aromatic amine;
pyrazoles;
quinazolines;
secondary amino compound		EC 2.7.11.26 (tau-protein kinase) inhibitor
dizocilpine maleate
Dizocilpine Maleate: A potent noncompetitive antagonist of the NMDA receptor (RECEPTORS, N-METHYL-D-ASPARTATE) used mainly as a research tool. The drug has been considered for the wide variety of neurodegenerative conditions or disorders in which NMDA receptors may play an important role. Its use has been primarily limited to animal and tissue experiments because of its psychotropic effects.. dizocilpine maleate : A maleate salt obtained by reaction of dizocilpine with one equivalent of maleic acid.		2.110maleate salt;
tetracyclic antidepressant		anaesthetic;
anticonvulsant;
neuroprotective agent;
nicotinic antagonist;
NMDA receptor antagonist
antimycin a
Antimycin A: An antibiotic substance produced by Streptomyces species. It inhibits mitochondrial respiration and may deplete cellular levels of ATP. Antimycin A1 has been used as a fungicide, insecticide, and miticide. (From Merck Index, 12th ed). antimycin A : A nine-membered bis-lactone having methyl substituents at the 2- and 6-positions, an n-hexyl substituent at the 8-position, an acyloxy substituent at the 7-position and an aroylamido substituent at the 3-position. It is produced by Streptomyces bacteria and has found commercial use as a fish poison.		2.2510amidobenzoic acid
bafilomycin a1
bafilomycin A1: from Streptomyces griseus; structure given in first source. bafilomycin A1 : The most used of the bafilomycins, a family of toxic macrolide antibiotics derived from Streptomyces griseus.		3.8940cyclic hemiketal;
macrolide antibiotic;
oxanes		apoptosis inducer;
autophagy inhibitor;
bacterial metabolite;
EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor;
EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor;
ferroptosis inhibitor;
fungicide;
potassium ionophore;
toxin
1,2-dioleoyloxy-3-(trimethylammonium)propane
1,2-dioleoyloxy-3-(trimethylammonium)propane: fluorescent probe for phospholipids; RN & structure given in first source		2.1110
1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol
1,2-dilinolenoyl-3-(4-aminobutyryl)propane-1,2,3-triol: RN refers to the (all-Z)-isomer		2.0510
5'-oleoyl cytarabine
elaidic acid-cytarabine: a 5'-elaidic acid (C18:1, unsaturated fatty acid) ester of cytarabine		3.1610pyrimidine nucleoside
pregna-4,17-diene-3,16-dione
pregna-4,17-diene-3,16-dione: steroid from guggulu extract; RN & N1 from C1 Form index; RN given refers to cpd without isomeric designation; structure in first source; antagonist of farnesoid X receptor		2.1103-hydroxy steroidandrogen
everolimus
[no description available]		15.43253cyclic acetal;
cyclic ketone;
ether;
macrolide lactam;
primary alcohol;
secondary alcohol		anticoronaviral agent;
antineoplastic agent;
geroprotector;
immunosuppressive agent;
mTOR inhibitor
laq824
LAQ824: Histone deacetylase inhibitor		8.6230
ixabepilone
[no description available]		4.35301,3-thiazoles;
beta-hydroxy ketone;
epoxide;
lactam;
macrocycle		antineoplastic agent;
microtubule-destabilising agent
1-oleoyl-2-stearoylphosphatidylcholine
1-oleoyl-2-stearoylphosphatidylcholine: RN given refers to the (Z)-isomer; RN for cpd without isomeric designation not available 4/91		2.0510
terbogrel
[no description available]		3.2110diterpene glycoside
ganglioside, gd2
[no description available]		3.1610
axitinib
[no description available]		7.0691aryl sulfide;
benzamides;
indazoles;
pyridines		antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
scy-635
[no description available]		2.1110
azlocillin
Azlocillin: A semisynthetic ampicillin-derived acylureido penicillin.. azlocillin : A semisynthetic penicillin having a 6beta-{(2R)-2-[(2-oxoimidazolidine-1-carbonyl)amino]-2-phenylacetyl}amino side-group. It is an antibiotic used in treating infections caused by Pseudomonas aeruginosa, Escherichia coli and Haemophilus influenzae.		2.0510penicillin allergen;
penicillin;
semisynthetic derivative		antibacterial drug
tanespimycin
CP 127374: analog of herbimycin A		6.082201,4-benzoquinones;
ansamycin;
carbamate ester;
organic heterobicyclic compound;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
Hsp90 inhibitor
2-[(3-iodophenyl)methylthio]-5-pyridin-4-yl-1,3,4-oxadiazole
[no description available]		2.0310aryl sulfide
beta-escin
[no description available]		2.8530
dantrolene sodium
dantrolene sodium (anhydrous) : The anhydrous sodium salt of dantrolene.		2.0510
nitrofurantoin
Nitrofurantoin: A urinary anti-infective agent effective against most gram-positive and gram-negative organisms. Although sulfonamides and antibiotics are usually the agents of choice for urinary tract infections, nitrofurantoin is widely used for prophylaxis and long-term suppression.. nitrofurantoin : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group. An antibiotic that damages bacterial DNA.		2.7830imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic;
organooxygen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
aminopurvalanol a
aminopurvalanol A: casein kinase I alpha inhibitor; structure in first source		2.0310monochlorobenzenes;
purvalanol		protein kinase inhibitor
nifurtimox
Nifurtimox: A nitrofuran thiazine that has been used against TRYPANOSOMIASIS.		3.5620nitrofuran antibiotic
butylscopolammonium bromide
Butylscopolammonium Bromide: Antimuscarinic quaternary ammonium derivative of scopolamine used to treat cramps in gastrointestinal, urinary, uterine, and biliary tracts, and to facilitate radiologic visualization of the gastrointestinal tract.		2.0610
gadolinium dtpa
Gadolinium DTPA: A complex of gadolinium with a chelating agent, diethylenetriamine penta-acetic acid (DTPA see PENTETIC ACID), that is given to enhance the image in cranial and spinal MRIs. (From Martindale, The Extra Pharmacopoeia, 30th ed, p706)		2.0810gadolinium coordination entityMRI contrast agent
roxithromycin
(E)-roxithromycin : A major geometrical isomer of roxithromycin.		2.0510roxithromycinenvironmental contaminant;
xenobiotic
fumagillin
[no description available]		3.1510antibiotic antifungal drug;
carboxylic ester;
dicarboxylic acid monoester;
meroterpenoid;
organooxygen heterocyclic antibiotic;
spiro-epoxide		angiogenesis inhibitor;
antibacterial drug;
antimicrobial agent;
antiprotozoal drug;
fungal metabolite;
methionine aminopeptidase 2 inhibitor
beraprost
beraprost: stable prostacyclin analog; structure given in first source. beraprost : An organic heterotricyclic compound that is (3aS,8bS)-2,3,3a,8b-tetrahydro-1H-benzo[b]cyclopenta[d]furan in which the hydrogens at positions 1R, 2R and 5 are replaced by (3S)-3-hydroxy-4-methyloct-1-en-6-yn-1-yl, hydroxy and 3-carboxypropyl groups, respectively. It is a prostaglandin receptor agonist which is approved to treat pulmonary arterial hypertension in Asia.		4.640enyne;
monocarboxylic acid;
organic heterotricyclic compound;
secondary alcohol;
secondary allylic alcohol		anti-inflammatory agent;
antihypertensive agent;
platelet aggregation inhibitor;
prostaglandin receptor agonist;
vasodilator agent
lanreotide
[no description available]		2.0510
u 62840
U 62840: stereoisomeric benzindene prostaglandin analog; structure given in first source		4.3630carbotricyclic compound;
carboxylic acid		antihypertensive agent;
cardiovascular drug;
human blood serum metabolite;
platelet aggregation inhibitor;
vasodilator agent;
vitamin K antagonist
perfosfamide
[no description available]		2.0310
soblidotin
soblidotin: a dolastatin 10 derivative; RN refers to (2S-(1(1R*(R*),2S*),2R*(1S*,2S*)))-isomer; structure given in first source. soblidotin : A tetrapeptide derivative of dolastatin 10. It is an inhibitor of tubulin polymerization which exhibits potent antitumor activity.		2.0210tetrapeptideantineoplastic agent;
apoptosis inducer;
microtubule-destabilising agent
bay 12-9566
Bay 12-9566: an angiogenesis inhibitor with matrix metalloproteinase inhibitory activity		3.1110biphenyls;
organochlorine compound
cvt 313
CVT 313: a potent inhibitor of CDK2 that prevents neointimal proliferation; structure given in first source		2.0310
pki 166
[no description available]		2.4520
pd 184352
2-(2-chloro-4-iodophenylamino)-N-cyclopropylmethoxy-3,4-difluorobenzamide: inhibits MAP kinase kinase; structure in first source		6.1591aminobenzoic acid
laulimalide
laulimalide: isolated from Cacospongia mycofijiensis; structure in first source. laulimalide : A macrolide with formula C30H42O7 that is isolated from the marine sponges, Cacospongia mycofijiensis and Hyattella sp.		2.0210carboxylic ester;
epoxide;
macrolide;
secondary alcohol;
secondary allylic alcohol		animal metabolite;
antimitotic;
antineoplastic agent;
marine metabolite;
microtubule-stabilising agent
lu 208075
ambrisentan: an ET(A) receptor antagonist and antihypertensive agent; studied for use in pulmonary arterial hypertension		3.930diarylmethane
bibx 1382bs
BIBX 1382BS: an ErbB receptor kinase inhibitor; no further information available 4/2001		2.5120substituted aniline
vildagliptin
[no description available]		2.1710amino acid amide
sk-7041
SK-7041: an antineoplastic agent; structure in first source		2.0310
yc137
YC137: small molecule inhibitor of Bcl-2; structure in first source		2.3110
cysmethynil
cysmethynil: an Icmt inhibitor with antineoplastic activity; structure in first source		2.1310
panobinostat
Panobinostat: An indole and hydroxamic acid derivative that acts as a HISTONE DEACETYLASE inhibitor. It is used as an antineoplastic agent in combination with BORTEZOMIB and DEXAMETHASONE for the treatment of MULTIPLE MYELOMA.. panobinostat : A hydroxamic acid obtained by formal condensation of the carboxy group of (2E)-3-[4-({[2-(2-methylindol-3-yl)ethyl]amino}methyl)phenyl]prop-2-enoic acid with the amino group of hydroxylamine. A histone deacetylase inhibitor used (as its lactate salt) in combination with bortezomib and dexamethasone for the treatment of multiple myeloma.		6.1691cinnamamides;
hydroxamic acid;
methylindole;
secondary amino compound		angiogenesis modulating agent;
antineoplastic agent;
EC 3.5.1.98 (histone deacetylase) inhibitor
bromopyruvate
[no description available]		2.55202-oxo monocarboxylic acid anion
acetylcarnitine
O-acetyl-L-carnitine : An O-acyl-L-carnitine where the acyl group specified is acetyl. It facilitates movement of acetyl-CoA into the matrices of mammalian mitochondria during the oxidation of fatty acids.		2.0510O-acetylcarnitine;
saturated fatty acyl-L-carnitine		human metabolite;
Saccharomyces cerevisiae metabolite
staurosporine
staurosporinium : Conjugate acid of staurosporine.		7.09270ammonium ion derivative
loa
lithocholic acid acetate: structure in first source		3.0610
1,25-dihydroxyergocalciferol
1,25-dihydroxyergocalciferol: RN given refers to (3beta,5Z,7E,22E)-isomer. 1alpha,25-dihydroxyvitamin D2 : A hydroxycalciol that is vitamin D2 bearing additional hydroxy substituents at positions 1alpha and 25.		2.0310hydroxycalciol;
seco-ergostane;
vitamin D		bone density conservation agent;
human xenobiotic metabolite;
nutraceutical
shu 508
SHU 508: intravenous saccharide echo contrast agent with transpulmonary capacity for left heart contrast; appears in Japanese literature as SH/TA-508		6.321
hypericum
Hypericum: Genus of perennial plants in the family CLUSIACEAE (sometimes classified as Hypericaceae). Herbal and homeopathic preparations are used for depression, neuralgias, and a variety of other conditions. Hypericum contains flavonoids; GLYCOSIDES; mucilage, TANNINS; volatile oils (OILS, ESSENTIAL), hypericin and hyperforin.. 6-formamidopenicillanic acid : A penicillanic acid having a (6R)-formamido substituent.		5.2362penicillanic acids
phosphocreatine
Phosphocreatine: An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996). phosphagen : Any of a group of guanidine or amidine phosphates that function as storage depots for high-energy phosphate in muscle with the purpose of regenerating ATP from ADP during muscular contraction.. N-phosphocreatine : A phosphoamino acid consisting of creatine having a phospho group attached at the primary nitrogen of the guanidino group.		2.0710phosphagen;
phosphoamino acid		human metabolite;
mouse metabolite
sl 327
SL 327: a MEK inhibitor. SL-327 : A nitrile that is acrylonitrile in which the hydrogen attached to the same carbon as the cyano group has been replaced by an o-(trifluoromethyl)phenyl group, while the remaining hydrogens of the ethenyl group have been replaced by amino and (4-aminophenyl)sulfanyl groups. The configuration of the double bond is not specified. It is an inhibitor of MEK1 and MEK2.		2.0310
tws 119
[no description available]		2.0310pyrroles
krn 633
N-(2-chloro-4-((6,7-dimethoxy-4-quinazolinyl)oxy)phenyl)-N'-propylurea: a VEGF receptor-2 tyrosine kinase inhibitor; structure in first source		2.0310
((3z)-n-(3-chlorophenyl)-3-((3,5-dimethyl-4-((4-methylpiperazin-1-yl)carbonyl)-1h-pyrrol-2-yl)methylene)-n-methyl-2-oxo-2,3-dihydro-1h-indole-5-sulfonamide)
[no description available]		2.0310sulfonamide
c 1368
[no description available]		2.0310
pq 401
PQ 401: an IGF receptor type I antagonist; structure in first source		2.0310quinolines
chlorhexidine
Chlorhexidine: A disinfectant and topical anti-infective agent used also as mouthwash to prevent oral plaque.. chlorhexidine : A bisbiguanide compound with a structure consisting of two (p-chlorophenyl)guanide units linked by a hexamethylene bridge.		2.0810biguanides;
monochlorobenzenes		antibacterial agent;
antiinfective agent
formazans
Formazans: Colored azo compounds formed by the reduction of tetrazolium salts. Employing this reaction, oxidoreductase activity can be determined quantitatively in tissue sections by allowing the enzymes to act on their specific substrates in the presence of tetrazolium salts.		2.0510
nifurtoinol
nifurtoinol : An imidazolidine-2,4-dione that is hydantoin substituted at position 1 by a [(5-nitro-2-furyl)methylene]amino group and at position 3 by a hydroxymethyl group.		2.0510hydrazone;
imidazolidine-2,4-dione;
nitrofuran antibiotic;
organonitrogen heterocyclic antibiotic		antibacterial drug;
antiinfective agent;
hepatotoxic agent
gemifloxacin
Gemifloxacin: A naphthyridine and fluoroquinolone derivative antibacterial agent and DNA TOPOISOMERASE II inhibitor that is used for the treatment of community-acquired pneumonia and acute bacterial infections associated with chronic bronchitis.. gemifloxacin : A 1,4-dihydro-1,8-naphthyridine with a carboxy group at the 3-position, an oxo sustituent at the 4-position, a fluoro substituent at the 5-position and a substituted pyrrolin-1-yl group at the 7-position.		2.17101,8-naphthyridine derivative;
fluoroquinolone antibiotic;
monocarboxylic acid;
quinolone antibiotic		antibacterial drug;
antimicrobial agent;
topoisomerase IV inhibitor
st 1481
ST 1481: structure in first source		2.0210
fosinopril
[no description available]		2.0510
vacuolin-1
vacuolin-1: inhibits Ca2-dependent lysosomal exocytosis		2.4110
jnj 10198409
[no description available]		2.0310
eflucimibe
eflucimibe: a powerful and systemic acylcoenzyme A: cholesterol acyltransferase inhibitor		2.0510
lenvatinib
lenvatinib : A member of the class of quinolines that is the carboxamide of 4-{3-chloro-4-[(cyclopropylcarbamoyl)amino]phenoxy}-7-methoxyquinoline-6-carboxylic acid. A multi-kinase inhibitor and orphan drug used (as its mesylate salt) for the treatment of various types of thyroid cancer that do not respond to radioiodine.		4.1520aromatic amide;
aromatic ether;
cyclopropanes;
monocarboxylic acid amide;
monochlorobenzenes;
phenylureas;
quinolines		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
fibroblast growth factor receptor antagonist;
orphan drug;
vascular endothelial growth factor receptor antagonist
pd 0325901
mirdametinib: has antineoplastic activity; appears to be a MEK inhibitor. PD 0325901 : A hydroxamic acid ester that is benzhydroxamic acid (N-hydroxybenzamide) in which the hydroxamic acid group has been converted to the corresponding 2,3-dihydroxypropyl ester and in which the benzene ring has been substituted at position 2 by a (2-fluoro-4-iodophenyl)amino group and at positions 3 and 4 by fluorines (the R enantiomer).		2.5220difluorobenzene;
hydroxamic acid ester;
monofluorobenzenes;
organoiodine compound;
propane-1,2-diols;
secondary amino compound		antineoplastic agent;
EC 2.7.12.2 (mitogen-activated protein kinase kinase) inhibitor
midostaurin
midostaurin : An organic heterooctacyclic compound that is the N-benzoyl derivative of staurosporine.		6.98240benzamides;
gamma-lactam;
indolocarbazole;
organic heterooctacyclic compound		antineoplastic agent;
EC 2.7.11.13 (protein kinase C) inhibitor
bromotetrandrine
bromotetrandrine: structure in first source		2.0510
sincalide
Sincalide: An octapeptide hormone present in the intestine and brain. When secreted from the gastric mucosa, it stimulates the release of bile from the gallbladder and digestive enzymes from the pancreas.		2.4110oligopeptide
etomoxir
[no description available]		2.0510aromatic ether
gambogic acid
gambogic acid: RN given refers to (1R-(1alpha,1(Z),3abeta,5alpha,11beta,14aS*))-isomer		2.110pyranoxanthonesmetabolite
pentagastrin
Pentagastrin: A synthetic pentapeptide that has effects like gastrin when given parenterally. It stimulates the secretion of gastric acid, pepsin, and intrinsic factor, and has been used as a diagnostic aid.		2.0510organic molecular entity
nu 7026
2-(morpholin-4-yl)benzo(h)chromen-4-one: a radiosensitizing agent that inhibits DNA-dependent protein kinase; structure in first source		2.0310organic heterotricyclic compound;
organooxygen compound
f 12509a
F 12509A: a sphingosine kinase inhibitor; isolated from Trichopezizella barbata; structure in first source		2.0410
pbox-6
PBOX-6: structure in first source		2.4520
mocetinostat
mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).		3.0310aminopyrimidine;
benzamides;
pyridines;
secondary amino compound;
secondary carboxamide;
substituted aniline		antineoplastic agent;
apoptosis inducer;
autophagy inducer;
cardioprotective agent;
EC 3.5.1.98 (histone deacetylase) inhibitor;
hepatotoxic agent
mirabegron
mirabegron: a beta3-adrenergic receptor agonist; structure in first source. mirabegron : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 2-amino-1,3-thiazol-4-ylacetic acid with the anilino group of (1R)-2-{[2-(4-aminophenyl)ethyl]amino}-1-phenylethanol. Used for the treatment of overactive bladder syndrome.		3.41101,3-thiazoles;
aromatic amide;
ethanolamines;
monocarboxylic acid amide		beta-adrenergic agonist
k201 compound
K201 compound: structure given in first source		2.0110
cgp 74588
CGP 74588: a metabolite of STI-571; structure in first source		15.65348benzamides
rivaroxaban
Rivaroxaban: A morpholine and thiophene derivative that functions as a FACTOR XA INHIBITOR and is used in the treatment and prevention of DEEP-VEIN THROMBOSIS and PULMONARY EMBOLISM. It is also used for the prevention of STROKE and systemic embolization in patients with non-valvular ATRIAL FIBRILLATION, and for the prevention of atherothrombotic events in patients after an ACUTE CORONARY SYNDROME.. rivaroxaban : A monocarboxylic acid amide obtained by formal condensation of the carboxy group of 5-chlorothiophene-2-carboxylic acid with the amino group of 4-{4-[(5S)-5-(aminomethyl)-2-oxo-1,3-oxazolidin-3-yl]phenyl}morpholin-3-one. An anticoagulant used for prophylaxis of venous thromboembolism in patients with knee or hip replacement surgery.		2.6920aromatic amide;
lactam;
monocarboxylic acid amide;
morpholines;
organochlorine compound;
oxazolidinone;
thiophenes		anticoagulant;
EC 3.4.21.6 (coagulation factor Xa) inhibitor
dehydroxymethylepoxyquinomicin
dehydroxymethylepoxyquinomicin: an NF-kappaB inhibitor; structure in first source		2.0610
treosulfan
treosulfan: immunosuppressant; RN given refers to (S-(R*,R*))-isomer		2.4420methanesulfonate ester
pi103
PI103: pyridofuropyrimidine antineoplastic; a potent inhibitor of class I phosphatidylinositide 3-kinases (PI3K); structure in first soruce		2.4520aromatic amine;
morpholines;
organic heterotricyclic compound;
phenols;
tertiary amino compound		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
mTOR inhibitor
ct-32228
CT-32228: CT-32212 is the inactive isomer of CT-32228 used as a control; structure in first source		2.0310
gentamicin sulfate
[no description available]		2.0510
y 27632, dihydrochloride, (4(r)-trans)-isomer
[no description available]		2.0310
selexipag
selexipag: prostacyclin receptor agonist. selexipag : A member of the class of pyrazines that is N-(methanesulfonyl)-2-{4-[(propan-2-yl)(pyrazin-2-yl)amino]butoxy}acetamide carrying two additional phenyl substituents at positions 5 and 6 on the pyrazine ring. An orphan drug used for the treatment of pulmonary arterial hypertension. It is a prodrug for ACT-333679 (the free carboxylic acid).		3.5820aromatic amine;
ether;
monocarboxylic acid amide;
N-sulfonylcarboxamide;
pyrazines;
tertiary amino compound		orphan drug;
platelet aggregation inhibitor;
prodrug;
prostacyclin receptor agonist;
vasodilator agent
sorbitan monooleate
[no description available]		4.6111fatty acid ester
tofacitinib
tofacitinib : A pyrrolopyrimidine that is pyrrolo[2,3-d]pyrimidine substituted at position 4 by an N-methyl,N-(1-cyanoacetyl-4-methylpiperidin-3-yl)amino moiety. Used as its citrate salt to treat moderately to severely active rheumatoid arthritis.		4.0830N-acylpiperidine;
nitrile;
pyrrolopyrimidine;
tertiary amino compound		antirheumatic drug;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
hypothemycin
hypothemycin: a resorcylic acid lactone antibiotic; antifungal metabolite from Hypomyces trichothecoides. hypothemycin : A macrolide that is isolated from the cultured broth of Hypomyces subiculosus and shows antifungal activity and inhibits the growth of some human cancer cells.		2.0410aromatic ether;
diol;
enone;
epoxide;
macrolide;
phenols;
polyketide;
secondary alpha-hydroxy ketone		antifungal agent;
antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
fungal metabolite
cediranib
[no description available]		2.2110aromatic ether
tae226
TAE226: an adhesion kinase inhibitor, offers an attractive therapeutic approach in ovarian carcinoma; structure in first source		2.0510morpholines
ap23464
AP23464: a potent adenosine 5'-triphosphate (ATP)-based inhibitor of Src and Abl kinases		3.8230
sb 743921
[no description available]		2.1110
pitolisant
pitolisant: functions as both inverse agonist and antagonist of histamine H3 receptors; structure in first source		4.6111organochlorine compound
ps1145
PS1145: IkappaB kinase inhibitor; structure in first source		2.0310beta-carbolines
g(m1) ganglioside
G(M1) Ganglioside: A specific monosialoganglioside that accumulates abnormally within the nervous system due to a deficiency of GM1-b-galactosidase, resulting in GM1 gangliosidosis.. ganglioside GM1 : A sialotetraosylceramide consisting of a branched pentasaccharide made up from one sialyl residue, two galactose residues, one N-acetylgalactosamine residue and a glucose residue at the reducing end attached to N-stearoylsphingosine via a beta-linkage.		2.0310alpha-N-acetylneuraminosyl-(2->3)-[beta-D-galactosyl-(1->3)-N-acetyl-beta-D-galactosaminyl-(1->4)]-beta-D-galactosyl-(1->4)-beta-D-glucosyl-(1<->1')-N-acylsphingosine;
sialotetraosylceramide
osu 03012
OSU 03012: a PDK-1 inhibitor; structure in first source		2.7730antibiotic antifungal drug;
aromatic amide;
glycine derivative;
organofluorine compound;
phenanthrenes;
pyrazoles		antineoplastic agent;
apoptosis inducer;
EC 2.7.11.1 (non-specific serine/threonine protein kinase) inhibitor
masitinib
[no description available]		10.011421,3-thiazoles;
benzamides;
N-alkylpiperazine;
pyridines		antineoplastic agent;
antirheumatic drug;
tyrosine kinase inhibitor
bx795
BX795: structure in first source		2.4110ureas
pazopanib
pazopanib: a protein kinase inhibitor. pazopanib : A pyrimidine that is 5-(pyrimidin-2-yl}amino-2-methylbenzenesulfonamide substituted at position 4 by a (2,3-dimethylindazol-6-yl)(methyl)amino group. Used as its hydrochloride salt for treatment of kidney cancer.		9.95182aminopyrimidine;
indazoles;
sulfonamide		angiogenesis modulating agent;
antineoplastic agent;
tyrosine kinase inhibitor;
vascular endothelial growth factor receptor antagonist
azd 6244
AZD 6244: a MEK inhibitor		3.9640benzimidazoles;
bromobenzenes;
hydroxamic acid ester;
monochlorobenzenes;
organofluorine compound;
secondary amino compound		anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
a 443654
A 443654: an Akt kinase inhibitor; structure in first source		2.4110indoles
apilimod
[no description available]		2.4110
apixaban
[no description available]		2.4110aromatic ether;
lactam;
piperidones;
pyrazolopyridine		anticoagulant;
EC 3.4.21.6 (coagulation factor Xa) inhibitor
bibw 2992
[no description available]		4.240aromatic ether;
enamide;
furans;
monochlorobenzenes;
organofluorine compound;
quinazolines;
secondary carboxamide;
tertiary amino compound		antineoplastic agent;
tyrosine kinase inhibitor
artenimol
artenimol: derivative of antimalarial drug artemisinin (quinghaosu)		3.9421
pik 75
PIK 75: structure in first source		2.5520
binimetinib
binimetinib : A member of the class of benzimidazoles that is 1-methyl-1H-benzimidazole which is substituted at positions 4, 5, and 6 by fluorine, (4-bromo-2-fluorophenyl)nitrilo, and N-(2-hydroxyethoxy)aminocarbonyl groups, respectively. It is a MEK1 and MEK2 inhibitor (IC50= 12 nM). Approved by the FDA for the treatment of patients with unresectable or metastatic melanoma with a BRAF V600E or V600K mutation in combination with encorafenib.		6.1522benzimidazoles;
bromobenzenes;
hydroxamic acid ester;
monofluorobenzenes;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor
aee 788
AEE 788: structure in first source		2.96406-{4-[(4-ethylpiperazin-1-yl)methyl]phenyl}-N-(1-phenylethyl)-7H-pyrrolo[2,3-d]pyrimidin-4-amineangiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor;
epidermal growth factor receptor antagonist;
trypanocidal drug
saracatinib
[no description available]		2.5220aromatic ether;
benzodioxoles;
diether;
N-methylpiperazine;
organochlorine compound;
oxanes;
quinazolines;
secondary amino compound		anticoronaviral agent;
antineoplastic agent;
apoptosis inducer;
autophagy inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
radiosensitizing agent
alpha-synuclein
alpha-Synuclein: A synuclein that is a major component of LEWY BODIES and plays a role in SYNUCLEINOPATHIES, neurodegeneration and neuroprotection.		2.1510
on012380
ON012380: a non-ATP-competitive inhibitor of BCR-ABL; structure in first source		4.2350
ko 143
[no description available]		2.0410beta-carbolines;
tert-butyl ester
crenolanib
[no description available]		4.4270aminopiperidine;
aromatic ether;
benzimidazoles;
oxetanes;
quinolines;
tertiary amino compound		angiogenesis inhibitor;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
norvancomycin
norvancomycin: glycopeptide; adverse reactions tend to occur in older patients, those who use other antibiotic concomitantly or those who receive this agent longer than 14 days		2.4110
galidesivir
[no description available]		2.1110
volasertib
BI 6727: a polo-like kinase inhibitor with broad antitumor activity; structure in first source		2.2110
oxadiazoles
Oxadiazoles: Compounds containing five-membered heteroaromatic rings containing two carbons, two nitrogens, and one oxygen atom which exist in various regioisomeric forms.		2.8330
vinflunine
vinflunine: inhibits tubulin assembly; structure in first source. vinflunine : An organic heteropentacyclic compound and an organic heterotetracyclic compound that is vinorelbine in which the tetrahydropyridine moiety of the heterotetracyclic part of the molecule has been redced to the corresponding piperidine, and in which the ethyl group attached to this ring has been replaced by a 1,1-difluoroethyl group.		2.0510acetate ester;
methyl ester;
organic heteropentacyclic compound;
organic heterotetracyclic compound;
semisynthetic derivative;
vinca alkaloid		antineoplastic agent
baci-im
[no description available]		2.0510homodetic cyclic peptide;
polypeptide;
zwitterion		antibacterial agent;
antimicrobial agent
ribose
ribopyranose : The pyranose form of ribose.		2.4620D-ribose;
ribopyranose
acebutolol
alpha-D-glucosyl-(1->4)-alpha-D-mannose : An alpha-D-glucosyl-(1->4)-D-mannopyranose in which the anomeric hydroxy group has alpha configuration.		2.1110alpha-D-glucosyl-(1->4)-D-mannopyranose
regorafenib
[no description available]		15.255013(trifluoromethyl)benzenes;
aromatic ether;
monochlorobenzenes;
monofluorobenzenes;
phenylureas;
pyridinecarboxamide		antineoplastic agent;
hepatotoxic agent;
tyrosine kinase inhibitor
degrasyn
degrasyn: a JAK2 kinase inhibitor that induces rapid degradation of c-Myc protein in MM-1 multiple myeloma and other tumor cell lines; structure in first source		2.4520
abt-737
[no description available]		8.6790aromatic amine;
aryl sulfide;
biphenyls;
C-nitro compound;
monochlorobenzenes;
N-arylpiperazine;
N-sulfonylcarboxamide;
secondary amino compound;
tertiary amino compound		anti-allergic agent;
anti-inflammatory agent;
antineoplastic agent;
apoptosis inducer;
B-cell lymphoma 2 inhibitor
mp470
[no description available]		2.830N-arylpiperazine
nystatin a1
Nystatin: Macrolide antifungal antibiotic complex produced by Streptomyces noursei, S. aureus, and other Streptomyces species. The biologically active components of the complex are nystatin A1, A2, and A3.. nystatin : A heterogeneous mixture of polyene compounds produced by cultures of Streptomyces noursei. It mainly consists of three biologically active components designated nystatin A1, nystatin A2, and nystatin A3. It is used to treat oral and dermal fungal infections.. nystatin A1 : A polyene macrolide antibiotic; part of the nystatin complex produced by several Streptomyces species. It is an antifungal antibiotic used for the treatment of topical fungal infections caused by a broad spectrum of fungal pathogens comprising yeast-like and filamentous species.		2.4620nystatins
bay 63-2521
riociguat: guanylate cyclase stimulator; structure in first source. riociguat : A carbamate ester that is the methyl ester of {4,6-diamino-2-[1-(2-fluorobenzyl)-1H-pyrazolo[3,4-b]pyridin-3-yl]pyrimidin-5-yl}methylcarbamic acid. It is used for treatment of chronic thromboembolic pulmonary hypertension and pulmonary arterial hypertension		4.6140aminopyrimidine;
carbamate ester;
organofluorine compound;
pyrazolopyridine		antihypertensive agent;
soluble guanylate cyclase activator
bi 2536
[no description available]		2.830
inno-406
[no description available]		8.68191biaryl
kw 2449
KW 2449: has both multikinase inhibitory activity and antineoplastic activity; structure in first source		2.0610
nutlin-3a
nutlin 3: an MDM2 antagonist; structure in first source		3.0140stilbenoid
danusertib
[no description available]		11.0681piperazines
nvp-aew541
[no description available]		2.4420
abt 869
[no description available]		2.0310aromatic amine;
indazoles;
phenylureas		angiogenesis inhibitor;
antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
fr 180204
FR 180204: structure in first source		2.0310pyrazoles;
ring assembly
lbw242
LBW242: proapoptotic IAP inhibitor; low MW Smac (Second mitochondria-derived activator of caspases) mimetic; structure in first source		2.0410
ridaforolimus
[no description available]		3.2110macrolide lactam
ki11502
Ki11502: a multitargeted receptor tyrosine kinase inhibitor that induces growth arrest and apoptosis of human leukemia cells in vitro and in vivo; structure in first source. Ki11502 : A member of the class of quinolines that acts as a receptor tyrosine kinase inhibitor and apoptosis inducer with potential for use in treatment of leukemia and colorectal cancer.		2.110aromatic ether;
benzamides;
quinolines;
thioureas		antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
carfilzomib
[no description available]		2.6920epoxide;
morpholines;
tetrapeptide		antineoplastic agent;
proteasome inhibitor
mrk 560
MRK 560: a gamma-secretase inhibitor; MRK-560 is the (cis)-isomer; structure in first source		2.3110
sitagliptin phosphate
Sitagliptin Phosphate: A pyrazine-derived DIPEPTIDYL-PEPTIDASE IV INHIBITOR and HYPOGLYCEMIC AGENT that increases the levels of the INCRETIN hormones GLUCAGON-LIKE PEPTIDE-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). It is used in the treatment of TYPE 2 DIABETES.		2.1510
jnj 26854165
[no description available]		2.1510
gw 2580
5-(3-methoxy-4-((4-methoxybenzyl)oxy)benzyl)pyrimidine-2,4-diamine: a cFMS kinase inhibitor; structure in first source		2.7430
idelalisib
idelalisib: an antineoplastic agent and p110delta inhibitor; structure in first source. idelalisib : A member of the class of quinazolines that is 5-fluoro-3-phenylquinazolin-4-one in which the hydrogen at position 2 is replaced by a (1S)-1-(3H-purin-6-ylamino)propyl group. used for for the treatment of refractory indolent non-Hodgkin's lymphoma and relapsed chronic lymphocytic leukemia.		2.1310aromatic amine;
organofluorine compound;
purines;
quinazolines;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
crizotinib
Crizotinib: A piperidine and aminopyridine derivative that acts as an inhibitor of RECEPTOR PROTEIN-TYROSINE KINASES, including ANAPLASTIC LYMPHOMA KINASE (ALK) and HEPATOCYTE GROWTH FACTOR RECEPTOR (HGFR; c-Met). It is used in the treatment of NON-SMALL CELL LUNG CANCER.. crizotinib : A 3-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amine that has R configuration at the chiral centre. The active enantiomer, it acts as a kinase inhibitor and is used for the treatment of patients with locally advanced or metastatic non-small cell lung cancer (NSCLC)		6.251003-[1-(2,6-dichloro-3-fluorophenyl)ethoxy]-5-[1-(piperidin-4-yl)pyrazol-4-yl]pyridin-2-amineantineoplastic agent;
biomarker;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
cgp 57380
CGP 57380: inhibits the mitogen-activated protein kinase-interacting kinase Mnk1		2.0410pyrazolopyrimidine
zstk474
ZSTK-474 : A triamino-1,3,5-triazine that is 1,3,5-triazine in which two of the hydrogens have been replaced by morpholin-4-yl groups while the third hydrogen has been replaced by a 2-(difluoromethyl)benzimidazol-1-yl group. It is an inhibitor of phosphatidylinositol 3-kinase.		2.5420benzimidazoles;
morpholines;
organofluorine compound;
triamino-1,3,5-triazine		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
trametinib
[no description available]		3.0940acetamides;
aromatic amine;
cyclopropanes;
organofluorine compound;
organoiodine compound;
pyridopyrimidine;
ring assembly		anticoronaviral agent;
antineoplastic agent;
EC 2.7.11.24 (mitogen-activated protein kinase) inhibitor;
geroprotector
pha 767491
PHA 767491: a Cdc7 inhibitor; structure in first source		2.4110pyrrolopyridine
losartan potassium
Erythropoietin: Glycoprotein hormone, secreted chiefly by the KIDNEY in the adult and the LIVER in the FETUS, that acts on erythroid stem cells of the BONE MARROW to stimulate proliferation and differentiation.		5.36100
telomestatin
telomestatin: isolated from Spreptomyces anulatus; structure in first source		2.0310
at 13387
(2,4-dihydroxy-5-isopropylphenyl)-(5-(4-methylpiperazin-1-ylmethyl)-1,3-dihydroisoindol-2-yl)methanone: structure in first source. onalespib : A member of the class of isoindoles that is isoindole in which the amino group has been acylated by a 2,4-dihydroxy-5-isopropylbenzoyl group and in which position 5 of the isoidole moiety has been substituted by a (4-methylpiperazin-1-yl)methyl group. A second-generation Hsp90 inhibitor.		5.6632benzamides;
isoindoles;
N-alkylpiperazine;
resorcinols;
tertiary carboxamide		antineoplastic agent;
Hsp90 inhibitor
dextrothyroxine
[no description available]		4.6230
sepharose
agarose : A linear polysaccharide made up from alternating D-galactose and 3,6-anhydro-alpha-L-galactopyranose residues joined by alpha-(1->3)- and beta-(1->4)-linkages.		2.4920
dactolisib
dactolisib: antineoplastic agent that inhibits both phosphatidylinositol 3-kinase and mTOR. dactolisib : An imidazoquinoline that is 3-methyl-2-oxo-2,3-dihydro-1H-imidazo[4,5-c]quinoline substituted at position 1 by a 4-(1-cyanoisopropyl)phenyl group and at position 8 by a quinolin-3-yl group. A dual PI3K/mTOR inhibitor used in cancer treatment.		3.2450imidazoquinoline;
nitrile;
quinolines;
ring assembly;
ureas		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor;
mTOR inhibitor
n4-(2,2-dimethyl-3-oxo-4h-pyrid(1,4)oxazin-6-yl)-5-fluoro-n2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamine
N4-(2,2-dimethyl-3-oxo-4H-pyrid(1,4)oxazin-6-yl)-5-fluoro-N2-(3,4,5-trimethoxyphenyl)-2,4-pyrimidinediamine: a spleen tyrosine kinase (Syk) inhibitor; structure in first source		2.0310
pf 03491390
[no description available]		2.0510
mefloquine
Mefloquine: A phospholipid-interacting antimalarial drug (ANTIMALARIALS). It is very effective against PLASMODIUM FALCIPARUM with very few side effects.. mefloquine : A racemate composed of (+)-(11R,2'S)- and (-)-(11S,2'R)-enantiomers of mefloquine. An antimalarial agent which acts as a blood schizonticide; its mechanism of action is unknown.		2.0810
hypocrellin a
hypocrellin A: isolated from fungus Hypocrella bambusae sacc		7.0510
icatibant
icatibant: a potent bradykinin (B2) receptor antagonist; WIN 65365 is an L-Tic(7) stereoisomer. icatibant : A ten-membered synthetic oligopeptide consisting of D-Arg, Arg, Pro, Hyp, Gly, Thi, Ser, D-Tic, Oic, and Arg residues joined in sequrence. A bradykinin receptor antagonist used as its acetate salt for the treatment of acute attacks of hereditary angioedema in adult patients.		3.5110
3-(4-chlorophenyl)-adamantane-1-carboxylic acid (pyridin-4-ylmethyl)amide
[no description available]		2.4110organochlorine compound
macitentan
[no description available]		5.1270aromatic ether;
organobromine compound;
pyrimidines;
ring assembly;
sulfamides		antihypertensive agent;
endothelin receptor antagonist;
orphan drug
toceranib phosphate
toceranib phosphate: a tyrosine kinase inhibitor; structure in first source		3.8521
amodiaquine hydrochloride
[no description available]		2.4520
cytochrome c-t
Cytochromes c: Cytochromes of the c type that are found in eukaryotic MITOCHONDRIA. They serve as redox intermediates that accept electrons from MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX III and transfer them to MITOCHONDRIAL ELECTRON TRANSPORT COMPLEX IV.		4.75110
cosyntropin
Cosyntropin: A synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of ADRENOCORTICOTROPIC HORMONE. ACTH (1-24), a segment similar in all species, contains the biological activity that stimulates production of CORTICOSTEROIDS in the ADRENAL CORTEX.. cosyntropin : A synthetic peptide that is identical to the 24-amino acid segment at the N-terminal of adrenocorticotropic hormone (corticotropin). A segment similar in all species, it contains the biological activity that stimulates production of corticosteroids in the adrenal cortex. It is used diagnostically to investigate adrenocortical insufficiency.		2.0510
bivalirudin
bivalirudin: designed to bind to the alpha-thrombin catalytic site and anion-binding exosite for fibrin(ogen) recognition. bivalirudin : A synthetic peptide of 20 amino acids, comprising D-Phe, Pro, Arg, Pro, Gly, Gly, Gly, Gly, Asn, Gly, Asp, Phe, Glu, Glu, Ile, Pro, Glu, Glu, Tyr, and Leu in sequence. A congener of hirudin (a naturally occurring drug found in the saliva of the medicinal leech), it a specific and reversible inhibitor of thrombin, and is used as an anticoagulant.		2.0110polypeptideanticoagulant;
EC 3.4.21.5 (thrombin) inhibitor
atrial natriuretic factor
Atrial Natriuretic Factor: A potent natriuretic and vasodilatory peptide or mixture of different-sized low molecular weight PEPTIDES derived from a common precursor and secreted mainly by the HEART ATRIUM. All these peptides share a sequence of about 20 AMINO ACIDS.		2.110polypeptide
tannins
gallotannin : A class of hydrolysable tannins obtained by condensation of the carboxy group of gallic acid (and its polymeric derivatives) with the hydroxy groups of a monosaccharide (most commonly glucose).		2.0510tannin
enfuvirtide
Enfuvirtide: A synthetic 36-amino acid peptide that corresponds to the heptad repeat sequence of HIV-1 gp41. It blocks HIV cell fusion and viral entry and is used with other anti-retrovirals for combination therapy of HIV INFECTIONS and AIDS.. enfuvirtide : A synthetic 36-amino acid peptide consisting of N-acetyltyrosyl, threonyl, seryl, leucyl, isoleucyl, histidyl, seryl, leucyl, isoleucyl, alpha-glutamyl, alpha-glutamyl, seryl, glutaminyl, asparaginyl, glutaminyl, glutaminyl, alpha-glutamyl, lysyl, asparaginyl, alpha-glutamyl, alpha-glutamyl, alpha-glutamyl, leucyl, leucyl, alpha-glutamyl, leucyl, alpha-aspartyl, lysyl, tryptophyl, alanyl, seryl, leucyl, tryptophyl, asparaginyl, tryptophyl, and phenylalaninamide residues joined in sequence. An HIV fusion inhibitor, it was the first of a novel class of antiretroviral drugs used in combination therapy for the treatment of HIV-1 infection. It interferes with entry of HIV into cells by binding to the gp41 sub-unit of the viral envelope glycoprotein, so inhibiting fusion of viral and cellular membranes.		3.1310
adrenocorticotropin zinc
[no description available]		2.0510
hes1 protein, human
HES1 protein, human: RefSeq NM_005524		5.2152
abarelix
abarelix: RN & structure in first source. abarelix : A polypeptide compound composed of ten natural and non-natural amino acid resiudes in a linear sequence.		3.1210polypeptideantineoplastic agent;
hormone antagonist
bkt140
BKT140: a T140 analog and CXCR4 antagonist		2.110
glucagon
Glucagon: A 29-amino acid pancreatic peptide derived from proglucagon which is also the precursor of intestinal GLUCAGON-LIKE PEPTIDES. Glucagon is secreted by PANCREATIC ALPHA CELLS and plays an important role in regulation of BLOOD GLUCOSE concentration, ketone metabolism, and several other biochemical and physiological processes. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1511). glucagon : A 29-amino acid peptide hormone consisting of His, Ser, Gln, Gly, Thr, Phe, Thr, Ser, Asp, Tyr, Ser, Lys, Tyr, Leu, Asp, Ser, Arg, Arg, Ala, Gln, Asp, Phe, Val, Gln, Trp, Leu, Met, Asn and Thr residues joined in sequence.		5.4941peptide hormone
oligonucleotides
[no description available]		10.46143
r18 peptide
R18 peptide: a 20-mer peptide, derived from a phage library, that binds 14-3-3 tau protein; amino acid sequence in first source		2.0410
c-peptide
C-Peptide: The middle segment of proinsulin that is between the N-terminal B-chain and the C-terminal A-chain. It is a pancreatic peptide of about 31 residues, depending on the species. Upon proteolytic cleavage of proinsulin, equimolar INSULIN and C-peptide are released. C-peptide immunoassay has been used to assess pancreatic beta cell function in diabetic patients with circulating insulin antibodies or exogenous insulin. Half-life of C-peptide is 30 min, almost 8 times that of insulin.		2.1110
cellulose
DEAE-Cellulose: Cellulose derivative used in chromatography, as ion-exchange material, and for various industrial applications.		4.6111glycoside
endothelin-1
Endothelin-1: A 21-amino acid peptide produced in a variety of tissues including endothelial and vascular smooth-muscle cells, neurons and astrocytes in the central nervous system, and endometrial cells. It acts as a modulator of vasomotor tone, cell proliferation, and hormone production. (N Eng J Med 1995;333(6):356-63)		4.5940
phosphatidylcholines
Phosphatidylcholines: Derivatives of PHOSPHATIDIC ACIDS in which the phosphoric acid is bound in ester linkage to a CHOLINE moiety.		2.87301,2-diacyl-sn-glycero-3-phosphocholine
mk-8776
MK-8776: a checkpoint kinase 1 (CHK1) inhibitor; SCH900776 was renamed MK-8776; structure in first source		2.1710pyrazolopyrimidine
buparlisib
NVP-BKM120: a pan class I PI3 kinase inhibitor with antineoplastic activity; structure in first source		4.5511aminopyridine;
aminopyrimidine;
morpholines;
organofluorine compound		antineoplastic agent;
EC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
azd8330
[no description available]		2.4110pyridinecarboxamide
chlorophyll a
Chlorophyll: Porphyrin derivatives containing magnesium that act to convert light energy in photosynthetic organisms.. chlorophyll : A family of magnesium porphyrins, defined by the presence of a fifth ring beyond the four pyrrole-like rings. The rings can have various side chains which usually include a long phytol chain.		2.4520chlorophyll;
methyl ester		cofactor
lumacaftor
lumacaftor: a corrector of CF transmembrane conductance regulator (CTFR); structure in first source. lumacaftor : An aromatic amide obtained by formal condensation of the carboxy group of 1-(2,2-difluoro-1,3-benzodioxol-5-yl)cyclopropane-1-carboxylic acid with the aromatic amino group of 3-(6-amino-3-methylpyridin-2-yl)benzoic acid. Used for the treatment of cystic fibrosis.		2.610aromatic amide;
benzodioxoles;
benzoic acids;
cyclopropanes;
organofluorine compound;
pyridines		CFTR potentiator;
orphan drug
bi(otf)3
Bi(OTf)3: structure in first source		2.1710
pevonedistat
pevonedistat: a potent and selective inhibitor of NAE (NEDD8-activating enzyme). pevonedistat : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine which is substituted by a (1S)-2,3-dihydro-1H-inden-1-ylnitrilo group at position 4 and by a (1S,3S,4S)-3-hydroxy-4-[(sulfamoyloxy)methyl]cyclopentyl group at position 7. It is a potent and selective NEDD8-activating enzyme inhibitor with an IC50 of 4.7 nM, and currently under clinical investigation for the treatment of acute myeloid leukemia (AML) and myelodysplastic syndromes.		2.5920cyclopentanols;
indanes;
pyrrolopyrimidine;
secondary amino compound;
sulfamidate		antineoplastic agent;
apoptosis inducer
tg101209
[no description available]		2.0810N-alkylpiperazine;
N-arylpiperazine;
pyrimidines;
secondary amino compound;
sulfonamide		antineoplastic agent;
apoptosis inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
fedratinib
fedratinib: a selective small-molecule inhibitor of JAK2		2.5820sulfonamide
14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene
14-methyl-20-oxa-5,7,14,26-tetraazatetracyclo(19.3.1.1(2,6).1(8,12))heptacosa-1(25),2(26),3,5,8(27),9,11,16,21,23-decaene: has antineoplastic activity; also inhibits Fms-like tyrosine kinase-3; structure in first source		2.4110
hoe 33342
bisbenzimide ethoxide trihydrochloride: benzimidazole fluorescent dye		2.4720
sphingosine kinase
[no description available]		3.6690
igk
IgK: abnormal immunoglobin in leprous-Rubino negative sera; partly related to Fc fragment of IgA & to FAB fragments; possesses Kappa but not lambda light polypeptide chains		2.0210
calpain
Calpain: Cysteine proteinase found in many tissues. Hydrolyzes a variety of endogenous proteins including NEUROPEPTIDES; CYTOSKELETAL PROTEINS; proteins from SMOOTH MUSCLE; CARDIAC MUSCLE; liver; platelets; and erythrocytes. Two subclasses having high and low calcium sensitivity are known. Removes Z-discs and M-lines from myofibrils. Activates phosphorylase kinase and cyclic nucleotide-independent protein kinase. This enzyme was formerly listed as EC 3.4.22.4.		2.110
chitosan
[no description available]		5.5841
icotinib
[no description available]		3.1810
mesna
Mesna: A sulfhydryl compound used to prevent urothelial toxicity by inactivating metabolites from ANTINEOPLASTIC AGENTS, such as IFOSFAMIDE or CYCLOPHOSPHAMIDE.		7.4320organosulfonic acid
cerivastatin sodium
cerivastatin sodium : The sodium salt of cerivastatin. Formerly used to lower cholesterol and prevent cardiovascular disease, it was withdrawn from the market worldwide in 2001 following reports of a severe form of muscle toxicity.		2.0510organic sodium salt;
statin (synthetic)
monensin
[no description available]		2.0510
oxacillin sodium
[no description available]		2.0510organic sodium salt
raltegravir potassium
Raltegravir Potassium: A pyrrolidinone derivative and HIV INTEGRASE INHIBITOR that is used in combination with other ANTI-HIV AGENTS for the treatment of HIV INFECTION.		310
sarkosyl
sarkosyl: RN given is for sarkosyl L, the parent cpd; structure		2.110
sodium diatrizoate
histopaque: used for separating mononuclear & other cells. sodium amidotrizoate : The sodium salt of a benzoic acid having iodo substituents at the 2-, 4- and 6-positions and acetamido substituents at the 3- and 5-positions. It is used, often as a mixture with the meglumine salt, as an X-ray contrast medium in gastrointestinal studies, angiography, and urography.		2.0510organic sodium salt;
organoiodine compound		radioopaque medium
arginine
Teniposide: A semisynthetic derivative of PODOPHYLLOTOXIN that exhibits antitumor activity. Teniposide inhibits DNA synthesis by forming a complex with topoisomerase II and DNA. This complex induces breaks in double stranded DNA and prevents repair by topoisomerase II binding. Accumulated breaks in DNA prevent cells from entering into the mitotic phase of the cell cycle, and lead to cell death. Teniposide acts primarily in the G2 and S phases of the cycle.. teniposide : A furonaphthodioxole that is a synthetic derivative of podophyllotoxin with anti-tumour activity; causes single- and double-stranded breaks in DNA and DNA-protein cross-links and prevents repair by topoisomerase II binding.		2.0310
olaparib
[no description available]		2.8830cyclopropanes;
monofluorobenzenes;
N-acylpiperazine;
phthalazines		antineoplastic agent;
apoptosis inducer;
EC 2.4.2.30 (NAD(+) ADP-ribosyltransferase) inhibitor
thiostrepton
Thiostrepton: One of the CYCLIC PEPTIDES from Streptomyces that is active against gram-positive bacteria. In veterinary medicine, it has been used in mastitis caused by gram-negative organisms and in dermatologic disorders.. thiostrepton : A heterodetic cyclic peptide, in which the cyclisation step involves a formal lactonisation between the carboxy group of a quinaldic acid-based residue and a secondary alcohol. An antibiotic that inhibits bacterial protein synthesis. Also acts as an antitumor agent.		2.2110
cx 4945
[no description available]		2.8430
mln 8237
MLN 8237: an aurora kinase A inhibitor		2.0610benzazepine
lde225
sonidegib: specific Smoothened/Smo antagonist. sonidegib : A member of the classo of biphenyls that is the amide obtained by formal condensation of the carboxy group of 2-methyl-4'-(trifluoromethoxy)[1,1'-biphenyl]-3-carboxylic acid with the amino group of 6-(2,6-dimethylmorpholin-4-yl)pyridin-3-amine. Used (as its phosphate salt) for treatment of locally advanced basal cell carcinoma.		2.110aminopyridine;
aromatic ether;
benzamides;
biphenyls;
morpholines;
organofluorine compound;
tertiary amino compound		antineoplastic agent;
Hedgehog signaling pathway inhibitor;
SMO receptor antagonist
gdc 0449
HhAntag691: inhibits the hedgehog pathway and ABC transporters; has antineoplastic activity		4.0920benzamides;
monochlorobenzenes;
pyridines;
sulfone		antineoplastic agent;
Hedgehog signaling pathway inhibitor;
SMO receptor antagonist;
teratogenic agent
eapb0203
EAPB0203: antineoplastic; structure in first source		2.110
bms 777607
N-(4-(2-amino-3-chloropyridin-4-yloxy)-3-fluorophenyl)-4-ethoxy-1-(4-fluorophenyl)-2-oxo-1,2-dihydropyridine-3-carboxamide: a Met kinase inhibitor; structure in first source		2.110aromatic amide
sgi 1776
SGI 1776: a Pim kinase inhibitor; structure in first source		2.1110imidazoles
marinopyrrole a
marinopyrrole A: antibiotic from a marine Streptomyces sp.; structure in first source. (-)-marinopyrrole A : A member of the class of pyrroles that is 1'H-1,3'-bipyrrole substituted by four chloro groups at positions 4, 4', 5 and 5' and two 2-hydroxybenzoyl moieties at positions 2 and 2'. It is isolated from Streptomyces sp.CNQ-418 and exhibits cytotoxic and antibacterial activities.		2.2510aromatic ketone;
organochlorine compound;
phenols;
pyrroles		antibacterial agent;
antimicrobial agent;
antineoplastic agent;
bacterial metabolite;
marine metabolite
delanzomib
[no description available]		2.2510C-terminal boronic acid peptide;
phenylpyridine;
secondary alcohol;
threonine derivative		antineoplastic agent;
apoptosis inducer;
proteasome inhibitor
pci 32765
ibrutinib: a Btk protein inhibitor. ibrutinib : A member of the class of acrylamides that is (3R)-3-[4-amino-3-(4-phenoxyphenyl)pyrazolo[3,4-d]pyrimidin-1-yl]piperidine in which the piperidine nitrogen is replaced by an acryloyl group. A selective and covalent inhibitor of the enzyme Bruton's tyrosine kinase, it is used for treatment of B-cell malignancies.		3.4150acrylamides;
aromatic amine;
aromatic ether;
N-acylpiperidine;
pyrazolopyrimidine;
tertiary carboxamide		antineoplastic agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
ponatinib
[no description available]		15.44757(trifluoromethyl)benzenes;
acetylenic compound;
benzamides;
imidazopyridazine;
N-methylpiperazine		antineoplastic agent;
tyrosine kinase inhibitor
mk-1775
adavosertib: a Wee1 kinase inhibitor; structure in first source		2.2510piperazines
sgi-1027
SGI-1027: inhibits DNA methyltransferase 1; structure in first source		2.1310
mk 2206
MK 2206: a protein kinase inhibitor and antineoplastic agent		2.6320organic heterotricyclic compoundEC 2.7.1.137 (phosphatidylinositol 3-kinase) inhibitor
navitoclax
[no description available]		3.5920aryl sulfide;
monochlorobenzenes;
morpholines;
N-sulfonylcarboxamide;
organofluorine compound;
piperazines;
secondary amino compound;
sulfone;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
B-cell lymphoma 2 inhibitor
4,4-difluoro-4-bora-3a,4a-diaza-s-indacene
[no description available]		2.0810BODIPY compound
n-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide
N-(cyanomethyl)-4-(2-((4-(4-morpholinyl)phenyl)amino)-4-pyrimidinyl)benzamide: a Janus kinase 1 and Janus kinase 2 inhibitor; structure in first source. momelotinib : A benzamide obtained by formal condensation of the carboxy group of 4-{2-[4-(morpholin-4-yl)anilino]pyrimidin-4-yl}benzoic acid with the primary amino group of aminoacetonitrile. It is an ATP-competitive JAK1/JAK2 inhibitor with IC50 of 11 nM and 18 nM, respectively. Used for the treatment of patients with intermediate- or high-risk myelofibrosis.		2.4110aminopyrimidine;
benzamides;
morpholines;
nitrile;
secondary amino compound;
tertiary amino compound		anti-anaemic agent;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
cardiovascular agents
Cardiovascular Agents: Agents that affect the rate or intensity of cardiac contraction, blood vessel diameter, or blood volume.		2.0310
dcc-2036
rebastinib: an inhibitor of Tie2 tyrosine kinase receptor and antineoplastic agent		3.8630organofluorine compound;
phenylureas;
pyrazoles;
pyridinecarboxamide;
quinolines		tyrosine kinase inhibitor
cabozantinib
cabozantinib: a multikinase inhibitor. cabozantinib : A dicarboxylic acid diamide that is N-phenyl-N'-(4-fluorophenyl)cyclopropane-1,1-dicarboxamide in which the hydrogen at position 4 on the phenyl ring is substituted by a (6,7-dimethoxyquinolin-4-yl)oxy group. A multi-tyrosine kinase inhibitor, used (as its malate salt) for the treatment of progressive, metastatic, medullary thyroid cancer.		8.682aromatic ether;
dicarboxylic acid diamide;
organofluorine compound;
quinolines		antineoplastic agent;
tyrosine kinase inhibitor
incb-018424
[no description available]		5.84100nitrile;
pyrazoles;
pyrrolopyrimidine		antineoplastic agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
entrectinib
entrectinib: inhibits TRK, ROS1, and ALK receptor tyrosine kinases; structure in first source. entrectinib : A member of the class of indazoles that is 1H-indazole substituted by [4-(4-methylpiperazin-1-yl)-2-(tetrahydro-2H-pyran-4-ylamino)benzoyl]amino and 3,5-difluorobenzyl groups at positions 3 and 5, respectively. It is a potent inhibitor of TRKA, TRKB, TRKC, ROS1, and ALK (IC50 values of 0.1 to 1.7 nM), and used for the treatment of NTRK, ROS1 and ALK gene fusion-positive solid tumours.		3.3110benzamides;
difluorobenzene;
indazoles;
N-methylpiperazine;
oxanes;
secondary amino compound;
secondary carboxamide		antibacterial agent;
antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
4-phenyl-1-(1h-1,2,4-triazol-1-yl)-2-butanone
4-phenyl-1-(1H-1,2,4-triazol-1-yl)-2-butanone: inhibits heme oxidase; structure in first source		2.0810
mannans
[no description available]		2.2110
pexidartinib
pexidartinib: inhibits both CSF1R and c-kit receptor tyrosine kinase; structure in first source. pexidartinib : A pyrrolopyridine that is 5-chloro-1H-pyrrolo[2,3-b]pyridine which is substituted by a [6-({[6-(trifluoromethyl)pyridin-3-yl]methyl}amino)pyridin-3-yl]methyl group at position 3. It is a potent multi-targeted receptor tyrosine kinase inhibitor of CSF-1R, KIT, and FLT3 (IC50 of 20 nM, 10 nM and 160 nM, respectively). Approved by the FDA for the treatment of adult patients with symptomatic tenosynovial giant cell tumor (TGCT).		2.520aminopyridine;
organochlorine compound;
organofluorine compound;
pyrrolopyridine;
secondary amino compound		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
ixazomib
ixazomib: a proteasome inhibitor with antineoplastic activity; MLN2238 is the biologically active form of MLN9708; structure in first source. ixazomib : A glycine derivative that is the amide obtained by formal condensation of the carboxy group of N-(2,5-dichlorobenzoyl)glycine with the amino group of [(1R)-1-amino-3-methylbutyl]boronic acid. The active metabolite of ixazomib citrate, it is used in combination therapy for treatment of multiple myeloma.		2.7220benzamides;
boronic acids;
dichlorobenzene;
glycine derivative		antineoplastic agent;
apoptosis inducer;
drug metabolite;
orphan drug;
proteasome inhibitor
fit-039
FIT-039: CDK9 inhibitor; structure in first source		2.4110
eapb0503
EAPB0503: antineoplastic; structure in first source		2.110
azd2014
vistusertib: potent and selective dual mTORC1 and mTORC2 inhibitor; structure in first source		2.4110
(5-(2,4-bis((3s)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol
(5-(2,4-bis((3S)-3-methylmorpholin-4-yl)pyrido(2,3-d)pyrimidin-7-yl)-2-methoxyphenyl)methanol: a potent, selective, and orally bioavailable ATP-competitive mammalian target of rapamycin kinase inhibitor with in vitro and in vivo antitumor activity; structure in first source		2.110benzyl alcohols;
morpholines;
pyridopyrimidine;
tertiary amino compound		antineoplastic agent;
apoptosis inducer;
mTOR inhibitor
plx4032
[no description available]		7.55120aromatic ketone;
difluorobenzene;
monochlorobenzenes;
pyrrolopyridine;
sulfonamide		antineoplastic agent;
B-Raf inhibitor
gsk 1363089
GSK 1363089: a multikinase inhibitor that acts on Met, RON, Axl, and VEGFR; structure in first source		2.0610aromatic ether
glycolipids
[no description available]		4.6111
bay 869766
[no description available]		2.4110
baricitinib
[no description available]		6.3341azetidines;
nitrile;
pyrazoles;
pyrrolopyrimidine;
sulfonamide		anti-inflammatory agent;
antirheumatic drug;
antiviral agent;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
immunosuppressive agent
piperidines
Piperidines: A family of hexahydropyridines.		13.66626
bryostatin 1
bryostatin 1: a protein kinase C activator; macrocyclic lactone from marine Bryozoan Bugula neritina; RN given refers to (1S*-(1R*,3R*,5Z,7S*,8E,11R*,12R*(2E,4E),13E,15R*,17S*(S*),21S*,23S*,25R*))-isomer; structure given in first source; activates protein kinase c. bryostatin 1 : A member of the class of bryostatins that is (17E)-2-oxooxacyclohexacos-17-ene which is substituted by hydroxy groups at positions 4, 10, and 20; an acetoxy group at position 8; methyl groups at positions 9, 9, 18, and 19; 2-methoxy-2-oxoethylidene groups at positions 14 and 24; an (E,E)-octa-2,4-dienoyloxy group at position 21; and with oxygen bridges linking positions 6 to 10, 12 to 16, and 20 to 24. It is one of the most abundant member of the class of bryostatins.		2.0210
interleukin-8
Interleukin-8: A member of the CXC chemokine family that plays a role in the regulation of the acute inflammatory response. It is secreted by variety of cell types and induces CHEMOTAXIS of NEUTROPHILS and other inflammatory cells.		6.7592
dabrafenib
[no description available]		2.1101,3-thiazoles;
aminopyrimidine;
organofluorine compound;
sulfonamide		anticoronaviral agent;
antineoplastic agent;
B-Raf inhibitor
1-(4-(3-bromophenoxy)butyl)-1h-imidazole
1-(4-(3-bromophenoxy)butyl)-1H-imidazole: structure in first source		2.0810
4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide
4-(cyclopropylamino)-2-((4-(4-(ethylsulfonyl)piperazin-1-yl)phenyl)amino)pyrimidine-5-carboxamide: a protein kinase inhibitor; structure in first source		2.4110
ribociclib
ribociclib: inhibits both CDK4 and CDK6		2.5320
gx 15-070
obatoclax: a pan-Bcl-2 inhibitor potentially useful in treating mantle cell lymphoma		2.0410
5-(4-amino-1-propan-2-yl-3-pyrazolo[3,4-d]pyrimidinyl)-1,3-benzoxazol-2-amine
sapanisertib: an mTOR inhibitor		4.6111benzoxazole
ly2784544
[no description available]		2.4110pyridazines
sb 1518
[no description available]		2.4110
unc 0638
UNC 0638: inhibits lysine methyltransferases G9a and GLP; structure in first source		2.110quinazolines
nvp-bsk805
[no description available]		2.110
wzb117
WZB117: structure in first source		2.4110
xmd 8-92
XMD8-92 : A dimethylpyrimido[4,5-b][1,4]benzodiazepin-6-one carrying at C-2 on the pyrimidine ring a [2-ethoxy-4-(4-hydroxypiperidin-1-yl)phenyl]amino substituent. It is an inhibitor of the BMK1 kinase pathway.		2.1710pyrimidobenzodiazepineprotein kinase inhibitor
hh-gv678
flumatinib: an antineoplastic agent and tyrosine kinase inhibitor		4.1250
dinaciclib
[no description available]		2.4110pyrazolopyrimidine
bix 01294
BIX 01294: structure in first source		2.110
calcipotriene
calcipotriene: a topical dermatologic for the treatment of moderate plaque psoriasis; structure in first source. calcipotriol hydrate : A hydrate that is the monohydrate form of calcipotriol. It is used in combination with betamethasone dipropionate, a corticosteroid, for the topical treatment of plaque psoriasis in adult patients.		2.3110hydrateantipsoriatic
gilteritinib
gilteritinib: an FLT3/AXL protein tyrosine kinase inhibitor. gilteritinib : A member of the class of pyrazines that is pyrazine-2-carboxamide which is substituted by {3-methoxy-4-[4-(4-methylpiperazin-1-yl)piperidin-1-yl]phenyl}nitrilo, (oxan-4-yl)nitrilo and ethyl groups at positions 3,5 and 6, respectively. It is a potent inhibitor of FLT3 and AXL tyrosine kinase receptors (IC50 = 0.29 nM and 0.73 nM, respectively). Approved by the FDA for the treatment of acute myeloid leukemia in patients who have a FLT3 gene mutation.		2.4110aromatic amine;
monomethoxybenzene;
N-methylpiperazine;
oxanes;
piperidines;
primary carboxamide;
pyrazines;
secondary amino compound		antineoplastic agent;
apoptosis inducer;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
glpg0634
[no description available]		2.4110
abt-199
venetoclax: A BCL-2 inhibitor with antineoplastic activity that is used in the treatment of CHRONIC LYMPHOCYTIC LEUKEMIA associated with chromosome 17p deletion; structure in first source.. venetoclax : A member of the class of pyrrolopyridines that is a potent inhibitor of the antiapoptotic protein B-cell lymphoma 2. It is used for treamtment of chronic lymphocytic leukemia with 17p deletion.		6.6752aromatic ether;
C-nitro compound;
monochlorobenzenes;
N-alkylpiperazine;
N-arylpiperazine;
N-sulfonylcarboxamide;
oxanes;
pyrrolopyridine		antineoplastic agent;
apoptosis inducer;
B-cell lymphoma 2 inhibitor
ipi-145
[no description available]		2.1510isoquinolines
delgocitinib
delgocitinib: a Janus kinase inhibitor. delgocitinib : A pyrrolopyrimidine that is 7H-pyrrolo[2,3-d]pyrimidine substituted by a (3S,4R)-1-(cyanoacetyl)-3-methyl-1,6-diazaspiro[3.4]octan-6-yl group at position 4. It is a pan-Janus kinase (JAK) inhibitor and is approved for treatment of atopic dermatitis (AD) in Japan.		2.4110azaspiro compound;
N-acylazetidine;
nitrile;
pyrrolopyrimidine;
tertiary amino compound;
tertiary carboxamide		anti-inflammatory drug;
antipsoriatic;
antiseborrheic;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor
bms-911543
N,N-dicyclopropyl-4-((1,5-dimethyl-1H-pyrazol-3-yl)amino)-6-ethyl-1-methyl-1,6-dihydroimidazo(4,5-d)pyrrolo(2,3b)pyridine-7-carboxamide: has antineoplastic activity; structure in first source		2.110
spautin-1
[no description available]		2.110
azd4547
[no description available]		2.1310benzamides;
N-arylpiperazine;
pyrazoles		fibroblast growth factor receptor antagonist
eliglustat tartrate
agalsidase beta: recombinant protein for treatment of Fabry disease. eliglustat tartrate : A tartrate that is the hemitartrate salt of eliglustat. A ceramide glucosyltransferase inhibitor used (as its tartrate salt) for treatment of Gaucher's disease.		2.0710tartrate saltEC 2.4.1.80 (ceramide glucosyltransferase) inhibitor
oligomycin a
[no description available]		2.5720antibiotic antifungal agent;
diketone;
oligomycin;
pentol		antineoplastic agent;
EC 3.6.3.14 (H(+)-transporting two-sector ATPase) inhibitor;
nematicide
3-(2,6-dichloro-3,5-dimethoxyphenyl)-1-(6-(4-(4-ethylpiperazin-1-yl)-phenylamino)pyrimidin-4-yl)-1-methylurea
infigratinib: structure in first source. BGJ-398 : A member of the class of phenylureas that is urea in which a hydrogen attached to one of the nitrogens is replaced by a 2,6-dichloro-3,5-dimethoxyphenyl group, while the hydrogens attached to the other nitrogen are replaced by a methyl group and a 6-{[4-(4-ethylpiperazin-1-yl)phenyl]amino}pyrimidin-4-yl group. It is a potent and selective fibroblast growth factor receptor inhibitor.		5.7361aminopyrimidine;
dichlorobenzene;
N-alkylpiperazine;
N-arylpiperazine;
phenylureas		antineoplastic agent;
fibroblast growth factor receptor antagonist
vasoactive intestinal peptide
Vasoactive Intestinal Peptide: A highly basic, 28 amino acid neuropeptide released from intestinal mucosa. It has a wide range of biological actions affecting the cardiovascular, gastrointestinal, and respiratory systems and is neuroprotective. It binds special receptors (RECEPTORS, VASOACTIVE INTESTINAL PEPTIDE).		3.5620
natriuretic peptide, brain
Natriuretic Peptide, Brain: A PEPTIDE that is secreted by the BRAIN and the HEART ATRIA, stored mainly in cardiac ventricular MYOCARDIUM. It can cause NATRIURESIS; DIURESIS; VASODILATION; and inhibits secretion of RENIN and ALDOSTERONE. It improves heart function. It contains 32 AMINO ACIDS.		3.1550polypeptide
heme
Heme: The color-furnishing portion of hemoglobin. It is found free in tissues and as the prosthetic group in many hemeproteins.. ferroheme : Any iron(II)--porphyrin coordination complex.. ferroheme b : Heme b in which the iron has oxidation state +2.. heme : A heme is any tetrapyrrolic chelate of iron.		521
incb039110
INCB039110: a JAK1 inhibitor; structure in first source		2.4110
leukotoxin
leukotoxin: do not confuse with leukotoxin which is 9,10-epoxy-12-octadecenoate		2.0610
cudc-907
[no description available]		2.2510
ascorbic acid
Ascorbic Acid: A six carbon compound related to glucose. It is found naturally in citrus fruits and many vegetables. Ascorbic acid is an essential nutrient in human diets, and necessary to maintain connective tissue and bone. Its biologically active form, vitamin C, functions as a reducing agent and coenzyme in several metabolic pathways. Vitamin C is considered an antioxidant.. L-ascorbic acid : The L-enantiomer of ascorbic acid and conjugate acid of L-ascorbate.. L-ascorbate : The L-enantiomer of ascorbate and conjugate base of L-ascorbic acid, arising from selective deprotonation of the 3-hydroxy group. Required for a range of essential metabolic reactions in all animals and plants.. vitamin C : Any member of a group of vitamers that belong to the chemical structural class called butenolides that exhibit biological activity against vitamin C deficiency in animals. The vitamers include L-ascorbic acid and its salt, ionized and oxidized forms.		2.9740ascorbic acid;
vitamin C		coenzyme;
cofactor;
flour treatment agent;
food antioxidant;
food colour retention agent;
geroprotector;
plant metabolite;
skin lightening agent
novobiocin
Novobiocin: An antibiotic compound derived from Streptomyces niveus. It has a chemical structure similar to coumarin. Novobiocin binds to DNA gyrase, and blocks adenosine triphosphatase (ATPase) activity. (From Reynolds, Martindale The Extra Pharmacopoeia, 30th ed, p189). novobiocin : A coumarin-derived antibiotic obtained from Streptomyces niveus.		3.1550carbamate ester;
ether;
hexoside;
hydroxycoumarin;
monocarboxylic acid amide;
monosaccharide derivative;
phenols		antibacterial agent;
antimicrobial agent;
EC 5.99.1.3 [DNA topoisomerase (ATP-hydrolysing)] inhibitor;
Escherichia coli metabolite;
hepatoprotective agent
tetracycline
Tetracycline: A naphthacene antibiotic that inhibits AMINO ACYL TRNA binding during protein synthesis.. tetracycline : A broad-spectrum polyketide antibiotic produced by the Streptomyces genus of actinobacteria.		2.4520
chlortetracycline
Chlortetracycline: A TETRACYCLINE with a 7-chloro substitution.. chlortetracycline : A member of the class of tetracyclines with formula C22H23ClN2O8 isolated from Streptomyces aureofaciens.		2.0510
oxytetracycline, anhydrous
Oxytetracycline: A TETRACYCLINE analog isolated from the actinomycete STREPTOMYCES RIMOSUS and used in a wide variety of clinical conditions.. oxytetracycline : A tetracycline used for treatment of infections caused by a variety of Gram positive and Gram negative microorganisms including Mycoplasma pneumoniae, Pasteurella pestis, Escherichia coli, Haemophilus influenzae (respiratory infections), and Diplococcus pneumoniae.		2.0510
minocycline
Minocycline: A TETRACYCLINE analog, having a 7-dimethylamino and lacking the 5 methyl and hydroxyl groups, which is effective against tetracycline-resistant STAPHYLOCOCCUS infections.. minocycline : A tetracycline analogue having a dimethylamino group at position 7 and lacking the methyl and hydroxy groups at position 5.		4.3650
dicumarol
Dicumarol: An oral anticoagulant that interferes with the metabolism of vitamin K. It is also used in biochemical experiments as an inhibitor of reductases.		2.0510hydroxycoumarinanticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor;
Hsp90 inhibitor;
vitamin K antagonist
piroxicam
[no description available]		2.7630benzothiazine;
monocarboxylic acid amide;
pyridines		analgesic;
antirheumatic drug;
cyclooxygenase 1 inhibitor;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-steroidal anti-inflammatory drug
acenocoumarol
Acenocoumarol: A coumarin that is used as an anticoagulant. Its actions and uses are similar to those of WARFARIN. (From Martindale, The Extra Pharmacopoeia, 30th ed, p233). acenocoumarol : A hydroxycoumarin that is warfarin in which the hydrogen at position 4 of the phenyl substituent is replaced by a nitro group.		2.0510C-nitro compound;
hydroxycoumarin;
methyl ketone		anticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
lfm a13
LFM-A13 : An enamide obtained by formal condensation of the carboxy group of (2Z)-2-cyano-3-hydroxybut-2-enoic acid with the amino group of 2,5-dibromoaniline. It is a dual-function inhibitor of Bruton's tyrosine kinase (BTK) and Polo-like kinases (PLK) that exhibits anticancer properties.		2.0310aromatic amide;
dibromobenzene;
enamide;
enol;
nitrile;
secondary carboxamide		antineoplastic agent;
apoptosis inducer;
EC 2.7.10.2 (non-specific protein-tyrosine kinase) inhibitor;
EC 2.7.11.21 (polo kinase) inhibitor;
geroprotector;
platelet aggregation inhibitor
mobic
Meloxicam: A benzothiazine and thiazole derivative that acts as a NSAID and cyclooxygenase-2 (COX-2) inhibitor. It is used in the treatment of RHEUMATOID ARTHRITIS; OSTEOARTHRITIS; and ANKYLOSING SPONDYLITIS.. meloxicam : A benzothiazine that is piroxicam in which the pyridin-2-yl group is replaced by a 5-methyl-1,3-thiazol-2-yl group. A non-steroidal anti-inflammatory drug and selective inhibitor of COX-2, it is used particularly for the management of rheumatoid arthritis.		2.05101,3-thiazoles;
benzothiazine;
monocarboxylic acid amide		analgesic;
antirheumatic drug;
cyclooxygenase 2 inhibitor;
non-steroidal anti-inflammatory drug
mobiflex
tenoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain and inflammation in osteoarthritis and rheumatoid arthritis. It is also indicated for short term treatment of acute musculoskeletal disorders including strains, sprains and other soft-tissue injuries.		2.0510heteroaryl hydroxy compound;
monocarboxylic acid amide;
pyridines;
thienothiazine		antipyretic;
EC 1.14.99.1 (prostaglandin-endoperoxide synthase) inhibitor;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
warfarin
Warfarin: An anticoagulant that acts by inhibiting the synthesis of vitamin K-dependent coagulation factors. Warfarin is indicated for the prophylaxis and/or treatment of venous thrombosis and its extension, pulmonary embolism, and atrial fibrillation with embolization. It is also used as an adjunct in the prophylaxis of systemic embolism after myocardial infarction. Warfarin is also used as a rodenticide.. warfarin : A racemate comprising equal amounts of (R)- and (S)-warfarin. Extensively used as both an anticoagulant drug and as a pesticide against rats and mice.. 4-hydroxy-3-(3-oxo-1-phenylbutyl)-1-benzopyran-2-one : A member of the class of coumarins that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenyl-3-oxo-1-butyl group.		4.7990benzenes;
hydroxycoumarin;
methyl ketone
phenprocoumon
Phenprocoumon: Coumarin derivative that acts as a long acting oral anticoagulant.. phenprocoumon : A hydroxycoumarin that is 4-hydroxycoumarin which is substituted at position 3 by a 1-phenylpropyl group.		2.0510hydroxycoumarinanticoagulant;
EC 1.6.5.2 [NAD(P)H dehydrogenase (quinone)] inhibitor
tipranavir
tipranavir: inhibits HIV-1 protease. tipranavir : A pyridine-2-sulfonamide substituted at C-5 by a trifluoromethyl group and at the sulfonamide nitrogen by a dihydropyrone-containing m-tolyl substituent. It is an HIV-1 protease inhibitor.		2.0410sulfonamideantiviral drug;
HIV protease inhibitor
rolitetracycline
Rolitetracycline: A pyrrolidinylmethyl TETRACYCLINE.. rolitetracycline : A derivative of tetracycline in which the amide function is substituted with a pyrrolidinomethyl group.		2.0510
mna 715
2-cyano-3-hydroxy-N-(4-(trifluoromethyl)phenyl)-2-hepten-6-ynamide: structure in first source; a derivative of A77 1726, the active metabolite of the antirheumatic drug leflunomide, where the isoxazole ring has opened to become a nitrile and an alkyne		2.0110
tigecycline
[no description available]		2.1510
lornoxicam
lornoxicam : A thienothiazine-derived monocarboxylic acid amide obtained by formal condensation of the carboxy group of 6-chloro-4-hydroxy-2-methylthieno[2,3-e][1,2]thiazine-3-carboxylic acid 1,1-dioxide with the amino group of 2-aminopyridine. Used for the treatment of pain, primarily resulting from inflammatory diseases of the joints, osteoarthritis, surgery, sciatica and other inflammations.		2.0510heteroaryl hydroxy compound;
monocarboxylic acid amide;
organochlorine compound;
pyridines;
thienothiazine		antipyretic;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug
s 1 (combination)
S 1 (combination): consists of tegafur, 5-chloro-2,4-dihydroxyuridine & potassium oxonate; an inhibitor of fluorouracil(5-FU) degradation; prolongs the blood 5-FU level as well as increases selective toxicity to tumor; used for the treatment of colon cancer		4.0640
byl719
[no description available]		4.9421proline derivative
epidermal growth factor
Epidermal Growth Factor: A 6-kDa polypeptide growth factor initially discovered in mouse submaxillary glands. Human epidermal growth factor was originally isolated from urine based on its ability to inhibit gastric secretion and called urogastrone. Epidermal growth factor exerts a wide variety of biological effects including the promotion of proliferation and differentiation of mesenchymal and EPITHELIAL CELLS. It is synthesized as a transmembrane protein which can be cleaved to release a soluble active form.		6.35110
transforming growth factor beta
Transforming Growth Factor beta: A factor synthesized in a wide variety of tissues. It acts synergistically with TGF-alpha in inducing phenotypic transformation and can also act as a negative autocrine growth factor. TGF-beta has a potential role in embryonal development, cellular differentiation, hormone secretion, and immune function. TGF-beta is found mostly as homodimer forms of separate gene products TGF-beta1, TGF-beta2 or TGF-beta3. Heterodimers composed of TGF-beta1 and 2 (TGF-beta1.2) or of TGF-beta2 and 3 (TGF-beta2.3) have been isolated. The TGF-beta proteins are synthesized as precursor proteins.		7.85321
ceritinib
ceritinib: an anaplastic lymphoma kinase inhibitor. ceritinib : A member of the class of aminopyrimidines that is 2,6-diamino-5-chloropyrimidine in which the amino groups at positions 2 and 6 are respectively carrying 2-methoxy-4-(piperidin-4-yl)-5-methylphenyl and 2-(isopropylsulfonyl)phenyl substituents. Used for the treatment of ALK-positive metastatic non-small cell lung cancer.		2.7620aminopyrimidine;
aromatic ether;
organochlorine compound;
piperidines;
secondary amino compound;
sulfone		antineoplastic agent;
EC 2.7.10.1 (receptor protein-tyrosine kinase) inhibitor
rg7112
[no description available]		2.1310
azd1208
[no description available]		2.2110
vx-970
berzosertib: an ATR kinase inhibitor		2.4110sulfonamide
gt0918
proxalutamide: has antineoplastic activity		3.4110
tas-116
[no description available]		4.641
3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl ester
3-(6-isobutyl-9-methoxy-1,4-dioxo-1,2,3,4,6,7,12,12a-octahydropyrazino(1',2'-1,6)pyrido(3,4-b)indol-3-yl)propionic acid tert-butyl ester: a breast cancer resistance protein (BCRP) inhibitor; structure in first source		2.4720
ajmaline
[no description available]		2.0510
bgp 15
BGP 15: A PARP (poy(ADP)-ribose polymerase) inhibitor; structure in first source; do not confuse with BGP-15 calcipotriene cpd		2.0710
cpi203
CPI203: a BET protein bromodomain inhibitor		2.1310
fti 277
FTI 277: a ras CAAX (C - Cys; A - aliphatic amino acid; X - Ser or Met) peptidomimetic; inhibits farnesyltransferase; blocks Ras oncogenic signaling by accumulating Ras/Raf complexes in the cytoplasm; structure given in first source		2.0210
curcumin glucuronide
curcumin glucuronide: a curcumin metabolite		2.2510diarylheptanoid
selinexor
selinexor: inhibits karyopherin XPO1		2.5720
osimertinib
osimertinib: an EGFR tyrosine kinase inhibitor. osimertinib : A member of the class of aminopyrimidines that is 4-(1-methylindol-3-yl)pyrimidin-2-amine in which one of the amino hydrogens is replaced by a 2-methoxy-4-[2-(dimethylamino)ethyl](methyl)amino-5-acrylamidophenyl group. Used (as the mesylate salt) for treatment of EGFR T790M mutation positive non-small cell lung cancer.		2.6920acrylamides;
aminopyrimidine;
biaryl;
indoles;
monomethoxybenzene;
secondary amino compound;
secondary carboxamide;
substituted aniline;
tertiary amino compound		antineoplastic agent;
epidermal growth factor receptor antagonist
arsenic trisulfide
[no description available]		2.4420
aki603
AKI603: an aurora-A kinase inhibitor with antineoplastic activity; structure in first source		2.5220
hirudin
Hirudin: A 65-residue polypeptide from LEECHES.		2.0110
imetelstat
[no description available]		9.7493
glutaminase
[no description available]		2.4110
cyclin d1
Cyclin D1: Protein encoded by the bcl-1 gene which plays a critical role in regulating the cell cycle. Overexpression of cyclin D1 is the result of bcl-1 rearrangement, a t(11;14) translocation, and is implicated in various neoplasms.		4.07140
ldc4297
LDC4297: a CDK7 inhibitor with antineoplastic activity; structure in first source. LDC4297 : A pyrazolotriazine that is pyrazolo[1,5-a][1,3,5]triazine substituted by a piperidin-3-yloxy group, [2-(1H-pyrazol-1-yl)benzyl]nitrilo group and an isopropyl group at positions 2, 4 and 8 respectively. It is a potent and selective CDK7 inhibitor and exhibits antiviral activity.		2.4110aromatic ether;
piperidines;
pyrazoles;
pyrazolotriazine;
secondary amino compound		antineoplastic agent;
antiviral agent;
apoptosis inducer;
EC 2.7.11.22 (cyclin-dependent kinase) inhibitor
oligomycins
Oligomycins: A closely related group of toxic substances elaborated by various strains of Streptomyces. They are 26-membered macrolides with lactone moieties and double bonds and inhibit various ATPases, causing uncoupling of phosphorylation from mitochondrial respiration. Used as tools in cytochemistry. Some specific oligomycins are RUTAMYCIN, peliomycin, and botrycidin (formerly venturicidin X).		2.5720
asbestos, crocidolite
Asbestos, Crocidolite: A lavender, acid-resistant asbestos.		2.0310
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone
benzyloxycarbonylvalyl-alanyl-aspartyl fluoromethyl ketone: an interleukin-1beta converting enzyme (ICE)-like protease inhibitor		3.5580
nitrophenols
Nitrophenols: PHENOLS carrying nitro group substituents.		3.6790
lewis x antigen
Lewis X Antigen: A trisaccharide antigen expressed on glycolipids and many cell-surface glycoproteins. In the blood the antigen is found on the surface of NEUTROPHILS; EOSINOPHILS; and MONOCYTES. In addition, Lewis X antigen is a stage-specific embryonic antigen.		2.0110
1 alpha,24-dihydroxyvitamin d3
1 alpha,24-dihydroxyvitamin D3: RN refers to (1alpha,3beta,5Z,7E)-isomer; formulated in ointment at a concentration of 4 microg/g, for treatment of mild psoriasis		2.7730
pladienolide b
pladienolide B: structure in first source		3.1510
adrenomedullin
Adrenomedullin: A 52-amino acid peptide with multi-functions. It was originally isolated from PHEOCHROMOCYTOMA and ADRENAL MEDULLA but is widely distributed throughout the body including lung and kidney tissues. Besides controlling fluid-electrolyte homeostasis, adrenomedullin is a potent vasodilator and can inhibit pituitary ACTH secretion.		3.1310
epoetin alfa
Epoetin Alfa: A recombinant glycosylated form of erythropoietin which stimulates the differentiation and proliferation of erythroid precursors. It is used for the treatment of ANEMIA associated with CHRONIC RENAL FAILURE in dialysis and predialysis patients.		2.0610
neferine
neferine: isolated from green seed embryo of Nelumbo nucifera Gaertn		2.7630
oridonin
[no description available]		2.8130
vitamin b 12
Vitamin B 12: A cobalt-containing coordination compound produced by intestinal micro-organisms and found also in soil and water. Higher plants do not concentrate vitamin B 12 from the soil and so are a poor source of the substance as compared with animal tissues. INTRINSIC FACTOR is important for the assimilation of vitamin B 12.		2.4420
oblimersen
oblimersen: targets the Bcl-2 oncogene good efficacy with low toxicity tumour regressions		12.271
s 8932
[no description available]		3.3510aromatic amine;
C-nucleoside;
carboxylic ester;
nitrile;
phosphoramidate ester;
pyrrolotriazine		anticoronaviral agent;
antiviral drug;
prodrug
cyclosporine
Cyclosporine: A cyclic undecapeptide from an extract of soil fungi. It is a powerful immunosupressant with a specific action on T-lymphocytes. It is used for the prophylaxis of graft rejection in organ and tissue transplantation. (From Martindale, The Extra Pharmacopoeia, 30th ed).		8.16310
silybin
Silybin: The major active component of silymarin flavonoids extracted from seeds of the MILK THISTLE, Silybum marianum; it is used in the treatment of HEPATITIS; LIVER CIRRHOSIS; and CHEMICAL AND DRUG INDUCED LIVER INJURY, and has antineoplastic activity; silybins A and B are diastereomers.		3.4811
apicidin
apicidin: structure in first source		2.0210
lactoferrin
Lactoferrin: An iron-binding protein that was originally characterized as a milk protein. It is widely distributed in secretory fluids and is found in the neutrophilic granules of LEUKOCYTES. The N-terminal part of lactoferrin possesses a serine protease which functions to inactivate the TYPE III SECRETION SYSTEM used by bacteria to export virulence proteins for host cell invasion.		7.3110
catalpol
catalpol: component of dihuang; RN given refers to (1aS-(1aalpha,1bbeta,2beta,5abeta,6beta,6aalpha))-isomer; RN for cpd without isomeric designation not avail 12/92		4.6111
icg 001
ICG 001: PRI-724 is an enantiomer of ICG-001; binds to cAMP response element-binding protein; structure in first source		2.1710
n-benzyladriamycin-14-valerate
[no description available]		2.0310
thromboplastin
Thromboplastin: Constituent composed of protein and phospholipid that is widely distributed in many tissues. It serves as a cofactor with factor VIIa to activate factor X in the extrinsic pathway of blood coagulation.		2.0310
muramidase
Muramidase: A basic enzyme that is present in saliva, tears, egg white, and many animal fluids. It functions as an antibacterial agent. The enzyme catalyzes the hydrolysis of 1,4-beta-linkages between N-acetylmuramic acid and N-acetyl-D-glucosamine residues in peptidoglycan and between N-acetyl-D-glucosamine residues in chitodextrin. EC 3.2.1.17.		2.4820
amyloid beta-peptides
amyloid beta-protein (1-40): although acutely neurotoxic in both rat & monkey cerebral cortex, neuronal degeneration in primates resembles more closely to that found in Alzheimer's disease; amino acid sequence has been determined		2.110
exudates
Malaysia: A parliamentary democracy with a constitutional monarch in southeast Asia, consisting of 11 states (West Malaysia) on the Malay Peninsula and two states (East Malaysia) on the island of BORNEO. It is also called the Federation of Malaysia. Its capital is Kuala Lumpur. Before 1963 it was the Union of Malaya. It reorganized in 1948 as the Federation of Malaya, becoming independent from British Malaya in 1957 and becoming Malaysia in 1963 as a federation of Malaya, Sabah, Sarawak, and Singapore (which seceded in 1965). The form Malay- probably derives from the Tamil malay, mountain, with reference to its geography. (From Webster's New Geographical Dictionary, 1988, p715 & Room, Brewer's Dictionary of Names, 1992, p329)		3.98120
technetium tc 99m dimercaptosuccinic acid
Technetium Tc 99m Dimercaptosuccinic Acid: A nontoxic radiopharmaceutical that is used in the diagnostic imaging of the renal cortex.		2.7430
at 9283
[no description available]		2.4110
entecavir
entecavir (anhydrous) : Guanine substituted at the 9 position by a 4-hydroxy-3-(hydroxymethyl)-2-methylidenecyclopentyl group. A synthetic analogue of 2'-deoxyguanosine, it is a nucleoside reverse transcriptase inhibitor with selective antiviral activity against hepatitis B virus. Entecavir is phosphorylated intracellularly to the active triphosphate form, which competes with deoxyguanosine triphosphate, the natural substrate of hepatitis B virus reverse transcriptase, inhibiting every stage of the enzyme's activity, although it has no activity against HIV. It is used for the treatment of chronic hepatitis B.		2.05102-aminopurines;
oxopurine;
primary alcohol;
secondary alcohol		antiviral drug;
EC 2.7.7.49 (RNA-directed DNA polymerase) inhibitor
acyclovir
Acyclovir: A GUANOSINE analog that acts as an antimetabolite. Viruses are especially susceptible. Used especially against herpes.. acyclovir : An oxopurine that is guanine substituted by a (2-hydroxyethoxy)methyl substituent at position 9. Used in the treatment of viral infections.		2.45202-aminopurines;
oxopurine		antimetabolite;
antiviral drug
levoleucovorin
Levoleucovorin: A folate analog consisting of the pharmacologically active isomer of LEUCOVORIN.. (6S)-5-formyltetrahydrofolic acid : The pharmacologically active (6S)-stereoisomer of 5-formyltetrahydrofolic acid.		6.01425-formyltetrahydrofolic acidantineoplastic agent;
metabolite
cyclic gmp
Cyclic GMP: Guanosine cyclic 3',5'-(hydrogen phosphate). A guanine nucleotide containing one phosphate group which is esterified to the sugar moiety in both the 3'- and 5'-positions. It is a cellular regulatory agent and has been described as a second messenger. Its levels increase in response to a variety of hormones, including acetylcholine, insulin, and oxytocin and it has been found to activate specific protein kinases. (From Merck Index, 11th ed). 3',5'-cyclic GMP : A 3',5'-cyclic purine nucleotide in which the purine nucleobase is specified as guanidine.		2.1103',5'-cyclic purine nucleotide;
guanyl ribonucleotide		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
plant metabolite;
Saccharomyces cerevisiae metabolite
guanosine diphosphate
Guanosine Diphosphate: A guanine nucleotide containing two phosphate groups esterified to the sugar moiety.		2.0110guanosine 5'-phosphate;
purine ribonucleoside 5'-diphosphate		Escherichia coli metabolite;
mouse metabolite;
uncoupling protein inhibitor
guanosine triphosphate
Guanosine Triphosphate: Guanosine 5'-(tetrahydrogen triphosphate). A guanine nucleotide containing three phosphate groups esterified to the sugar moiety.		2.7130guanosine 5'-phosphate;
purine ribonucleoside 5'-triphosphate		Escherichia coli metabolite;
mouse metabolite;
uncoupling protein inhibitor
guanine
[no description available]		5.51312-aminopurines;
oxopurine;
purine nucleobase		algal metabolite;
Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
inosine
[no description available]		2.0510inosines;
purines D-ribonucleoside		Escherichia coli metabolite;
human metabolite;
mouse metabolite;
Saccharomyces cerevisiae metabolite
folic acid
folcysteine: used to promote fertility in chickens. vitamin B9 : Any B-vitamin that exhibits biological activity against vitamin B9 deficiency. Vitamin B9 refers to the many forms of folic acid and its derivatives, including tetrahydrofolic acid (the active form), methyltetrahydrofolate (the primary form found in blood), methenyltetrahydrofolate, folinic acid amongst others. They are present in abundance in green leafy vegetables, citrus fruits, and animal products. Lack of vitamin B9 leads to anemia, a condition in which the body cannot produce sufficient number of red blood cells. Symptoms of vitamin B9 deficiency include fatigue, muscle weakness, and pale skin.		3.0340folic acids;
N-acyl-amino acid		human metabolite;
mouse metabolite;
nutrient
3-methyladenine
N3-methyladenine: structure in first source		3.0240
rifampin
Rifampin: A semisynthetic antibiotic produced from Streptomyces mediterranei. It has a broad antibacterial spectrum, including activity against several forms of Mycobacterium. In susceptible organisms it inhibits DNA-dependent RNA polymerase activity by forming a stable complex with the enzyme. It thus suppresses the initiation of RNA synthesis. Rifampin is bactericidal, and acts on both intracellular and extracellular organisms. (From Gilman et al., Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed, p1160)		4.7161cyclic ketal;
hydrazone;
N-iminopiperazine;
N-methylpiperazine;
rifamycins;
semisynthetic derivative;
zwitterion		angiogenesis inhibitor;
antiamoebic agent;
antineoplastic agent;
antitubercular agent;
DNA synthesis inhibitor;
EC 2.7.7.6 (RNA polymerase) inhibitor;
Escherichia coli metabolite;
geroprotector;
leprostatic drug;
neuroprotective agent;
pregnane X receptor agonist;
protein synthesis inhibitor
clozapine
Clozapine: A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.. clozapine : A benzodiazepine that is 5H-dibenzo[b,e][1,4]diazepine substituted by a chloro group at position 8 and a 4-methylpiperazin-1-yl group at position 11. It is a second generation antipsychotic used in the treatment of psychiatric disorders like schizophrenia.		2.7230benzodiazepine;
N-arylpiperazine;
N-methylpiperazine;
organochlorine compound		adrenergic antagonist;
dopaminergic antagonist;
EC 3.4.21.26 (prolyl oligopeptidase) inhibitor;
environmental contaminant;
GABA antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
xenobiotic
dacarbazine
(E)-dacarbazine : A dacarbazine in which the N=N double bond adopts a trans-configuration.		10.6214dacarbazine
didanosine
Didanosine: A dideoxynucleoside compound in which the 3'-hydroxy group on the sugar moiety has been replaced by a hydrogen. This modification prevents the formation of phosphodiester linkages which are needed for the completion of nucleic acid chains. Didanosine is a potent inhibitor of HIV replication, acting as a chain-terminator of viral DNA by binding to reverse transcriptase; ddI is then metabolized to dideoxyadenosine triphosphate, its putative active metabolite.. didanosine : A purine 2',3'-dideoxyribonucleoside that is inosine in which the hydroxy groups at both the 2' and the 3' positions on the sugar moiety have been replaced by hydrogen. An antiviral drug, it is used as a medication to treat HIV/AIDS.		2.0510purine 2',3'-dideoxyribonucleosideantimetabolite;
antiviral drug;
EC 2.4.2.1 (purine-nucleoside phosphorylase) inhibitor;
geroprotector;
HIV-1 reverse transcriptase inhibitor
ganciclovir
[no description available]		2.44202-aminopurines;
oxopurine		antiinfective agent;
antiviral drug
valacyclovir
Valacyclovir: A prodrug of acyclovir that is used in the treatment of HERPES ZOSTER and HERPES SIMPLEX VIRUS INFECTION of the skin and mucous membranes, including GENITAL HERPES.		2.0410L-valyl esterantiviral drug
sildenafil
sildenafil : A pyrazolo[4,3-d]pyrimidin-7-one having a methyl substituent at the 1-position, a propyl substituent at the 3-position and a 2-ethoxy-5-[(4-methylpiperazin-1-yl)sulfonyl]phenyl group at the 5-position.		2.0510piperazines;
pyrazolopyrimidine;
sulfonamide		EC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
olanzapine
Olanzapine: A benzodiazepine derivative that binds SEROTONIN RECEPTORS; MUSCARINIC RECEPTORS; HISTAMINE H1 RECEPTORS; ADRENERGIC ALPHA-1 RECEPTORS; and DOPAMINE RECEPTORS. It is an antipsychotic agent used in the treatment of SCHIZOPHRENIA; BIPOLAR DISORDER; and MAJOR DEPRESSIVE DISORDER; it may also reduce nausea and vomiting in patients undergoing chemotherapy.. olanzapine : A benzodiazepine that is 10H-thieno[2,3-b][1,5]benzodiazepine substituted by a methyl group at position 2 and a 4-methylpiperazin-1-yl group at position 4.		2.0510benzodiazepine;
N-arylpiperazine;
N-methylpiperazine		antiemetic;
dopaminergic antagonist;
histamine antagonist;
muscarinic antagonist;
second generation antipsychotic;
serotonergic antagonist;
serotonin uptake inhibitor
penciclovir
penciclovir : A member of the class of 2-aminopurines that is guanine in which the hydrogen at position 9 is substituted by a 4-hydroxy-3-(hydroxymethyl)but-1-yl group. An antiviral drug, it is administered topically for treatment of herpes labialis. A prodrug, famciclovir, is used for oral administration.		2.05102-aminopurines;
propane-1,3-diols		antiviral drug
oxypurinol
Oxypurinol: A xanthine oxidase inhibitor.. alloxanthine : A pyrazolopyrimidine that is 4,5,6,7-tetrahydro-H-pyrazolo[3,4-d]pyrimidine substituted by oxo groups at positions 4 and 6.		2.0510pyrazolopyrimidinedrug metabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor
raltitrexed
[no description available]		2.0510N-acyl-amino acid
ro 3306
RO 3306: structure in first source		2.3110
allopurinol
Allopurinol: A XANTHINE OXIDASE inhibitor that decreases URIC ACID production. It also acts as an antimetabolite on some simpler organisms.. allopurinol : A bicyclic structure comprising a pyrazole ring fused to a hydroxy-substituted pyrimidine ring.		3.3260nucleobase analogue;
organic heterobicyclic compound		antimetabolite;
EC 1.17.3.2 (xanthine oxidase) inhibitor;
gout suppressant;
radical scavenger
2,2'-(hydroxynitrosohydrazono)bis-ethanamine
2,2'-(hydroxynitrosohydrazono)bis-ethanamine: a nitric oxide (NO) generating compound. 1,1-bis(2-aminoethyl)-2-hydroxy-3-oxotriazane : A nitroso compound that is triazane in which the the nitrogen at position 1 is substituted by two 2-aminoethyl groups, that at position 2 is substituted by a hydroxy group, and that at position 3 is substituted by an oxo group.		2.0310
leucovorin
5-formyltetrahydrofolic acid : A formyltetrahydrofolic acid in which the formyl group is located at position 5.		2.4520formyltetrahydrofolic acidEscherichia coli metabolite;
mouse metabolite
alanosine
[no description available]		2.0510
bl 4162a
anagrelide: imidazoquinazoline derivative which lowers platelet count probably by inhibiting thrombopoiesis and reduces platelet aggregation; used for thrombocythemia; structure in first source. 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.		4.5270imidazoquinazolineanticoagulant;
antifibrinolytic drug;
cardiovascular drug;
platelet aggregation inhibitor
pemetrexed
pemetrexed disodium : An organic sodium salt that is the disodium salt of N-{4-[2-(2-amino-4-oxo-4,7-dihydro-1H-pyrrolo[2,3-d]pyrimidin-5-yl)ethyl]benzoyl}-L-glutamic acid. Inhibits thymidylate synthase (TS), 421 dihydrofolate reductase (DHFR), and glycinamide ribonucleotide formyltransferase (GARFT).		6.5152N-acyl-L-glutamic acid;
pyrrolopyrimidine		antimetabolite;
antineoplastic agent;
EC 1.5.1.3 (dihydrofolate reductase) inhibitor;
EC 2.1.1.45 (thymidylate synthase) inhibitor;
EC 2.1.2.2 (phosphoribosylglycinamide formyltransferase) inhibitor
tirapazamine
Tirapazamine: A triazine derivative that introduces breaks into DNA strands in hypoxic cells, sensitizing tumor cells to the cytotoxic activity of other drugs and radiation.. tirapazamine : A member of the class of benzotriazines that is 1,2,4-benzotriazine carrying an amino substituent at position 3 and two oxido substituents at positions 1 and 4.		2.0510aromatic amine;
benzotriazines;
N-oxide		antibacterial agent;
antineoplastic agent;
apoptosis inducer
lometrexol
lometrexol: RN & structure given in first source;		3.110
sildenafil citrate
Sildenafil Citrate: A PHOSPHODIESTERASE TYPE-5 INHIBITOR; VASODILATOR AGENT and UROLOGICAL AGENT that is used in the treatment of ERECTILE DYSFUNCTION and PRIMARY PULMONARY HYPERTENSION.. sildenafil citrate : The citrate salt of sildenafil.		7.0291citrate saltEC 3.1.4.35 (3',5'-cyclic-GMP phosphodiesterase) inhibitor;
vasodilator agent
aprepitant
Aprepitant: A morpholine neurokinin-1 (NK1) receptor antagonist that is used in the management of nausea and vomiting caused by DRUG THERAPY, and for the prevention of POSTOPERATIVE NAUSEA AND VOMITING.. aprepitant : A morpholine-based antiemetic, which is or the prevention of acute and delayed nausea and vomiting associated with initial and repeat courses of highly emetogenic cancer chemotherapy. Aprepitant is a selective high-affinity antagonist of human substance P/neurokinin 1 (NK1) receptors.		2.1710(trifluoromethyl)benzenes;
cyclic acetal;
morpholines;
triazoles		antidepressant;
antiemetic;
neurokinin-1 receptor antagonist;
peripheral nervous system drug;
substance P receptor antagonist
hymenialdisine
[no description available]		2.4220
vardenafil dihydrochloride
Vardenafil Dihydrochloride: A piperazine derivative, PHOSPHODIESTERASE 5 INHIBITOR and VASODILATOR AGENT that is used as a UROLOGICAL AGENT in the treatment of ERECTILE DYSFUNCTION.		3.6220
rifabutin
[no description available]		2.0510
isogranulatimide
isogranulatimide: G2 checkpoint inhibitor; structure in first source		2.0310
ag-879
AG-879: structure given in first source		2.4110
hesperadin
[no description available]		2.7220
trypan blue
Trypan Blue: A diazo-naphthalene sulfonate that is widely used as a stain.. trypan blue : An organosulfonate salt that is the tetrasodium salt of 3,3'-[(3,3'-dimethylbiphenyl-4,4'-diyl)didiazene-2,1-diyl]bis(5-amino-4-hydroxynaphthalene-2,7-disulfonic acid).		2.1710
nintedanib
nintedanib : A member of the class of oxindoles that is a kinase inhibitor used (in the form of its ethylsulfonate salt) for the treatment of idiopathic pulmonary fibrosis and cancer.		4.2240
methylnitronitrosoguanidine
Methylnitronitrosoguanidine: A nitrosoguanidine derivative with potent mutagenic and carcinogenic properties.. N-methyl-N'-nitro-N-nitrosoguanidine : An N-nitroguanidine compound having nitroso and methyl substituents at the N'-position		2.7630nitroso compoundalkylating agent
8-hydroxy-2'-deoxyguanosine
8-Hydroxy-2'-Deoxyguanosine: Common oxidized form of deoxyguanosine in which C-8 position of guanine base has a carbonyl group.. 8-hydroxy-2'-deoxyguanosine : Guanosine substituted at the purine 8-position by a hydroxy group. It is used as a biomarker of oxidative DNA damage.		2.2110guanosinesbiomarker
amg531
[no description available]		3.9530
debromohymenialdisine
[no description available]		2.0310
bmn 673
talazoparib: inhibits both PARP1 and PARP2; structure in first source		2.2110
pf-477736
PF 00477736: a Chk1 inhibitor; structure in first source. PF-00477736 : A diazepinoindole that is 8-amino-4,5-dihydro-6H-[1,2]diazepino[4,5,6-cd]indol-6-one which is substituted at position 2 by a 1-methylpyrazol-4-yl group and in which the amino group at position 8 has undergone condensation with the carboxy group of (2R)-2-cyclohexylglycine to give the corresponding carboxamide. It is an inhibitor of checkpoint kinase 1 (Chk 1).		2.1110
bay 80-6946
copanlisib: an antineoplastic agent with PI3K inhibitory activity; structure in first source. copanlisib : An imidazoquinazoline that is 2,3-dihydroimidazo[1,2-c]quinazoline substituted by (2-aminopyrimidine-5-carbonyl)amino, methoxy, and 3-(morpholin-4-yl)propoxy groups at positions 5, 7 and 8, respectively. It is a intravenous pan-class I PI3K inhibitor used for the treatment of relapsed follicular lymphoma in patients who have received at least 2 prior systemic therapies.		2.1310
alcian blue
Alcian Blue: A copper-containing dye used as a gelling agent for lubricants, for staining of bacteria and for the dyeing of histiocytes and fibroblasts in vivo.		2.0510
eye
[no description available]		2.0710
quillaja saponins
Quillaja Saponins: Natural detergents made up of a heterogeneous mixture of molecules having a triterpenoid core structure. They vary in aglycone (sapogenin) and sugar moieties, including glucose.		2.1310
ferric carboxymaltose
ferric carboxymaltose: effective for treatment of postpartum anemia		2.1110
acetylcellulose
acetylcellulose: coating compound. cellulose acetate : A glucan derivative obtained through the esterification of cellulose by acetic anhydride or acetic acid, resulting in the substitution of some of the hydroxy groups of cellulose by acetyl groups. It is used in a variety of applications including base material for photographic film, clothing, membrane filters, coatings, food packaging, and as a frame material for eyeglasses.		4.6111
molnupiravir
molnupiravir: prodrug that’s metabolized into N4-hydroxycytidine (NHC), a ribonucleoside analog. molnupiravir : A nucleoside analogue that is N(4)-hydroxycytidine in which the 5'-hydroxy group is replaced by a (2-methylpropanoyl)oxy group. It is the prodrug of the active antiviral ribonucleoside analog N(4)-hydroxycytidine (EIDD-1931), has activity against a number of RNA viruses including SARS-CoV-2, MERS-CoV, and seasonal and pandemic influenza viruses. It is currently in phase III trials for the treatment of patients with COVID-19.		2.610isopropyl ester;
ketoxime;
nucleoside analogue		anticoronaviral agent;
antiviral drug;
prodrug
carbidopa
Carbidopa: An inhibitor of DOPA DECARBOXYLASE that prevents conversion of LEVODOPA to dopamine. It is used in PARKINSON DISEASE to reduce peripheral adverse effects of LEVODOPA. It has no anti-parkinson activity by itself.. carbidopa : The hydrate of 3-(3,4-dihydroxyphenyl)propanoic acid in which the hydrogens alpha- to the carboxyl group are substituted by hydrazinyl and methyl groups (S-configuration). Carbidopa is a dopa decarboxylase inhibitor, so prevents conversion of levodopa to dopamine. It has no antiparkinson activity by itself, but is used in the management of Parkinson's disease to reduce peripheral adverse effects of levodopa.		2.1710
pseudolaric acid b
[no description available]		2.2510
salarin c
salarin C: has antineoplastic activity; isolated from the sponge Fascaplysinopsis; structure in first source		2.1310
concanavalin a
Concanavalin A: A MANNOSE/GLUCOSE binding lectin isolated from the jack bean (Canavalia ensiformis). It is a potent mitogen used to stimulate cell proliferation in lymphocytes, primarily T-lymphocyte, cultures.		3.420
metallothionein
Metallothionein: A low-molecular-weight (approx. 10 kD) protein occurring in the cytoplasm of kidney cortex and liver. It is rich in cysteinyl residues and contains no aromatic amino acids. Metallothionein shows high affinity for bivalent heavy metals.		2.4110
phosphorus radioisotopes
Phosphorus Radioisotopes: Unstable isotopes of phosphorus that decay or disintegrate emitting radiation. P atoms with atomic weights 28-34 except 31 are radioactive phosphorus isotopes.		2.0210
leptin
Leptin: A 16-kDa peptide hormone secreted from WHITE ADIPOCYTES. Leptin serves as a feedback signal from fat cells to the CENTRAL NERVOUS SYSTEM in regulation of food intake, energy balance, and fat storage.		8.8721
pyrimidinones
Pyrimidinones: Heterocyclic compounds known as 2-pyrimidones (or 2-hydroxypyrimidines) and 4-pyrimidones (or 4-hydroxypyrimidines) with the general formula C4H4N2O.		3.2650
filipin
Filipin: A complex of polyene antibiotics obtained from Streptomyces filipinensis. Filipin III alters membrane function by interfering with membrane sterols, inhibits mitochondrial respiration, and is proposed as an antifungal agent. Filipins I, II, and IV are less important.		2.0510
phenanthrenes
Phenanthrenes: POLYCYCLIC AROMATIC HYDROCARBONS composed of three fused BENZENE rings.. phenanthrenes : Any benzenoid aromatic compound that consists of a phenanthrene skeleton and its substituted derivatives thereof.		3.790
ConditionIndicatedRelationship StrengthStudiesTrials
Bone Cancer
[description not available]		013.035911
Osteogenic Sarcoma
[description not available]		05.13101
Bone Neoplasms
Tumors or cancer located in bone tissue or specific BONES.		013.035911
Osteosarcoma
A sarcoma originating in bone-forming cells, affecting the ends of long bones. It is the most common and most malignant of sarcomas of the bones, and occurs chiefly among 10- to 25-year-old youths. (From Stedman, 25th ed)		05.13101
Breast Cancer
[description not available]		015.39317
Breast Neoplasms
Tumors or cancer of the human BREAST.		117.39317
Erythremia
[description not available]		011.07353
Polycythemia Vera
A myeloproliferative disorder of unknown etiology, characterized by abnormal proliferation of all hematopoietic bone marrow elements and an absolute increase in red cell mass and total blood volume, associated frequently with splenomegaly, leukocytosis, and thrombocythemia. Hematopoiesis is also reactive in extramedullary sites (liver and spleen). In time myelofibrosis occurs.		113.07353
Adverse Drug Event
[description not available]		014.885817
Drug-Related Side Effects and Adverse Reactions
Disorders that result from the intended use of PHARMACEUTICAL PREPARATIONS. Included in this heading are a broad variety of chemically-induced adverse conditions due to toxicity, DRUG INTERACTIONS, and metabolic effects of pharmaceuticals.		014.885817
Acute Liver Injury, Drug-Induced
[description not available]		09.72361
Chemical and Drug Induced Liver Injury
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, herbal and dietary supplements and chemicals from the environment.		09.72361
Innate Inflammatory Response
[description not available]		014.725517
Inflammation
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.		019.725517
Benign Neoplasms
[description not available]		019.531216
Neoplasms
New abnormal growth of tissue. Malignant neoplasms show a greater degree of anaplasia and have the properties of invasion and metastasis, compared to benign neoplasms.		124.2462432
Plasmodium falciparum Malaria
[description not available]		04.2731
Malaria, Falciparum
Malaria caused by PLASMODIUM FALCIPARUM. This is the severest form of malaria and is associated with the highest levels of parasites in the blood. This disease is characterized by irregularly recurring febrile paroxysms that in extreme cases occur with acute cerebral, renal, or gastrointestinal manifestations.		04.2731
Acute Confusional Senile Dementia
[description not available]		08.62144
Alzheimer Disease
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)		08.62144
Congenital Zika Syndrome
[description not available]		02.2510
Disease Models, Animal
Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases.		020.7731183
Zika Virus Infection
A viral disease transmitted by the bite of AEDES mosquitoes infected with ZIKA VIRUS. Its mild DENGUE-like symptoms include fever, rash, headaches and ARTHRALGIA. The viral infection during pregnancy, in rare cases, is associated with congenital brain and ocular abnormalities, called Congenital Zika Syndrome, including MICROCEPHALY and may also lead to GUILLAIN-BARRE SYNDROME.		02.2510
2019 Novel Coronavirus Disease
[description not available]		015.386018
Viral Diseases
[description not available]		03.4220
Virus Diseases
A general term for diseases caused by viruses.		03.4220
Astrocytoma, Grade IV
[description not available]		011.045010
Experimental Neoplasms
[description not available]		07.96281
Granulocytic Leukemia, Chronic
[description not available]		031.365,061634
Glioblastoma
A malignant form of astrocytoma histologically characterized by pleomorphism of cells, nuclear atypia, microhemorrhage, and necrosis. They may arise in any region of the central nervous system, with a predilection for the cerebral hemispheres, basal ganglia, and commissural pathways. Clinical presentation most frequently occurs in the fifth or sixth decade of life with focal neurologic signs or seizures.		113.045010
Leukemia, Myelogenous, Chronic, BCR-ABL Positive
Clonal hematopoetic disorder caused by an acquired genetic defect in PLURIPOTENT STEM CELLS. It starts in MYELOID CELLS of the bone marrow, invades the blood and then other organs. The condition progresses from a stable, more indolent, chronic phase (LEUKEMIA, MYELOID, CHRONIC PHASE) lasting up to 7 years, to an advanced phase composed of an accelerated phase (LEUKEMIA, MYELOID, ACCELERATED PHASE) and BLAST CRISIS.		133.365,061634
Ph 1 Chromosome
[description not available]		022.4144971
Thrombocythemia
[description not available]		06.61181
Gastrointestinal Stromal Neoplasm
[description not available]		028.562,120311
Cancer of Stomach
[description not available]		016.021863
Stomach Neoplasms
Tumors or cancer of the STOMACH.		120.713726
Gastrointestinal Stromal Tumors
All tumors in the GASTROINTESTINAL TRACT arising from mesenchymal cells (MESODERM) except those of smooth muscle cells (LEIOMYOMA) or Schwann cells (SCHWANNOMA).		130.562,120311
Chronic Illness
[description not available]		016.614715
Chronic Disease
Diseases which have one or more of the following characteristics: they are permanent, leave residual disability, are caused by nonreversible pathological alteration, require special training of the patient for rehabilitation, or may be expected to require a long period of supervision, observation, or care (Dictionary of Health Services Management, 2d ed). For epidemiological studies chronic disease often includes HEART DISEASES; STROKE; CANCER; and diabetes (DIABETES MELLITUS, TYPE 2).		016.614715
Granulocytic Leukemia, Chronic, Stable Phase
[description not available]		024.18574255
Cancer of Gastrointestinal Tract
[description not available]		026.11805202
Recrudescence
[description not available]		023.15423155
Focal Segmental Glomerulosclerosis
[description not available]		02.7620
Glomerulosclerosis, Focal Segmental
A clinicopathological syndrome or diagnostic term for a type of glomerular injury that has multiple causes, primary or secondary. Clinical features include PROTEINURIA, reduced GLOMERULAR FILTRATION RATE, and EDEMA. Kidney biopsy initially indicates focal segmental glomerular consolidation (hyalinosis) or scarring which can progress to globally sclerotic glomeruli leading to eventual KIDNEY FAILURE.		02.7620
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		09.57203
Proteinuria
The presence of proteins in the urine, an indicator of KIDNEY DISEASES.		04.7261
Disease Exacerbation
[description not available]		025.58621297
Blast Phase
[description not available]		020.4731468
Blast Crisis
An advanced phase of chronic myelogenous leukemia, characterized by a rapid increase in the proportion of immature white blood cells (blasts) in the blood and bone marrow to greater than 30%.		020.4731468
Acute Lymphoid Leukemia
[description not available]		028.35501122
Acute Disease
Disease having a short and relatively severe course.		013.98587
Precursor Cell Lymphoblastic Leukemia-Lymphoma
A neoplasm characterized by abnormalities of the lymphoid cell precursors leading to excessive lymphoblasts in the marrow and other organs. It is the most common cancer in children and accounts for the vast majority of all childhood leukemias.		129.731,503366
Dry Eye
[description not available]		07.3110
Dry Eye Syndromes
Corneal and conjunctival dryness due to deficient tear production, predominantly in menopausal and post-menopausal women. Filamentary keratitis or erosion of the conjunctival and corneal epithelium may be caused by these disorders. Sensation of the presence of a foreign body in the eye and burning of the eyes may occur.		02.3110
Rupture, Spontaneous
Tear or break of an organ, vessel or other soft part of the body, occurring in the absence of external force.		05.29110
Local Neoplasm Recurrence
[description not available]		022.1744592
Malignant Melanoma
[description not available]		021.7510125
Cancer of Skin
[description not available]		018.2716024
Melanoma
A malignant neoplasm derived from cells that are capable of forming melanin, which may occur in the skin of any part of the body, in the eye, or, rarely, in the mucous membranes of the genitalia, anus, oral cavity, or other sites. It occurs mostly in adults and may originate de novo or from a pigmented nevus or malignant lentigo. Melanomas frequently metastasize widely, and the regional lymph nodes, liver, lungs, and brain are likely to be involved. The incidence of malignant skin melanomas is rising rapidly in all parts of the world. (Stedman, 25th ed; from Rook et al., Textbook of Dermatology, 4th ed, p2445)		121.4720250
Skin Neoplasms
Tumors or cancer of the SKIN.		120.2716024
Diabetes Mellitus
A heterogeneous group of disorders characterized by HYPERGLYCEMIA and GLUCOSE INTOLERANCE.		06.891
Eosinophilia, Tropical
[description not available]		013935
Acute Myelogenous Leukemia
[description not available]		014.19969
Eosinophilia
Abnormal increase of EOSINOPHILS in the blood, tissues or organs.		115935
Leukemia, Myeloid, Acute
Clonal expansion of myeloid blasts in bone marrow, blood, and other tissue. Myeloid leukemias develop from changes in cells that normally produce NEUTROPHILS; BASOPHILS; EOSINOPHILS; and MONOCYTES.		116.19969
Cancer of Liver
[description not available]		016.2422415
Liver Neoplasms
Tumors or cancer of the LIVER.		016.2422415
Hemorrhage, Retinal
[description not available]		03.4770
Day Blindness
[description not available]		03.3360
Retinal Diseases
Diseases involving the RETINA.		04.1250
Graft-Versus-Host Disease
[description not available]		015.829923
Graft vs Host Disease
The clinical entity characterized by anorexia, diarrhea, loss of hair, leukopenia, thrombocytopenia, growth retardation, and eventual death brought about by the GRAFT VS HOST REACTION.		117.829923
Chylopericardium
[description not available]		05.48130
Pericardial Effusion
Fluid accumulation within the PERICARDIUM. Serous effusions are associated with pericardial diseases. Hemopericardium is associated with trauma. Lipid-containing effusion (chylopericardium) results from leakage of THORACIC DUCT. Severe cases can lead to CARDIAC TAMPONADE.		05.48130
Bacteremia
The presence of viable bacteria circulating in the blood. Fever, chills, tachycardia, and tachypnea are common acute manifestations of bacteremia. The majority of cases are seen in already hospitalized patients, most of whom have underlying diseases or procedures which render their bloodstreams susceptible to invasion.		02.4110
Cancer of Rectum
[description not available]		09.891090
Intestinal Obstruction
Any impairment, arrest, or reversal of the normal flow of INTESTINAL CONTENTS toward the ANAL CANAL.		04.1350
Rectal Neoplasms
Tumors or cancer of the RECTUM.		111.891090
Urinary Retention
Inability to empty the URINARY BLADDER with voiding (URINATION).		02.4920
Anemia, Hypoplastic
[description not available]		03.4470
Anemia, Aplastic
A form of anemia in which the bone marrow fails to produce adequate numbers of peripheral blood elements.		03.4470
Cell Transformation, Neoplastic
Cell changes manifested by escape from control mechanisms, increased growth potential, alterations in the cell surface, karyotypic abnormalities, morphological and biochemical deviations from the norm, and other attributes conferring the ability to invade, metastasize, and kill.		013.29981
Leukemia, Pre-B-Cell
[description not available]		07.08280
Precursor B-Cell Lymphoblastic Leukemia-Lymphoma
A leukemia/lymphoma found predominately in children and adolescents and characterized by a high number of lymphoblasts and solid tumor lesions. Frequent sites involve LYMPH NODES, skin, and bones. It most commonly presents as leukemia.		07.08280
Low Bone Density
[description not available]		02.5420
Cherubism
A fibro-osseous hereditary disease of the jaws. The swollen jaws and raised eyes give a cherubic appearance; multiple radiolucencies are evident upon radiographic examination.		03.240
Bone Diseases, Metabolic
Diseases that affect the METABOLIC PROCESSES of BONE TISSUE.		02.5420
Diabetes Mellitus, Adult-Onset
[description not available]		08.04221
Diabetes Mellitus, Type 2
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.		08.04221
Anasarca
[description not available]		013.45549
Hemorrhage, Vitreous
[description not available]		02.4110
Edema
Abnormal fluid accumulation in TISSUES or body cavities. Most cases of edema are present under the SKIN in SUBCUTANEOUS TISSUE.		013.45549
Vitreous Hemorrhage
Hemorrhage into the VITREOUS BODY.		02.4110
Adenocarcinoma Of Kidney
[description not available]		012.04239
Cancer of Kidney
[description not available]		012.672911
Carcinoma, Renal Cell
A heterogeneous group of sporadic or hereditary carcinoma derived from cells of the KIDNEYS. There are several subtypes including the clear cells, the papillary, the chromophobe, the collecting duct, the spindle cells (sarcomatoid), or mixed cell-type carcinoma.		012.04239
Kidney Neoplasms
Tumors or cancers of the KIDNEY.		114.672911
Epiretinal Membrane
A membrane on the vitreal surface of the retina resulting from the proliferation of one or more of three retinal elements: (1) fibrous astrocytes; (2) fibrocytes; and (3) RETINAL PIGMENT EPITHELIUM. Localized epiretinal membranes may occur at the posterior pole of the eye without clinical signs or may cause marked loss of vision as a result of covering, distorting, or detaching the FOVEA CENTRALIS. Epiretinal membranes may cause vascular leakage and secondary retinal edema. In younger individuals some membranes appear to be developmental in origin and occur in otherwise normal eyes. The majority occur in association with RETINAL HOLES, ocular concussions, retinal inflammation, or after ocular surgery. (Newell, Ophthalmology: Principles and Concepts, 7th ed, p291)		02.3110
Neovascularization, Optic Disc
[description not available]		03.3360
Macular Holes
[description not available]		02.3110
Diabetic Retinopathy
Disease of the RETINA as a complication of DIABETES MELLITUS. It is characterized by the progressive microvascular complications, such as ANEURYSM, interretinal EDEMA, and intraocular PATHOLOGIC NEOVASCULARIZATION.		02.3110
Retinal Perforations
Perforations through the whole thickness of the retina including the macula as the result of inflammation, trauma, degeneration, etc. The concept includes retinal breaks, tears, dialyses, and holes.		02.3110
Retinal Neovascularization
Formation of new blood vessels originating from the retinal veins and extending along the inner (vitreal) surface of the retina.		03.3360
Complications, Parasitic Pregnancy
[description not available]		02.3110
Infections, Plasmodium
[description not available]		02.3110
Malaria
A protozoan disease caused in humans by four species of the PLASMODIUM genus: PLASMODIUM FALCIPARUM; PLASMODIUM VIVAX; PLASMODIUM OVALE; and PLASMODIUM MALARIAE; and transmitted by the bite of an infected female mosquito of the genus ANOPHELES. Malaria is endemic in parts of Asia, Africa, Central and South America, Oceania, and certain Caribbean islands. It is characterized by extreme exhaustion associated with paroxysms of high FEVER; SWEATING; shaking CHILLS; and ANEMIA. Malaria in ANIMALS is caused by other species of plasmodia.		02.3110
Pregnancy
The status during which female mammals carry their developing young (EMBRYOS or FETUSES) in utero before birth, beginning from FERTILIZATION to BIRTH.		013.829817
Cancer of Prostate
[description not available]		013.425711
Prostatic Neoplasms
Tumors or cancer of the PROSTATE.		115.425711
Carcinogenesis
The origin, production or development of cancer through genotypic and phenotypic changes which upset the normal balance between cell proliferation and cell death. Carcinogenesis generally requires a constellation of steps, which may occur quickly or over a period of many years.		010.84289
Chondrosarcoma, Mesenchymal
A rare aggressive variant of chondrosarcoma, characterized by a biphasic histologic pattern of small compact cells intermixed with islands of cartilaginous matrix. Mesenchymal chondrosarcomas have a predilection for flat bones; long tubular bones are rarely affected. They tend to occur in the younger age group and are highly metastatic. (DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1456)		02.4110
Schistosoma mansoni Infection
[description not available]		03.0640
Schistosomiasis mansoni
Schistosomiasis caused by Schistosoma mansoni. It is endemic in Africa, the Middle East, South America, and the Caribbean and affects mainly the bowel, spleen, and liver.		03.0640
Cancer of Esophagus
[description not available]		09.91332
Esophageal Neoplasms
Tumors or cancer of the ESOPHAGUS.		09.91332
Myeloproliferative Disorders
Conditions which cause proliferation of hemopoietically active tissue or of tissue which has embryonic hemopoietic potential. They all involve dysregulation of multipotent MYELOID PROGENITOR CELLS, most often caused by a mutation in the JAK2 PROTEIN TYROSINE KINASE.		115.051253
Congenital Limb Deformities
[description not available]		02.6920
Acro-Osteolysis
A condition with congenital and acquired forms causing recurrent ulcers in the fingers and toes. The congenital form exhibits autosomal dominant inheritance; the acquired form is found in workers who handle VINYL CHLORIDE. When acro-osteolysis is accompanied by generalized OSTEOPOROSIS and skull deformations, it is called HAJDU-CHENEY SYNDROME.		02.6920
Hutchinson Gilford Progeria Syndrome
[description not available]		02.6920
Abnormalities, Skin
[description not available]		03.420
Progeria
An abnormal congenital condition, associated with defects in the LAMIN TYPE A gene, which is characterized by premature aging in children, where all the changes of cell senescence occur. It is manifested by premature graying; hair loss; hearing loss (DEAFNESS); cataracts (CATARACT); ARTHRITIS; OSTEOPOROSIS; DIABETES MELLITUS; atrophy of subcutaneous fat; skeletal hypoplasia; elevated urinary HYALURONIC ACID; and accelerated ATHEROSCLEROSIS. Many affected individuals develop malignant tumors, especially SARCOMA.		02.6920
Skin Abnormalities
Congenital structural abnormalities of the skin.		03.420
Abdominal Aortic Aneurysm
[description not available]		03.9640
Aortic Aneurysm, Abdominal
An abnormal balloon- or sac-like dilatation in the wall of the ABDOMINAL AORTA which gives rise to the visceral, the parietal, and the terminal (iliac) branches below the aortic hiatus at the diaphragm.		03.9640
Digestive System Fistula
An abnormal passage communicating between any components of the digestive system, or between any part of the digestive system and surrounding organ(s).		02.3110
Autoimmune Thrombocytopenia
[description not available]		03.3160
Purpura, Thrombocytopenic, Idiopathic
Thrombocytopenia occurring in the absence of toxic exposure or a disease associated with decreased platelets. It is mediated by immune mechanisms, in most cases IMMUNOGLOBULIN G autoantibodies which attach to platelets and subsequently undergo destruction by macrophages. The disease is seen in acute (affecting children) and chronic (adult) forms.		03.3160
Cardiac Toxicity
[description not available]		06.54141
Cardiotoxicity
Damage to the HEART or its function secondary to exposure to toxic substances such as drugs used in CHEMOTHERAPY; IMMUNOTHERAPY; or RADIATION.		06.54141
Cancer of Colon
[description not available]		07.6280
Colonic Neoplasms
Tumors or cancer of the COLON.		19.6280
Cardiac Failure
[description not available]		015.625621
Heart Failure
A heterogeneous condition in which the heart is unable to pump out sufficient blood to meet the metabolic need of the body. Heart failure can be caused by structural defects, functional abnormalities (VENTRICULAR DYSFUNCTION), or a sudden overload beyond its capacity. Chronic heart failure is more common than acute heart failure which results from sudden insult to cardiac function, such as MYOCARDIAL INFARCTION.		015.625621
Cardiovascular Stroke
[description not available]		03.5370
Myocardial Infarction
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).		03.5370
Granulocytic Leukemia
[description not available]		013.72985
Leukemia, Myeloid
Form of leukemia characterized by an uncontrolled proliferation of the myeloid lineage and their precursors (MYELOID PROGENITOR CELLS) in the bone marrow and other sites.		013.72985
Chordoma
A malignant tumor arising from the embryonic remains of the notochord. It is also called chordocarcinoma, chordoepithelioma, and notochordoma. (Dorland, 27th ed)		09.48244
Desmoid
[description not available]		011.62278
Fibromatosis, Aggressive
A childhood counterpart of abdominal or extra-abdominal desmoid tumors, characterized by firm subcutaneous nodules that grow rapidly in any part of the body but do not metastasize. The adult form of abdominal fibromatosis is FIBROMATOSIS, ABDOMINAL. (Stedman, 25th ed)		113.62278
Hepatocellular Carcinoma
[description not available]		015.49347
Carcinoma, Hepatocellular
A primary malignant neoplasm of epithelial liver cells. It ranges from a well-differentiated tumor with EPITHELIAL CELLS indistinguishable from normal HEPATOCYTES to a poorly differentiated neoplasm. The cells may be uniform or markedly pleomorphic, or form GIANT CELLS. Several classification schemes have been suggested.		010.49347
Cancer of Pancreas
[description not available]		013.917813
Pancreatic Neoplasms
Tumors or cancer of the PANCREAS. Depending on the types of ISLET CELLS present in the tumors, various hormones can be secreted: GLUCAGON from PANCREATIC ALPHA CELLS; INSULIN from PANCREATIC BETA CELLS; and SOMATOSTATIN from the SOMATOSTATIN-SECRETING CELLS. Most are malignant except the insulin-producing tumors (INSULINOMA).		115.917813
Spinal Neoplasms
New abnormal growth of tissue in the SPINE.		07.7102
Thrombopenia
[description not available]		013.634321
Anemia
A reduction in the number of circulating ERYTHROCYTES or in the quantity of HEMOGLOBIN.		013.844319
Neutropenia
A decrease in the number of NEUTROPHILS found in the blood.		013.315730
Thrombocytopenia
A subnormal level of BLOOD PLATELETS.		013.634321
Diseases, Metabolic
[description not available]		06.0852
Metabolic Diseases
Generic term for diseases caused by an abnormal metabolic process. It can be congenital due to inherited enzyme abnormality (METABOLISM, INBORN ERRORS) or acquired due to disease of an endocrine organ or failure of a metabolically important organ such as the liver. (Stedman, 26th ed)		06.0852
Canine Diseases
[description not available]		07.21182
Acute Respiratory Distress Syndrome
[description not available]		013.243
Respiratory Distress Syndrome
A syndrome characterized by progressive life-threatening RESPIRATORY INSUFFICIENCY in the absence of known LUNG DISEASES, usually following a systemic insult such as surgery or major TRAUMA.		013.243
Chromosomal Translocation
[description not available]		019.341874
Lassitude
[description not available]		010.34197
Cramp
[description not available]		09.77123
Fatigue
The state of weariness following a period of exertion, mental or physical, characterized by a decreased capacity for work and reduced efficiency to respond to stimuli.		010.34197
Muscle Cramp
A sustained and usually painful contraction of muscle fibers. This may occur as an isolated phenomenon or as a manifestation of an underlying disease process (e.g., UREMIA; HYPOTHYROIDISM; MOTOR NEURON DISEASE; etc.). (From Adams et al., Principles of Neurology, 6th ed, p1398)		09.77123
Leukemia, Lymphoblastic, Acute, T Cell
[description not available]		06.3172
Precursor T-Cell Lymphoblastic Leukemia-Lymphoma
A leukemia/lymphoma found predominately in children and young adults and characterized LYMPHADENOPATHY and THYMUS GLAND involvement. It most frequently presents as a lymphoma, but a leukemic progression in the bone marrow is common.		18.3172
Genetic Predisposition
[description not available]		011.85473
Vitiligo
A disorder consisting of areas of macular depigmentation, commonly on extensor aspects of extremities, on the face or neck, and in skin folds. Age of onset is often in young adulthood and the condition tends to progress gradually with lesions enlarging and extending until a quiescent state is reached.		04.8470
Bednar Tumor
[description not available]		014.951003
Dermatofibrosarcoma
A sarcoma of the deep layers of the skin. The tumors are locally aggressive tends to recur but rarely metastatic. It can be classified into variants depending on the cell type tumors are derived from or by its characteristics: Pigmented variant from MELANIN-containing DERMAL DENDRITIC CELLS; Myxoid variant, myxoid STROMAL CELLS; Giant cell variant characterized by GIANT CELLS in the tumors; and Fibrosarcomatous variant chracterized by tumor areas histologically indistinguishable from FIBROSARCOMA.		116.951003
Enlarged Spleen
[description not available]		08.59241
Minimal Disease, Residual
[description not available]		019.518552
Adenopathy
[description not available]		02.4110
Chronic Lung Injury
[description not available]		02.8930
Edema, Pulmonary
[description not available]		06.4181
Pulmonary Edema
Excessive accumulation of extravascular fluid in the lung, an indication of a serious underlying disease or disorder. Pulmonary edema prevents efficient PULMONARY GAS EXCHANGE in the PULMONARY ALVEOLI, and can be life-threatening.		06.4181
Infections, Soft Tissue
[description not available]		02.4110
Soft Tissue Infections
Infections of non-skeletal tissue, i.e., exclusive of bone, ligaments, cartilage, and fibrous tissue. The concept is usually referred to as skin and soft tissue infections and usually subcutaneous and muscle tissue are involved. The predisposing factors in anaerobic infections are trauma, ischemia, and surgery. The organisms often derive from the fecal or oral flora, particularly in wounds associated with intestinal surgery, decubitus ulcer, and human bites. (From Cecil Textbook of Medicine, 19th ed, p1688)		02.4110
Epithelial Ovarian Cancer
[description not available]		02.6920
Cancer of Ovary
[description not available]		012.324311
Carcinoma, Ovarian Epithelial
A malignant neoplasm that originates in cells on the surface EPITHELIUM of the ovary and is the most common form of ovarian cancer. There are five histologic subtypes: papillary serous, endometrioid, mucinous, clear cell, and transitional cell. Mutations in BRCA1, OPCML, PRKN, PIK3CA, AKT1, CTNNB1, RRAS2, and CDH1 genes are associated with this cancer.		14.6920
Ovarian Neoplasms
Tumors or cancer of the OVARY. These neoplasms can be benign or malignant. They are classified according to the tissue of origin, such as the surface EPITHELIUM, the stromal endocrine cells, and the totipotent GERM CELLS.		114.324311
Hospital-Acquired Condition
[description not available]		02.7730
Leucocythaemia
[description not available]		015.631755
Endocarditis, Loeffler
[description not available]		017.542568
Leukemia
A progressive, malignant disease of the blood-forming organs, characterized by distorted proliferation and development of leukocytes and their precursors in the blood and bone marrow. Leukemias were originally termed acute or chronic based on life expectancy but now are classified according to cellular maturity. Acute leukemias consist of predominately immature cells; chronic leukemias are composed of more mature cells. (From The Merck Manual, 2006)		117.631755
Hypereosinophilic Syndrome
A heterogeneous group of disorders with the common feature of prolonged eosinophilia of unknown cause and associated organ system dysfunction, including the heart, central nervous system, kidneys, lungs, gastrointestinal tract, and skin. There is a massive increase in the number of EOSINOPHILS in the blood, mimicking leukemia, and extensive eosinophilic infiltration of the various organs.		119.542568
Licheniform Eruptions
[description not available]		06.41210
Dermatitis Medicamentosa
[description not available]		010.81721
Lichen Ruber Planus
[description not available]		03.3350
Lichen Planus
An inflammatory, pruritic disease of the skin and mucous membranes, which can be either generalized or localized. It is characterized by distinctive purplish, flat-topped papules having a predilection for the trunk and flexor surfaces. The lesions may be discrete or coalesce to form plaques. Histologically, there is a saw-tooth pattern of epidermal hyperplasia and vacuolar alteration of the basal layer of the epidermis along with an intense upper dermal inflammatory infiltrate composed predominantly of T-cells. Etiology is unknown.		08.3350
Angiogenesis, Pathologic
[description not available]		012.52701
Autoimmune Chronic Hepatitis
[description not available]		02.9840
Hepatitis, Infectious
[description not available]		02.4110
Hepatitis A
INFLAMMATION of the LIVER in humans caused by a member of the HEPATOVIRUS genus, HUMAN HEPATITIS A VIRUS. It can be transmitted through fecal contamination of food or water.		02.4110
Hepatitis, Autoimmune
A chronic self-perpetuating hepatocellular INFLAMMATION of unknown cause, usually with HYPERGAMMAGLOBULINEMIA and serum AUTOANTIBODIES.		02.9840
Agnogenic Myeloid Metaplasia
[description not available]		011.21404
Primary Myelofibrosis
A de novo myeloproliferation arising from an abnormal stem cell. It is characterized by the replacement of bone marrow by fibrous tissue, a process that is mediated by CYTOKINES arising from the abnormal clone.		113.21404
Ache
[description not available]		08.69145
Pain
An unpleasant sensation induced by noxious stimuli which are detected by NERVE ENDINGS of NOCICEPTIVE NEURONS.		08.69145
Heritable Pulmonary Arterial Hypertension
[description not available]		010.72175
Anoxemia
[description not available]		07.35212
Pulmonary Hypertension
[description not available]		021.269713
Pulmonary Arterial Hypertension
A progressive rare pulmonary disease characterized by high blood pressure in the PULMONARY ARTERY.		04.1340
Hypoxia
Sub-optimal OXYGEN levels in the ambient air of living organisms.		07.35212
Hypertension, Pulmonary
Increased VASCULAR RESISTANCE in the PULMONARY CIRCULATION, usually secondary to HEART DISEASES or LUNG DISEASES.		120.9719426
Familial Primary Pulmonary Hypertension
Familial or idiopathic hypertension in the PULMONARY CIRCULATION which is not secondary to other disease.		010.72175
Diarrhea
An increased liquidity or decreased consistency of FECES, such as running stool. Fecal consistency is related to the ratio of water-holding capacity of insoluble solids to total water, rather than the amount of water present. Diarrhea is not hyperdefecation or increased fecal weight.		018.253019
Leukocytosis
A transient increase in the number of leukocytes in a body fluid.		09.01201
Aortic Stenosis
[description not available]		02.4110
Calcification, Pathologic
[description not available]		02.5220
Aortic Valve Stenosis
A pathological constriction that can occur above (supravalvular stenosis), below (subvalvular stenosis), or at the AORTIC VALVE. It is characterized by restricted outflow from the LEFT VENTRICLE into the AORTA.		02.4110
Calcinosis
Pathologic deposition of calcium salts in tissues.		02.5220
Cancer of Intestines
[description not available]		09.23422
Intestinal Neoplasms
Tumors or cancer of the INTESTINES.		09.23422
Glial Cell Tumors
[description not available]		011.74317
Glioma
Benign and malignant central nervous system neoplasms derived from glial cells (i.e., astrocytes, oligodendrocytes, and ependymocytes). Astrocytes may give rise to astrocytomas (ASTROCYTOMA) or glioblastoma multiforme (see GLIOBLASTOMA). Oligodendrocytes give rise to oligodendrogliomas (OLIGODENDROGLIOMA) and ependymocytes may undergo transformation to become EPENDYMOMA; CHOROID PLEXUS NEOPLASMS; or colloid cysts of the third ventricle. (From Escourolle et al., Manual of Basic Neuropathology, 2nd ed, p21)		011.74317
Allergic Contact Dermatitis
[description not available]		02.4110
Dermatitis, Occupational
A recurrent contact dermatitis caused by substances found in the work place.		02.4110
Dermatitis, Allergic Contact
A contact dermatitis due to allergic sensitization to various substances. These substances subsequently produce inflammatory reactions in the skin of those who have acquired hypersensitivity to them as a result of prior exposure.		02.4110
Asthma, Bronchial
[description not available]		08.9112
Asthma
A form of bronchial disorder with three distinct components: airway hyper-responsiveness (RESPIRATORY HYPERSENSITIVITY), airway INFLAMMATION, and intermittent AIRWAY OBSTRUCTION. It is characterized by spasmodic contraction of airway smooth muscle, WHEEZING, and dyspnea (DYSPNEA, PAROXYSMAL).		110.9112
Pleural Effusion
Presence of fluid in the pleural cavity resulting from excessive transudation or exudation from the pleural surfaces. It is a sign of disease and not a diagnosis in itself.		015.62285
Hyperglycemia, Postprandial
Abnormally high BLOOD GLUCOSE level after a meal.		03.7490
Paraneoplastic Syndromes
In patients with neoplastic diseases a wide variety of clinical pictures which are indirect and usually remote effects produced by tumor cell metabolites or other products.		03.3360
Hyperglycemia
Abnormally high BLOOD GLUCOSE level.		08.7490
Dysplastic Nevus Syndrome, Hereditary
[description not available]		03.8830
Benign Meningeal Neoplasms
[description not available]		06.6873
Angioblastic Meningioma
[description not available]		06.6973
Corneal Angiogenesis
[description not available]		02.4110
Meningeal Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the meningeal coverings of the brain and spinal cord.		06.6873
Meningioma
A relatively common neoplasm of the CENTRAL NERVOUS SYSTEM that arises from arachnoidal cells. The majority are well differentiated vascular tumors which grow slowly and have a low potential to be invasive, although malignant subtypes occur. Meningiomas have a predilection to arise from the parasagittal region, cerebral convexity, sphenoidal ridge, olfactory groove, and SPINAL CANAL. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2056-7)		06.6973
Corneal Neovascularization
New blood vessels originating from the corneal blood vessels and extending from the limbus into the adjacent CORNEAL STROMA. Neovascularization in the superficial and/or deep corneal stroma is a sequel to numerous inflammatory diseases of the ocular anterior segment, such as TRACHOMA, viral interstitial KERATITIS, microbial KERATOCONJUNCTIVITIS, and the immune response elicited by CORNEAL TRANSPLANTATION.		02.4110
Hemorrhagic Thrombocythemia
[description not available]		06.49110
Thrombocythemia, Essential
A clinical syndrome characterized by repeated spontaneous hemorrhages and a remarkable increase in the number of circulating platelets.		06.49110
Erythrocytosis
[description not available]		04.9681
Hypermelanosis
[description not available]		08.32241
Hyperpigmentation
Excessive pigmentation of the skin, usually as a result of increased epidermal or dermal melanin pigmentation, hypermelanosis. Hyperpigmentation can be localized or generalized. The condition may arise from exposure to light, chemicals or other substances, or from a primary metabolic imbalance.		08.32241
Electron Transport Chain Deficiencies, Mitochondrial
[description not available]		02.4110
Inborn Errors of Metabolism
[description not available]		02.4110
Metabolism, Inborn Errors
Errors in metabolic processes resulting from inborn genetic mutations that are inherited or acquired in utero.		02.4110
Mitochondrial Diseases
Diseases caused by abnormal function of the MITOCHONDRIA. They may be caused by mutations, acquired or inherited, in mitochondrial DNA or in nuclear genes that code for mitochondrial components. They may also be the result of acquired mitochondria dysfunction due to adverse effects of drugs, infections, or other environmental causes.		02.4110
Margins of Excision
The edges of tissue removed in a surgery for assessment of the effectiveness of a surgical procedure in achieving the local control of a neoplasm and the adequacy of tumor removal. When the margin is negative or not involved by tumor (e.g., CANCER) it suggests all of the tumor has been removed by the surgery.		05.0770
Cardiovascular Diseases
Pathological conditions involving the CARDIOVASCULAR SYSTEM including the HEART; the BLOOD VESSELS; or the PERICARDIUM.		016.656044
Cirrhosis
[description not available]		013.28635
Active Hyperemia
[description not available]		02.4110
Fibrosis
Any pathological condition where fibrous connective tissue invades any organ, usually as a consequence of inflammation or other injury.		013.28635
Hyperemia
The presence of an increased amount of blood in a body part or an organ leading to congestion or engorgement of blood vessels. Hyperemia can be due to increase of blood flow into the area (active or arterial), or due to obstruction of outflow of blood from the area (passive or venous).		02.4110
Pulmonary Arterial Remodeling
[description not available]		03.460
Acute Brain Injuries
[description not available]		02.8630
Brain Hemorrhage, Cerebral
[description not available]		03.6280
Brain Injuries
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.		02.8630
Cerebral Hemorrhage
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.		03.6280
Hematologic Malignancies
[description not available]		017.14473
Hematologic Neoplasms
Neoplasms located in the blood and blood-forming tissue (the bone marrow and lymphatic tissue). The commonest forms are the various types of LEUKEMIA, of LYMPHOMA, and of the progressive, life-threatening forms of the MYELODYSPLASTIC SYNDROMES.		012.14473
Hyperkeratosis Palmaris et Plantaris
[description not available]		04.150
Blood Diseases
[description not available]		010.72203
Hematologic Diseases
Disorders of the blood and blood forming tissues.		010.72203
Cancer of Pituitary
[description not available]		02.610
Pituitary Neoplasms
Neoplasms which arise from or metastasize to the PITUITARY GLAND. The majority of pituitary neoplasms are adenomas, which are divided into non-secreting and secreting forms. Hormone producing forms are further classified by the type of hormone they secrete. Pituitary adenomas may also be characterized by their staining properties (see ADENOMA, BASOPHIL; ADENOMA, ACIDOPHIL; and ADENOMA, CHROMOPHOBE). Pituitary tumors may compress adjacent structures, including the HYPOTHALAMUS, several CRANIAL NERVES, and the OPTIC CHIASM. Chiasmal compression may result in bitemporal HEMIANOPSIA.		02.610
Body Weight
The mass or quantity of heaviness of an individual. It is expressed by units of pounds or kilograms.		09.35214
Depression
Depressive states usually of moderate intensity in contrast with MAJOR DEPRESSIVE DISORDER present in neurotic and psychotic disorders.		09.2760
Cirrhosis, Liver
[description not available]		06.89231
Liver Cirrhosis
Liver disease in which the normal microcirculation, the gross vascular anatomy, and the hepatic architecture have been variably destroyed and altered with fibrous septa surrounding regenerated or regenerating parenchymal nodules.		06.89231
Myofibromatosis
A condition characterized by multiple formations of myofibromas (LEIOMYOMA).		03.8790
Diabetic Glomerulosclerosis
[description not available]		02.9840
Diabetic Nephropathies
KIDNEY injuries associated with diabetes mellitus and affecting KIDNEY GLOMERULUS; ARTERIOLES; KIDNEY TUBULES; and the interstitium. Clinical signs include persistent PROTEINURIA, from microalbuminuria progressing to ALBUMINURIA of greater than 300 mg/24 h, leading to reduced GLOMERULAR FILTRATION RATE and END-STAGE RENAL DISEASE.		02.9840
Aura
[description not available]		02.8330
Absence Seizure
[description not available]		02.8530
Absence Status
[description not available]		02.610
Epilepsy
A disorder characterized by recurrent episodes of paroxysmal brain dysfunction due to a sudden, disorderly, and excessive neuronal discharge. Epilepsy classification systems are generally based upon: (1) clinical features of the seizure episodes (e.g., motor seizure), (2) etiology (e.g., post-traumatic), (3) anatomic site of seizure origin (e.g., frontal lobe seizure), (4) tendency to spread to other structures in the brain, and (5) temporal patterns (e.g., nocturnal epilepsy). (From Adams et al., Principles of Neurology, 6th ed, p313)		02.8330
Seizures
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or seizure disorder.		02.8530
Status Epilepticus
A prolonged seizure or seizures repeated frequently enough to prevent recovery between episodes occurring over a period of 20-30 minutes. The most common subtype is generalized tonic-clonic status epilepticus, a potentially fatal condition associated with neuronal injury and respiratory and metabolic dysfunction. Nonconvulsive forms include petit mal status and complex partial status, which may manifest as behavioral disturbances. Simple partial status epilepticus consists of persistent motor, sensory, or autonomic seizures that do not impair cognition (see also EPILEPSIA PARTIALIS CONTINUA). Subclinical status epilepticus generally refers to seizures occurring in an unresponsive or comatose individual in the absence of overt signs of seizure activity. (From N Engl J Med 1998 Apr 2;338(14):970-6; Neurologia 1997 Dec;12 Suppl 6:25-30)		02.610
Infections, Coronavirus
[description not available]		013.452311
Pneumonia, Viral
Inflammation of the lung parenchyma that is caused by a viral infection.		013.452311
Coronavirus Infections
Virus diseases caused by the CORONAVIRUS genus. Some specifics include transmissible enteritis of turkeys (ENTERITIS, TRANSMISSIBLE, OF TURKEYS); FELINE INFECTIOUS PERITONITIS; and transmissible gastroenteritis of swine (GASTROENTERITIS, TRANSMISSIBLE, OF SWINE).		013.452311
Cicatrization
The formation of fibrous tissue in the place of normal tissue during the process of WOUND HEALING. It includes scar tissue formation occurring in healing internal organs as well as in the skin after surface injuries.		02.4110
Dermatosclerosis
[description not available]		04.88120
Angioma, Sclerosing
[description not available]		02.8530
Cicatrix
The fibrous tissue that replaces normal tissue during the process of WOUND HEALING.		02.4110
Scleroderma, Localized
A term used to describe a variety of localized asymmetrical SKIN thickening that is similar to those of SYSTEMIC SCLERODERMA but without the disease features in the multiple internal organs and BLOOD VESSELS. Lesions may be characterized as patches or plaques (morphea), bands (linear), or nodules.		18.01240
Histiocytoma, Benign Fibrous
A benign tumor composed, wholly or in part, of cells with the morphologic characteristics of HISTIOCYTES and with various fibroblastic components. Fibrous histiocytomas can occur anywhere in the body. When they occur in the skin, they are called dermatofibromas or sclerosing hemangiomas. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 5th ed, p1747)		02.8530
Cutaneous Fistula
An abnormal passage or communication leading from an internal organ to the surface of the body.		02.4820
Cancer of Larynx
[description not available]		02.6120
Diseases of Pharynx
[description not available]		02.4110
Complication, Postoperative
[description not available]		05.63161
Laryngeal Neoplasms
Cancers or tumors of the LARYNX or any of its parts: the GLOTTIS; EPIGLOTTIS; LARYNGEAL CARTILAGES; LARYNGEAL MUSCLES; and VOCAL CORDS.		02.6120
Postoperative Complications
Pathologic processes that affect patients after a surgical procedure. They may or may not be related to the disease for which the surgery was done, and they may or may not be direct results of the surgery.		05.63161
Hematochezia
The passage of bright red blood from the rectum. The blood may or may not be mixed with formed stool in the form of blood, blood clots, bloody stool or diarrhea.		09.22291
Gastrointestinal Hemorrhage
Bleeding in any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM.		09.22291
Diffuse Mixed Small and Large Cell Lymphoma
[description not available]		07.09101
Lymphoma, Non-Hodgkin
Any of a group of malignant tumors of lymphoid tissue that differ from HODGKIN DISEASE, being more heterogeneous with respect to malignant cell lineage, clinical course, prognosis, and therapy. The only common feature among these tumors is the absence of giant REED-STERNBERG CELLS, a characteristic of Hodgkin's disease.		19.09101
Mast-Cell Leukemia
[description not available]		05.29170
Leukemia, Mast-Cell
A form of systemic mastocytosis (MASTOCYTOSIS, SYSTEMIC) characterized by the presence of large numbers of tissue MAST CELLS in the peripheral blood without skin lesions. It is a high-grade LEUKEMIA disease with bone marrow smear of		05.29170
Carcinoma, Ductal, Pancreatic
[description not available]		06.38111
Carcinoma, Pancreatic Ductal
Carcinoma that arises from the PANCREATIC DUCTS. It accounts for the majority of cancers derived from the PANCREAS.		06.38111
Eczema, Atopic
[description not available]		03.5240
Dermatitis, Atopic
A chronic inflammatory genetically determined disease of the skin marked by increased ability to form reagin (IgE), with increased susceptibility to allergic rhinitis and asthma, and hereditary disposition to a lowered threshold for pruritus. It is manifested by lichenification, excoriation, and crusting, mainly on the flexural surfaces of the elbow and knee. In infants it is known as infantile eczema.		03.5240
Aggressive Systemic Mastocytosis
A form of systemic mastocytosis in which patients have impaired organ functions due to multifocal infiltrates of pathological MAST CELLS in bone marrow, liver, spleen, gastrointestinal tract, or skeletal system. The cytomorphology shows a low to high grade.		013.08683
Mast Cell Activation Disease
[description not available]		011.22301
Mastocytosis
A rare neoplastic disorder characterized by a clonal proliferation of MAST CELLS, associated with KIT-D816 mutations, and accompanied by aberrant mast cell activation. The abnormal increase of MAST CELLS may occur in only the skin (MASTOCYTOSIS, CUTANEOUS), in extracutaneous tissues involving multiple organs (MASTOCYTOSIS, SYSTEMIC), or in solid tumors (MASTOCYTOMA).		011.22301
Mastocytosis, Systemic
A group of disorders caused by the abnormal proliferation of MAST CELLS in a variety of extracutaneous tissues including bone marrow, liver, spleen, lymph nodes, and gastrointestinal tract. Systemic mastocytosis is commonly seen in adults. These diseases are categorized on the basis of clinical features, pathologic findings, and prognosis.		013.08683
Respiration Disorders
Diseases of the respiratory system in general or unspecified or for a specific respiratory disease not available.		03.5240
Cardiac Tamponade
Compression of the heart by accumulated fluid (PERICARDIAL EFFUSION) or blood (HEMOPERICARDIUM) in the PERICARDIUM surrounding the heart. The affected cardiac functions and CARDIAC OUTPUT can range from minimal to total hemodynamic collapse.		08.4560
Lung Injury, Acute
[description not available]		07.7891
Acute Lung Injury
A condition of lung damage that is characterized by bilateral pulmonary infiltrates (PULMONARY EDEMA) rich in NEUTROPHILS, and in the absence of clinical HEART FAILURE. This can represent a spectrum of pulmonary lesions, endothelial and epithelial, due to numerous factors (physical, chemical, or biological).		07.7891
Fibroepithelial Neoplasms
[description not available]		03.5240
Cystosarcoma Phyllodes
[description not available]		03.5240
Injury, Myocardial Reperfusion
[description not available]		02.6320
Sclerosis
A pathological process consisting of hardening or fibrosis of an anatomical structure, often a vessel or a nerve.		06.9582
Gastric Volvulus
[description not available]		02.610
Insulin Sensitivity
[description not available]		05.47141
Insulin Resistance
Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS.		010.47141
Epulides, Giant Cell
[description not available]		03.6930
Granuloma, Giant Cell
A non-neoplastic inflammatory lesion, usually of the jaw or gingiva, containing large, multinucleated cells. It includes reparative giant cell granuloma. Peripheral giant cell granuloma refers to the gingiva (giant cell epulis); central refers to the jaw.		03.6930
Cancer of the Thyroid
[description not available]		011.01285
Thyroid Neoplasms
Tumors or cancer of the THYROID GLAND.		113.01285
Abnormalities, Autosome
[description not available]		016.6713312
Neoplasms, Cystic, Mucinous, and Serous
Neoplasms containing cyst-like formations or producing mucin or serum.		02.610
Acute Kidney Failure
[description not available]		04.14150
Acute Kidney Injury
Abrupt reduction in kidney function. Acute kidney injury encompasses the entire spectrum of the syndrome including acute kidney failure; ACUTE KIDNEY TUBULAR NECROSIS; and other less severe conditions.		04.14150
Kahler Disease
[description not available]		010341
Multiple Myeloma
A malignancy of mature PLASMA CELLS engaging in monoclonal immunoglobulin production. It is characterized by hyperglobulinemia, excess Bence-Jones proteins (free monoclonal IMMUNOGLOBULIN LIGHT CHAINS) in the urine, skeletal destruction, bone pain, and fractures. Other features include ANEMIA; HYPERCALCEMIA; and RENAL INSUFFICIENCY.		010341
22q11.2 Deletion Syndrome
[description not available]		02.610
DiGeorge Syndrome
Congenital syndrome characterized by a wide spectrum of characteristics including the absence of the THYMUS and PARATHYROID GLANDS resulting in T-cell immunodeficiency, HYPOCALCEMIA, defects in the outflow tract of the heart, and craniofacial anomalies.		02.610
Hepatitis B Virus Infection
[description not available]		08.5894
Hepatitis B
INFLAMMATION of the LIVER in humans caused by a member of the ORTHOHEPADNAVIRUS genus, HEPATITIS B VIRUS. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.		013.5894
B-Cell Chronic Lymphocytic Leukemia
[description not available]		011.36371
Leukemia, Lymphocytic, Chronic, B-Cell
A chronic leukemia characterized by abnormal B-lymphocytes and often generalized lymphadenopathy. In patients presenting predominately with blood and bone marrow involvement it is called chronic lymphocytic leukemia (CLL); in those predominately with enlarged lymph nodes it is called small lymphocytic lymphoma. These terms represent spectrums of the same disease.		011.36371
Adenocarcinoma, Basal Cell
[description not available]		013.1507
Cancer of Duodenum
[description not available]		06.96370
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		013.1507
Neuroendocrine Tumors
Tumors whose cells possess secretory granules and originate from the neuroectoderm, i.e., the cells of the ectoblast or epiblast that program the neuroendocrine system. Common properties across most neuroendocrine tumors include ectopic hormone production (often via APUD CELLS), the presence of tumor-associated antigens, and isozyme composition.		06.2280
Chronic Kidney Diseases
[description not available]		08.36104
Renal Insufficiency, Chronic
Conditions in which the KIDNEYS perform below the normal level for more than three months. Chronic kidney insufficiency is classified by five stages according to the decline in GLOMERULAR FILTRATION RATE and the degree of kidney damage (as measured by the level of PROTEINURIA). The most severe form is the end-stage renal disease (CHRONIC KIDNEY FAILURE). (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002)		08.36104
Cytokine Release Syndrome
A severe immune reaction characterized by excessive release of CYTOKINES. Symptoms include DYSPNEA; FEVER; HEADACHE; HYPOTENSION; NAUSEA; RASH; TACHYCARDIA; HYPOXIA; HYPERFERRITINEMIA, and MULTIPLE ORGAN FAILURE. It is associated with viral infections, SEPSIS; AUTOIMMUNE DISEASES and a variety of factors used in IMMUNOTHERAPY.		02.610
Brain Hemorrhage
[description not available]		03.7230
Intracranial Hemorrhages
Bleeding within the SKULL, including hemorrhages in the brain and the three membranes of MENINGES. The escape of blood often leads to the formation of HEMATOMA in the cranial epidural, subdural, and subarachnoid spaces.		03.7230
Familial Turner Syndrome
[description not available]		02.610
Mandibular Diseases
Diseases involving the MANDIBLE.		02.5320
Noonan Syndrome
A genetically heterogeneous, multifaceted disorder characterized by short stature, webbed neck, ptosis, skeletal malformations, hypertelorism, hormonal imbalance, CRYPTORCHIDISM, multiple cardiac abnormalities (most commonly including PULMONARY VALVE STENOSIS), and some degree of INTELLECTUAL DISABILITY. The phenotype bears similarities to that of TURNER SYNDROME that occurs only in females and has its basis in a 45, X karyotype abnormality. Noonan syndrome occurs in both males and females with a normal karyotype (46,XX and 46,XY). Mutations in a several genes (PTPN11, KRAS, SOS1, NF1 and RAF1) have been associated the NS phenotype. Mutations in PTPN11 are the most common. LEOPARD SYNDROME, a disorder that has clinical features overlapping those of Noonan Syndrome, is also due to mutations in PTPN11. In addition, there is overlap with the syndrome called neurofibromatosis-Noonan syndrome due to mutations in NF1.		02.610
Palmoplantaris Pustulosis
[description not available]		04.68100
Dermatoses
[description not available]		013.04336
Psoriasis
A common genetically determined, chronic, inflammatory skin disease characterized by rounded erythematous, dry, scaling patches. The lesions have a predilection for nails, scalp, genitalia, extensor surfaces, and the lumbosacral region. Accelerated epidermopoiesis is considered to be the fundamental pathologic feature in psoriasis.		09.68100
Skin Diseases
Diseases involving the DERMIS or EPIDERMIS.		013.04336
Colitis Gravis
[description not available]		03.6580
Colitis
Inflammation of the COLON section of the large intestine (INTESTINE, LARGE), usually with symptoms such as DIARRHEA (often with blood and mucus), ABDOMINAL PAIN, and FEVER.		05.6661
Colitis, Ulcerative
Inflammation of the COLON that is predominantly confined to the MUCOSA. Its major symptoms include DIARRHEA, rectal BLEEDING, the passage of MUCUS, and ABDOMINAL PAIN.		03.6580
Thyroid Diseases
Pathological processes involving the THYROID GLAND.		05.0931
Carcinoma, Non-Small Cell Lung
[description not available]		010.78334
Cancer of Lung
[description not available]		017.5614816
Carcinoma, Non-Small-Cell Lung
A heterogeneous aggregate of at least three distinct histological types of lung cancer, including SQUAMOUS CELL CARCINOMA; ADENOCARCINOMA; and LARGE CELL CARCINOMA. They are dealt with collectively because of their shared treatment strategy.		112.78334
Lung Neoplasms
Tumors or cancer of the LUNG.		119.5614816
Hemangioma, Capillary
A dull red, firm, dome-shaped hemangioma, sharply demarcated from surrounding skin, usually located on the head and neck, which grows rapidly and generally undergoes regression and involution without scarring. It is caused by proliferation of immature capillary vessels in active stroma, and is usually present at birth or occurs within the first two or three months of life. (Dorland, 27th ed)		03.7830
Pulmonary Veno Occlusive Disease
[description not available]		05.870
Pulmonary Veno-Occlusive Disease
Pathological process resulting in the fibrous obstruction of the small- and medium-sized PULMONARY VEINS and PULMONARY HYPERTENSION. Veno-occlusion can arise from fibrous proliferation of the VASCULAR INTIMA and VASCULAR MEDIA; THROMBOSIS; or a combination of both.		17.870
Hepatitis, Viral, Non-A, Non-B, Parenterally-Transmitted
[description not available]		02.8130
HIV Coinfection
[description not available]		06.86101
Hepatitis C
INFLAMMATION of the LIVER in humans caused by HEPATITIS C VIRUS, a single-stranded RNA virus. Its incubation period is 30-90 days. Hepatitis C is transmitted primarily by contaminated blood parenterally and is often associated with transfusion and intravenous drug abuse. However, in a significant number of cases, the source of hepatitis C infection is unknown.		02.8130
HIV Infections
Includes the spectrum of human immunodeficiency virus infections that range from asymptomatic seropositivity, thru AIDS-related complex (ARC), to acquired immunodeficiency syndrome (AIDS).		06.86101
Idiopathic Inflammatory Myopathies
[description not available]		02.610
Myositis
Inflammation of a muscle or muscle tissue.		02.610
Adenoma Sebaceum
Facial ANGIOFIBROMA in tuberous sclerosis		02.7630
Tuberous Sclerosis
Autosomal dominant neurocutaneous syndrome classically characterized by MENTAL RETARDATION; EPILEPSY; and skin lesions (e.g., adenoma sebaceum and hypomelanotic macules). There is, however, considerable heterogeneity in the neurologic manifestations. It is also associated with cortical tuber and HAMARTOMAS formation throughout the body, especially the heart, kidneys, and eyes. Mutations in two loci TSC1 and TSC2 that encode hamartin and tuberin, respectively, are associated with the disease.		02.7630
Angiomyolipoma
A benign tumor containing vascular, adipose, and muscle elements. It occurs most often in the kidney with smooth muscle elements (angiolipoleiomyoma) in association with tuberous sclerosis. (Dorland, 27th ed)		02.8130
Granulomas
[description not available]		03.7530
Granuloma
A relatively small nodular inflammatory lesion containing grouped mononuclear phagocytes, caused by infectious and noninfectious agents.		03.7530
Lymphomatoid Papulosis
Clinically benign, histologically malignant, recurrent cutaneous T-cell lymphoproliferative disorder characterized by an infiltration of large atypical cells surrounded by inflammatory cells. The atypical cells resemble REED-STERNBERG CELLS of HODGKIN DISEASE or the malignant cells of CUTANEOUS T-CELL LYMPHOMA. In some cases, lymphomatoid papulosis progresses to lymphomatous conditions including MYCOSIS FUNGOIDES; HODGKIN DISEASE; CUTANEOUS T-CELL LYMPHOMA; or ANAPLASTIC LARGE-CELL LYMPHOMA.		03.3360
Dysmyelopoietic Syndromes
[description not available]		010.61471
Myelodysplastic Syndromes
Clonal hematopoietic stem cell disorders characterized by dysplasia in one or more hematopoietic cell lineages. They predominantly affect patients over 60, are considered preleukemic conditions, and have high probability of transformation into ACUTE MYELOID LEUKEMIA.		015.61471
Kidney Failure
A severe irreversible decline in the ability of kidneys to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism.		03.3160
Neointima
The new and thickened layer of scar tissue that forms on a PROSTHESIS, or as a result of vessel injury especially following ANGIOPLASTY or stent placement.		02.8220
Constriction, Pathological
[description not available]		04.5551
Fistula
Abnormal communication most commonly seen between two internal organs, or between an internal organ and the surface of the body.		02.610
Constriction, Pathologic
The condition of an anatomical structure's being constricted beyond normal dimensions.		04.5551
Hyperplasia
An increase in the number of cells in a tissue or organ without tumor formation. It differs from HYPERTROPHY, which is an increase in bulk without an increase in the number of cells.		010.39131
Renal Insufficiency
Conditions in which the KIDNEYS perform below the normal level in the ability to remove wastes, concentrate URINE, and maintain ELECTROLYTE BALANCE; BLOOD PRESSURE; and CALCIUM metabolism. Renal insufficiency can be classified by the degree of kidney damage (as measured by the level of PROTEINURIA) and reduction in GLOMERULAR FILTRATION RATE.		03.3160
Bladder Cancer
[description not available]		04.8671
Bilharziasis
[description not available]		02.610
Urinary Bladder Neoplasms
Tumors or cancer of the URINARY BLADDER.		04.8671
Carcinoma, Transitional Cell
A malignant neoplasm derived from TRANSITIONAL EPITHELIAL CELLS, occurring chiefly in the URINARY BLADDER; URETERS; or RENAL PELVIS.		02.610
Schistosomiasis
Infection with flukes (trematodes) of the genus SCHISTOSOMA. Three species produce the most frequent clinical diseases: SCHISTOSOMA HAEMATOBIUM (endemic in Africa and the Middle East), SCHISTOSOMA MANSONI (in Egypt, northern and southern Africa, some West Indies islands, northern 2/3 of South America), and SCHISTOSOMA JAPONICUM (in Japan, China, the Philippines, Celebes, Thailand, Laos). S. mansoni is often seen in Puerto Ricans living in the United States.		02.610
Exanthem
[description not available]		011.67347
Exanthema
Diseases in which skin eruptions or rashes are a prominent manifestation. Classically, six such diseases were described with similar rashes; they were numbered in the order in which they were reported. Only the fourth (Duke's disease), fifth (ERYTHEMA INFECTIOSUM), and sixth (EXANTHEMA SUBITUM) numeric designations survive as occasional synonyms in current terminology.		011.67347
chronic COVID syndrome
[description not available]		02.610
Chylothorax
The presence of chyle in the thoracic cavity. (Dorland, 27th ed)		02.6320
Colonic Inertia
Symptom characterized by the passage of stool once a week or less.		03.9911
Constipation
Infrequent or difficult evacuation of FECES. These symptoms are associated with a variety of causes, including low DIETARY FIBER intake, emotional or nervous disturbances, systemic and structural disorders, drug-induced aggravation, and infections.		03.9911
Bile Duct Obstruction
[description not available]		02.7930
Liver Dysfunction
[description not available]		011.61102
Cholestasis
Impairment of bile flow due to obstruction in small bile ducts (INTRAHEPATIC CHOLESTASIS) or obstruction in large bile ducts (EXTRAHEPATIC CHOLESTASIS).		02.7930
Liver Diseases
Pathological processes of the LIVER.		06.61102
Peritoneal Carcinomatosis
[description not available]		013.84759
Peritoneal Neoplasms
Tumors or cancer of the PERITONEUM.		115.84759
Itching
[description not available]		04.2760
Pruritus
An intense itching sensation that produces the urge to rub or scratch the skin to obtain relief.		04.2760
Libman-Sacks Disease
[description not available]		03.0240
Lupus Erythematosus, Systemic
A chronic, relapsing, inflammatory, and often febrile multisystemic disorder of connective tissue, characterized principally by involvement of the skin, joints, kidneys, and serosal membranes. It is of unknown etiology, but is thought to represent a failure of the regulatory mechanisms of the autoimmune system. The disease is marked by a wide range of system dysfunctions, an elevated erythrocyte sedimentation rate, and the formation of LE cells in the blood or bone marrow.		03.0240
Cutaneous Mastocytosis
[description not available]		010.2160
Blood Clot
[description not available]		015.794837
Thrombosis
Formation and development of a thrombus or blood clot in the blood vessel.		015.794837
Esophageal Hernia
[description not available]		02.2110
Complication, Intraoperative
[description not available]		03.0640
Alveolitis, Fibrosing
[description not available]		09.77271
Sclerosis, Systemic
[description not available]		013.55563
Pulmonary Fibrosis
A process in which normal lung tissues are progressively replaced by FIBROBLASTS and COLLAGEN causing an irreversible loss of the ability to transfer oxygen into the bloodstream via PULMONARY ALVEOLI. Patients show progressive DYSPNEA finally resulting in death.		09.77271
Scleroderma, Systemic
A chronic multi-system disorder of CONNECTIVE TISSUE. It is characterized by SCLEROSIS in the SKIN, the LUNGS, the HEART, the GASTROINTESTINAL TRACT, the KIDNEYS, and the MUSCULOSKELETAL SYSTEM. Other important features include diseased small BLOOD VESSELS and AUTOANTIBODIES. The disorder is named for its most prominent feature (hard skin), and classified into subsets by the extent of skin thickening: LIMITED SCLERODERMA and DIFFUSE SCLERODERMA.		115.55563
Cholera Infantum
[description not available]		010.39126
Metastase
[description not available]		018.6317430
Neoplasm Metastasis
The transfer of a neoplasm from one organ or part of the body to another remote from the primary site.		018.6317430
Ewing Sarcoma
[description not available]		012.2192
Sarcoma, Ewing
A malignant tumor of the bone which always arises in the medullary tissue, occurring more often in cylindrical bones. The tumor occurs usually before the age of 20, about twice as frequently in males as in females.		07.2192
Drug Withdrawal Symptoms
[description not available]		05.5151
Substance Withdrawal Syndrome
Physiological and psychological symptoms associated with withdrawal from the use of a drug after prolonged administration or habituation. The concept includes withdrawal from smoking or drinking, as well as withdrawal from an administered drug.		05.5151
Bowel Diseases, Inflammatory
[description not available]		03.8821
Inflammatory Bowel Diseases
Chronic, non-specific inflammation of the GASTROINTESTINAL TRACT. Etiology may be genetic or environmental. This term includes CROHN DISEASE and ULCERATIVE COLITIS.		03.8821
Fibrous Histiocytoma of Tendon Sheath
[description not available]		04.0740
Sarcoma, Epithelioid
[description not available]		019.1412816
Giant Cell Tumor of Tendon Sheath
A tumor arising in the SYNOVIAL MEMBRANE; SYNOVIAL BURSA; or TENDON sheath. It is characterized by OSTEOCLAST-like GIANT CELLS; FOAM CELLS; pigmented HEMOSIDERIN-laden MACROPHAGES and inflammatory infiltrate. It is classified either as diffuse or localized tenosynovitis.		04.0740
Sarcoma
A connective tissue neoplasm formed by proliferation of mesodermal cells; it is usually highly malignant.		121.1412816
Soft Tissue Neoplasms
Neoplasms of whatever cell type or origin, occurring in the extraskeletal connective tissue framework of the body including the organs of locomotion and their various component structures, such as nerves, blood vessels, lymphatics, etc.		010.61221
Chloroma
[description not available]		05140
Sarcoma, Myeloid
An extramedullary tumor of immature MYELOID CELLS or MYELOBLASTS. Granulocytic sarcoma usually occurs with or follows the onset of ACUTE MYELOID LEUKEMIA.		05140
Algodystrophic Syndrome
[description not available]		02.2510
Bone Diseases
Diseases of BONES.		04.5651
Reflex Sympathetic Dystrophy
A syndrome characterized by severe burning pain in an extremity accompanied by sudomotor, vasomotor, and trophic changes in bone without an associated specific nerve injury. This condition is most often precipitated by trauma to soft tissue or nerve complexes. The skin over the affected region is usually erythematous and demonstrates hypersensitivity to tactile stimuli and erythema. (Adams et al., Principles of Neurology, 6th ed, p1360; Pain 1995 Oct;63(1):127-33)		02.2510
ATLL
[description not available]		03.5480
Leukemia-Lymphoma, Adult T-Cell
Aggressive T-Cell malignancy with adult onset, caused by HUMAN T-LYMPHOTROPIC VIRUS 1. It is endemic in Japan, the Caribbean basin, Southeastern United States, Hawaii, and parts of Central and South America and sub-Saharan Africa.		03.5480
Hemorrhage, Uterine
[description not available]		02.2110
Cancer of the Vagina
[description not available]		05.0890
Uterine Hemorrhage
Bleeding from blood vessels in the UTERUS, sometimes manifested as vaginal bleeding.		02.2110
Vaginal Neoplasms
Tumors or cancer of the VAGINA.		05.0890
Female Genital Neoplasms
[description not available]		03.8840
Genital Neoplasms, Female
Tumor or cancer of the female reproductive tract (GENITALIA, FEMALE).		03.8840
Nail Diseases
Diseases of the nail plate and tissues surrounding it. The concept is limited to primates.		08.29160
Incontinentia Pigmenti Achromians
[description not available]		05.9991
Bleeding
[description not available]		012.24211
Hemorrhage
Bleeding or escape of blood from a vessel.		07.24211
Thromboembolism
Obstruction of a blood vessel (embolism) by a blood clot (THROMBUS) in the blood stream.		02.4920
Stunted Growth
[description not available]		07.22112
Growth Disorders
Deviations from the average values for a specific age and sex in any or all of the following: height, weight, skeletal proportions, osseous development, or maturation of features. Included here are both acceleration and retardation of growth.		07.22112
Choroid Neovascularization
[description not available]		02.6120
Hypertriglyceridemia
A condition of elevated levels of TRIGLYCERIDES in the blood.		02.2110
B-Cell Lymphoma
[description not available]		010.2580
Lymphoma, B-Cell
A group of heterogeneous lymphoid tumors generally expressing one or more B-cell antigens or representing malignant transformations of B-lymphocytes.		05.2580
ER-Negative PR-Negative HER2-Negative Breast Cancer
[description not available]		03.0440
Invasiveness, Neoplasm
[description not available]		012.5602
Triple Negative Breast Neoplasms
Breast neoplasms that do not express ESTROGEN RECEPTORS; PROGESTERONE RECEPTORS; and do not overexpress the NEU RECEPTOR/HER-2 PROTO-ONCOGENE PROTEIN.		03.0440
MS (Multiple Sclerosis)
[description not available]		03.0240
Anterior Optic Neuritis
[description not available]		02.8130
Multiple Sclerosis
An autoimmune disorder mainly affecting young adults and characterized by destruction of myelin in the central nervous system. Pathologic findings include multiple sharply demarcated areas of demyelination throughout the white matter of the central nervous system. Clinical manifestations include visual loss, extra-ocular movement disorders, paresthesias, loss of sensation, weakness, dysarthria, spasticity, ataxia, and bladder dysfunction. The usual pattern is one of recurrent attacks followed by partial recovery (see MULTIPLE SCLEROSIS, RELAPSING-REMITTING), but acute fulminating and chronic progressive forms (see MULTIPLE SCLEROSIS, CHRONIC PROGRESSIVE) also occur. (Adams et al., Principles of Neurology, 6th ed, p903)		110.0240
Optic Neuritis
Inflammation of the optic nerve. Commonly associated conditions include autoimmune disorders such as MULTIPLE SCLEROSIS, infections, and granulomatous diseases. Clinical features include retro-orbital pain that is aggravated by eye movement, loss of color vision, and contrast sensitivity that may progress to severe visual loss, an afferent pupillary defect (Marcus-Gunn pupil), and in some instances optic disc hyperemia and swelling. Inflammation may occur in the portion of the nerve within the globe (neuropapillitis or anterior optic neuritis) or the portion behind the globe (retrobulbar neuritis or posterior optic neuritis).		02.8130
Sensitivity and Specificity
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)		015.3711514
Leiomyosarcoma, Epithelioid
[description not available]		010.94370
Leiomyosarcoma
A sarcoma containing large spindle cells of smooth muscle. Although it rarely occurs in soft tissue, it is common in the viscera. It is the most common soft tissue sarcoma of the gastrointestinal tract and uterus. The median age of patients is 60 years. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1865)		015.94370
Germinoblastoma
[description not available]		06.54170
Lymphoma
A general term for various neoplastic diseases of the lymphoid tissue.		113.54170
Atheroma
[description not available]		04.8821
Atherogenesis
[description not available]		07.964
Elevated Cholesterol
[description not available]		05.6161
Hypercholesterolemia
A condition with abnormally high levels of CHOLESTEROL in the blood. It is defined as a cholesterol value exceeding the 95th percentile for the population.		05.6161
Atherosclerosis
A thickening and loss of elasticity of the walls of ARTERIES that occurs with formation of ATHEROSCLEROTIC PLAQUES within the ARTERIAL INTIMA.		07.964
Acute Symptom Flare
[description not available]		02.2510
Bronchiolitis, Exudative
[description not available]		04.94130
Bronchiolitis Obliterans
Inflammation of the BRONCHIOLES leading to an obstructive lung disease. Bronchioles are characterized by fibrous granulation tissue with bronchial exudates in the lumens. Clinical features include a nonproductive cough and DYSPNEA.		04.94130
Enlarged Liver
[description not available]		03.6930
Colicky Pain
[description not available]		06.86141
Abdominal Pain
Sensation of discomfort, distress, or agony in the abdominal region.		06.86141
Cancer of Head
[description not available]		09.62273
Hoarseness
An unnaturally deep or rough quality of voice.		03.1710
Head and Neck Neoplasms
Soft tissue tumors or cancer arising from the mucosal surfaces of the LIP; oral cavity; PHARYNX; LARYNX; and cervical esophagus. Other sites included are the NOSE and PARANASAL SINUSES; SALIVARY GLANDS; THYROID GLAND and PARATHYROID GLANDS; and MELANOMA and non-melanoma skin cancers of the head and neck. (from Holland et al., Cancer Medicine, 4th ed, p1651)		111.62273
Chronic Kidney Failure
[description not available]		06.38141
Kidney Failure, Chronic
The end-stage of CHRONIC RENAL INSUFFICIENCY. It is characterized by the severe irreversible kidney damage (as measured by the level of PROTEINURIA) and the reduction in GLOMERULAR FILTRATION RATE to less than 15 ml per min (Kidney Foundation: Kidney Disease Outcome Quality Initiative, 2002). These patients generally require HEMODIALYSIS or KIDNEY TRANSPLANTATION.		06.38141
Neurofibroma
A moderately firm, benign, encapsulated tumor resulting from proliferation of SCHWANN CELLS and FIBROBLASTS that includes portions of nerve fibers. The tumors usually develop along peripheral or cranial nerves and are a central feature of NEUROFIBROMATOSIS 1, where they may occur intracranially or involve spinal roots. Pathologic features include fusiform enlargement of the involved nerve. Microscopic examination reveals a disorganized and loose cellular pattern with elongated nuclei intermixed with fibrous strands. (From Adams et al., Principles of Neurology, 6th ed, p1016)		09.8140
Extravascular Hemolysis
[description not available]		05.551
Colorectal Cancer
[description not available]		010.49394
Hemolysis
The destruction of ERYTHROCYTES by many different causal agents such as antibodies, bacteria, chemicals, temperature, and changes in tonicity.		05.551
Colorectal Neoplasms
Tumors or cancer of the COLON or the RECTUM or both. Risk factors for colorectal cancer include chronic ULCERATIVE COLITIS; FAMILIAL POLYPOSIS COLI; exposure to ASBESTOS; and irradiation of the CERVIX UTERI.		112.49394
Orbital Diseases
Diseases of the bony orbit and contents except the eyeball.		03.4370
Blepharospasm
Excessive winking; tonic or clonic spasm of the orbicularis oculi muscle.		07.2510
Carcinoma, Ehrlich Tumor
A transplantable, poorly differentiated malignant tumor which appeared originally as a spontaneous breast carcinoma in a mouse. It grows in both solid and ascitic forms.		05.1631
Cardiac Diseases
[description not available]		07.41161
Heart Diseases
Pathological conditions involving the HEART including its structural and functional abnormalities.		07.41161
Malignant Mesothelioma
[description not available]		04.522
Neoplasms, Pleural
[description not available]		08.87134
Metaplasia
A condition in which there is a change of one adult cell type to another similar adult cell type.		03.6630
Acquired Autoimmune Hemolytic Anemia
[description not available]		02.5120
Anemia, Hemolytic, Autoimmune
Acquired hemolytic anemia due to the presence of AUTOANTIBODIES which agglutinate or lyse the patient's own RED BLOOD CELLS.		02.5120
Esophageal Squamous Cell Carcinoma
A carcinoma that originates usually from cells on the surface of the middle and lower third of the ESOPHAGUS. Tumor cells exhibit typical squamous morphology and form large polypoid lesions. Mutations in RNF6, LZTS1, TGFBR2, DEC1, and WWOX1 genes are associated with this cancer.		04.8821
Behavior Disorders
[description not available]		04.5511
Mental Disorders
Psychiatric illness or diseases manifested by breakdowns in the adaptational process expressed primarily as abnormalities of thought, feeling, and behavior producing either distress or impairment of function.		04.5511
Cancer, Second Primary
[description not available]		013.98639
Lentigines
[description not available]		02.8130
Cancer Syndromes, Hereditary
[description not available]		04.3740
Lentigo
Small circumscribed melanoses resembling, but differing histologically from, freckles. The concept includes senile lentigo ('liver spots') and nevoid lentigo (nevus spilus, lentigo simplex) and may also occur in association with multiple congenital defects or congenital syndromes (e.g., Peutz-Jeghers syndrome).		02.8130
Cough
A sudden, audible expulsion of air from the lungs through a partially closed glottis, preceded by inhalation. It is a protective response that serves to clear the trachea, bronchi, and/or lungs of irritants and secretions, or to prevent aspiration of foreign materials into the lungs.		04.580
Birth Weight
The mass or quantity of heaviness of an individual at BIRTH. It is expressed by units of pounds or kilograms.		04.4311
Diffuse Parenchymal Lung Disease
[description not available]		011.2354
Hibernation, Myocardial
[description not available]		04.4311
Tuberculosis, Drug-Resistant
[description not available]		05.3121
Chronic Hepatitis B
[description not available]		011.3961
Anterior Cerebral Circulation Infarction
[description not available]		04.7821
Apoplexy
[description not available]		07.0492
Diffuse Lymphocytic Lymphoma, Poorly-Differentiated
[description not available]		05.5131
Airflow Obstruction, Chronic
[description not available]		04.7721
Ductal Carcinoma
[description not available]		04.4311
Complications of Diabetes Mellitus
[description not available]		05.0531
Overweight
A status with BODY WEIGHT that is above certain standards. In the scale of BODY MASS INDEX, overweight is defined as having a BMI of 25.0-29.9 kg/m2. Overweight may or may not be due to increases in body fat (ADIPOSE TISSUE), hence overweight does not equal over fat.		04.4311
Bone Fractures
[description not available]		05.0931
Primary Graft Dysfunction
A form of ischemia-reperfusion injury occurring in the early period following transplantation. Significant pathophysiological changes in MITOCHONDRIA are the main cause of the dysfunction. It is most often seen in the transplanted lung, liver, or kidney and can lead to GRAFT REJECTION.		04.4311
Airway Remodeling
The structural changes in the number, mass, size and/or composition of the airway tissues.		05.341
Lower Urinary Tract Symptom
[description not available]		04.4311
Adolescent Obesity
[description not available]		04.4311
Allergic Rhinitis
[description not available]		04.4311
Thyroid Cancer, Anaplastic
[description not available]		04.4311
Encephalopathy, Traumatic
[description not available]		04.921
Familial Nonmedullary Thyroid Cancer
[description not available]		05.5731
Rheumatoid Arthritis
[description not available]		08.84201
Amaurosis
[description not available]		06.4731
Bone Loss, Osteoclastic
[description not available]		07.65132
Benign Neoplasms, Brain
[description not available]		013.576015
Clostridioides difficile Infection
[description not available]		04.4311
Alloxan Diabetes
[description not available]		07.45101
Autoimmune Diabetes
[description not available]		010.48135
Cutis Elastica
[description not available]		04.4311
E coli Infections
[description not available]		04.4311
Fasting Hypoglycemia
HYPOGLYCEMIA expressed in the postabsorptive state, after prolonged FASTING, or an overnight fast.		05.8581
Chronic Insomnia
[description not available]		04.4311
Hypermobility, Joint
[description not available]		04.4311
B16 Melanoma
[description not available]		07.71192
Muscle Disorders
[description not available]		05.6161
Morbid Obesity
[description not available]		04.7921
Age-Related Osteoporosis
[description not available]		07.5544
Experimental Lung Inflammation
Inflammation of any part, segment or lobe, of the lung parenchyma.		08.85152
Prediabetes
[description not available]		04.4311
Acute Hypercapnic Respiratory Failure
[description not available]		05.6532
Cancer of Salivary Gland
[description not available]		010.76117
Hemorrhagic Shock
[description not available]		05.2841
Pulmonary Consumption
[description not available]		05.2941
Deficiency, Vitamin D
[description not available]		04.4311
Injuries
Used with anatomic headings, animals, and sports for wounds and injuries. Excludes cell damage, for which pathology is used.		04.4311
Injury, Ischemia-Reperfusion
[description not available]		05.5251
Bone Loss, Perimenopausal
[description not available]		04.4311
Bacterial Infections, Gram-Negative
[description not available]		07.7354
Hangman Fracture
[description not available]		04.4311
Idiopathic Interstitial Pneumonia
[description not available]		04.4311
Eye Infections, Fungal
Infection by a variety of fungi, usually through four possible mechanisms: superficial infection producing conjunctivitis, keratitis, or lacrimal obstruction; extension of infection from neighboring structures - skin, paranasal sinuses, nasopharynx; direct introduction during surgery or accidental penetrating trauma; or via the blood or lymphatic routes in patients with underlying mycoses.		04.4311
Cell Transformation, Viral
An inheritable change in cells manifested by changes in cell division and growth and alterations in cell surface properties. It is induced by infection with a transforming virus.		05.9591
Delayed Effects, Prenatal Exposure
[description not available]		04.7921
Brain Injuries, Traumatic
A form of acquired brain injury which occurs when a sudden trauma causes damage to the brain.		04.921
Aging
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.		08.34144
Albuminuria
The presence of albumin in the urine, an indicator of KIDNEY DISEASES.		04.821
Arthritis, Rheumatoid
A chronic systemic disease, primarily of the joints, marked by inflammatory changes in the synovial membranes and articular structures, widespread fibrinoid degeneration of the collagen fibers in mesenchymal tissues, and by atrophy and rarefaction of bony structures. Etiology is unknown, but autoimmune mechanisms have been implicated.		08.84201
Blindness
The inability to see or the loss or absence of perception of visual stimuli. This condition may be the result of EYE DISEASES; OPTIC NERVE DISEASES; OPTIC CHIASM diseases; or BRAIN DISEASES affecting the VISUAL PATHWAYS or OCCIPITAL LOBE.		06.4731
Brain Neoplasms
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.		013.576015
Clostridium Infections
Infections with bacteria of the genus CLOSTRIDIUM and closely related CLOSTRIDIOIDES species.		04.4311
Connective Tissue Diseases
A heterogeneous group of disorders, some hereditary, others acquired, characterized by abnormal structure or function of one or more of the elements of connective tissue, i.e., collagen, elastin, or the mucopolysaccharides.		04.7621
Diabetes Mellitus, Type 1
A subtype of DIABETES MELLITUS that is characterized by INSULIN deficiency. It is manifested by the sudden onset of severe HYPERGLYCEMIA, rapid progression to DIABETIC KETOACIDOSIS, and DEATH unless treated with insulin. The disease may occur at any age, but is most common in childhood or adolescence.		112.48135
Ehlers-Danlos Syndrome
A heterogeneous group of autosomally inherited COLLAGEN DISEASES caused by defects in the synthesis or structure of FIBRILLAR COLLAGEN. There are numerous subtypes: classical, hypermobility, vascular, and others. Common clinical features include hyperextensible skin and joints, skin fragility and reduced wound healing capability.		04.4311
Escherichia coli Infections
Infections with bacteria of the species ESCHERICHIA COLI.		04.4311
Hypoglycemia
A syndrome of abnormally low BLOOD GLUCOSE level. Clinical hypoglycemia has diverse etiologies. Severe hypoglycemia eventually lead to glucose deprivation of the CENTRAL NERVOUS SYSTEM resulting in HUNGER; SWEATING; PARESTHESIA; impaired mental function; SEIZURES; COMA; and even DEATH.		010.8581
Sleep Initiation and Maintenance Disorders
Disorders characterized by impairment of the ability to initiate or maintain sleep. This may occur as a primary disorder or in association with another medical or psychiatric condition.		04.4311
Muscular Diseases
Acquired, familial, and congenital disorders of SKELETAL MUSCLE and SMOOTH MUSCLE.		05.6161
Necrosis
The death of cells in an organ or tissue due to disease, injury or failure of the blood supply.		08.45302
Neuroblastoma
A common neoplasm of early childhood arising from neural crest cells in the sympathetic nervous system, and characterized by diverse clinical behavior, ranging from spontaneous remission to rapid metastatic progression and death. This tumor is the most common intraabdominal malignancy of childhood, but it may also arise from thorax, neck, or rarely occur in the central nervous system. Histologic features include uniform round cells with hyperchromatic nuclei arranged in nests and separated by fibrovascular septa. Neuroblastomas may be associated with the opsoclonus-myoclonus syndrome. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2099-2101; Curr Opin Oncol 1998 Jan;10(1):43-51)		08.41203
Obesity
A status with BODY WEIGHT that is grossly above the recommended standards, usually due to accumulation of excess FATS in the body. The standards may vary with age, sex, genetic or cultural background. In the BODY MASS INDEX, a BMI greater than 30.0 kg/m2 is considered obese, and a BMI greater than 40.0 kg/m2 is considered morbidly obese (MORBID OBESITY).		010.23149
Obesity, Morbid
The condition of weighing two, three, or more times the ideal weight, so called because it is associated with many serious and life-threatening disorders. In the BODY MASS INDEX, morbid obesity is defined as having a BMI greater than 40.0 kg/m2.		04.7921
Osteoporosis
Reduction of bone mass without alteration in the composition of bone, leading to fractures. Primary osteoporosis can be of two major types: postmenopausal osteoporosis (OSTEOPOROSIS, POSTMENOPAUSAL) and age-related or senile osteoporosis.		07.5544
Pneumonia
Infection of the lung often accompanied by inflammation.		08.85152
Prediabetic State
The time period before the development of symptomatic diabetes. For example, certain risk factors can be observed in subjects who subsequently develop INSULIN RESISTANCE as in type 2 diabetes (DIABETES MELLITUS, TYPE 2).		04.4311
Respiratory Insufficiency
Failure to adequately provide oxygen to cells of the body and to remove excess carbon dioxide from them. (Stedman, 25th ed)		05.6532
Salivary Gland Neoplasms
Tumors or cancer of the SALIVARY GLANDS.		010.76117
Tuberculosis, Pulmonary
MYCOBACTERIUM infections of the lung.		05.2941
Uveitis
Inflammation of part or all of the uvea, the middle (vascular) tunic of the eye, and commonly involving the other tunics (sclera and cornea, and the retina). (Dorland, 27th ed)		04.8221
Vitamin D Deficiency
A nutritional condition produced by a deficiency of VITAMIN D in the diet, insufficient production of vitamin D in the skin, inadequate absorption of vitamin D from the diet, or abnormal conversion of vitamin D to its bioactive metabolites. It is manifested clinically as RICKETS in children and OSTEOMALACIA in adults. (From Cecil Textbook of Medicine, 19th ed, p1406)		04.4311
Wounds and Injuries
Damage inflicted on the body as the direct or indirect result of an external force, with or without disruption of structural continuity.		04.4311
Reperfusion Injury
Adverse functional, metabolic, or structural changes in tissues that result from the restoration of blood flow to the tissue (REPERFUSION) following ISCHEMIA.		05.5251
Osteoporosis, Postmenopausal
Metabolic disorder associated with fractures of the femoral neck, vertebrae, and distal forearm. It occurs commonly in women within 15-20 years after menopause, and is caused by factors associated with menopause including estrogen deficiency.		04.4311
Spinal Fractures
Broken bones in the vertebral column.		04.4311
Gram-Negative Bacterial Infections
Infections caused by bacteria that show up as pink (negative) when treated by the gram-staining method.		07.7354
Lung Diseases, Interstitial
A diverse group of lung diseases that affect the lung parenchyma. They are characterized by an initial inflammation of PULMONARY ALVEOLI that extends to the interstitium and beyond leading to diffuse PULMONARY FIBROSIS. Interstitial lung diseases are classified by their etiology (known or unknown causes), and radiological-pathological features.		011.2354
Tuberculosis, Multidrug-Resistant
Tuberculosis resistant to chemotherapy with two or more ANTITUBERCULAR AGENTS, including at least ISONIAZID and RIFAMPICIN. The problem of resistance is particularly troublesome in tuberculous OPPORTUNISTIC INFECTIONS associated with HIV INFECTIONS. It requires the use of second line drugs which are more toxic than the first line regimens. TB with isolates that have developed further resistance to at least three of the six classes of second line drugs is defined as EXTENSIVELY DRUG-RESISTANT TUBERCULOSIS.		05.3121
Hepatitis B, Chronic
INFLAMMATION of the LIVER in humans caused by HEPATITIS B VIRUS lasting six months or more. It is primarily transmitted by parenteral exposure, such as transfusion of contaminated blood or blood products, but can also be transmitted via sexual or intimate personal contact.		06.3961
Brain Infarction
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.		09.7821
Stroke
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)		07.0492
Lymphoma, Mantle-Cell
A form of non-Hodgkin lymphoma having a usually diffuse pattern with both small and medium lymphocytes and small cleaved cells. It accounts for about 5% of adult non-Hodgkin lymphomas in the United States and Europe. The majority of mantle-cell lymphomas are associated with a t(11;14) translocation resulting in overexpression of the CYCLIN D1 gene (GENES, BCL-1).		05.5131
Pulmonary Disease, Chronic Obstructive
A disease of chronic diffuse irreversible airflow obstruction. Subcategories of COPD include CHRONIC BRONCHITIS and PULMONARY EMPHYSEMA.		04.7721
Carcinoma, Ductal
Malignant neoplasms involving the ductal systems of any of a number of organs, such as the MAMMARY GLANDS, the PANCREAS, the PROSTATE, or the LACRIMAL GLAND.		04.4311
Fractures, Bone
Breaks in bones.		05.0931
Rhinitis, Allergic
An inflammation of the NASAL MUCOSA triggered by ALLERGENS.		04.4311
Thyroid Carcinoma, Anaplastic
An aggressive THYROID GLAND malignancy which generally occurs in IODINE-deficient areas in people with previous thyroid pathology such as GOITER. It is associated with CELL DEDIFFERENTIATION of THYROID CARCINOMA (e.g., FOLLICULAR THYROID CARCINOMA; PAPILLARY THYROID CANCER). Typical initial presentation is a rapidly growing neck mass which upon metastasis is associated with DYSPHAGIA; NECK PAIN; bone pain; DYSPNEA; and NEUROLOGIC DEFICITS.		04.4311
Carcinoma, Anaplastic
[description not available]		08.61301
Cyst
[description not available]		02.9840
Cancer of ILEUM
[description not available]		04.17150
Carcinoma
A malignant neoplasm made up of epithelial cells tending to infiltrate the surrounding tissues and give rise to metastases. It is a histological type of neoplasm and not a synonym for cancer.		110.61301
Ectopic Lymph Nodes
[description not available]		02.2510
Connective Tissue Neoplasms
[description not available]		011.01191
Biliary Tract Cancer
[description not available]		07.4720
Biliary Tract Neoplasms
Tumors or cancer in the BILIARY TRACT including the BILE DUCTS and the GALLBLADDER.		02.4720
Weight Reduction
[description not available]		04.3970
Anorexia
The lack or loss of APPETITE accompanied by an aversion to food and the inability to eat. It is the defining characteristic of the disorder ANOREXIA NERVOSA.		02.9130
Weight Loss
Decrease in existing BODY WEIGHT.		04.3970
HbS Disease
[description not available]		03.0240
Sickle Cell Trait
The condition of being heterozygous for hemoglobin S.		02.4820
Anemia, Cooley's
[description not available]		02.5320
Anemia, Sickle Cell
A disease characterized by chronic hemolytic anemia, episodic painful crises, and pathologic involvement of many organs. It is the clinical expression of homozygosity for hemoglobin S.		15.0240
beta-Thalassemia
A disorder characterized by reduced synthesis of the beta chains of hemoglobin. There is retardation of hemoglobin A synthesis in the heterozygous form (thalassemia minor), which is asymptomatic, while in the homozygous form (thalassemia major, Cooley's anemia, Mediterranean anemia, erythroblastic anemia), which can result in severe complications and even death, hemoglobin A synthesis is absent.		02.5320
Arteriosclerosis, Coronary
[description not available]		03.4670
Coronary Artery Disease
Pathological processes of CORONARY ARTERIES that may derive from a congenital abnormality, atherosclerotic, or non-atherosclerotic cause.		03.4670
Thrombotic Microangiopathies
Diseases that result in THROMBOSIS in MICROVASCULATURE. The two most prominent diseases are PURPURA, THROMBOTIC THROMBOCYTOPENIC; and HEMOLYTIC-UREMIC SYNDROME. Multiple etiological factors include VASCULAR ENDOTHELIAL CELL damage due to SHIGA TOXIN; FACTOR H deficiency; and aberrant VON WILLEBRAND FACTOR formation.		03.3860
Chronic Hepatitis C
[description not available]		03.3920
Hepatitis C, Chronic
INFLAMMATION of the LIVER in humans that is caused by HEPATITIS C VIRUS lasting six months or more. Chronic hepatitis C can lead to LIVER CIRRHOSIS.		03.3920
Encephalitis, JC Polyomavirus
[description not available]		02.2510
Leukoencephalopathy, Progressive Multifocal
An opportunistic viral infection of the central nervous system associated with conditions that impair cell-mediated immunity (e.g., ACQUIRED IMMUNODEFICIENCY SYNDROME and other IMMUNOLOGIC DEFICIENCY SYNDROMES; HEMATOLOGIC NEOPLASMS; IMMUNOSUPPRESSION; and COLLAGEN DISEASES). The causative organism is JC Polyomavirus (JC VIRUS) which primarily affects oligodendrocytes, resulting in multiple areas of demyelination. Clinical manifestations include DEMENTIA; ATAXIA; visual disturbances; and other focal neurologic deficits, generally progressing to a vegetative state within 6 months. (From Joynt, Clinical Neurology, 1996, Ch26, pp36-7)		02.2510
Hypogammaglobulinemia
[description not available]		04.9142
Agammaglobulinemia
An immunologic deficiency state characterized by an extremely low level of generally all classes of gamma-globulin in the blood.		04.9142
Diathesis
[description not available]		02.9430
Macrophage Activation Syndrome
A serious complication of childhood systemic inflammatory disorders that is thought to be caused by excessive activation and proliferation of T-LYMPHOCYTES and MACROPHAGES. It is seen predominantly in children with systemic onset JUVENILE IDIOPATHIC ARTHRITIS.		02.2510
Cancer of Jejunum
[description not available]		05.97240
B-Cell Leukemia
[description not available]		03.9440
Anal Cancer
[description not available]		04.8110
Anus Neoplasms
Tumors or cancer of the ANAL CANAL.		04.8110
Cafe-au-Lait Spots with Pulmonic Stenosis
[description not available]		012.76292
Elephantiasis Neuromatosis
[description not available]		08.45112
Neurofibromatosis 1
An autosomal dominant inherited disorder (with a high frequency of spontaneous mutations) that features developmental changes in the nervous system, muscles, bones, and skin, most notably in tissue derived from the embryonic NEURAL CREST. Multiple hyperpigmented skin lesions and subcutaneous tumors are the hallmark of this disease. Peripheral and central nervous system neoplasms occur frequently, especially OPTIC NERVE GLIOMA and NEUROFIBROSARCOMA. NF1 is caused by mutations which inactivate the NF1 gene (GENES, NEUROFIBROMATOSIS 1) on chromosome 17q. The incidence of learning disabilities is also elevated in this condition. (From Adams et al., Principles of Neurology, 6th ed, pp1014-18) There is overlap of clinical features with NOONAN SYNDROME in a syndrome called neurofibromatosis-Noonan syndrome. Both the PTPN11 and NF1 gene products are involved in the SIGNAL TRANSDUCTION pathway of Ras (RAS PROTEINS).		114.76292
Neurofibroma, Plexiform
A type of neurofibroma manifesting as a diffuse overgrowth of subcutaneous tissue, usually involving the face, scalp, neck, and chest but occasionally occurring in the abdomen or pelvis. The tumors tend to progress, and may extend along nerve roots to eventually involve the spinal roots and spinal cord. This process is almost always a manifestation of NEUROFIBROMATOSIS 1. (From Adams et al., Principles of Neurology, 6th ed, p1016; J Pediatr 1997 Nov;131(5):678-82)		110.45112
Indigestion
[description not available]		02.2510
Dyspepsia
Impaired digestion, especially after eating.		02.2510
Dermatitis, Eczematous
[description not available]		02.5820
Eczema
A pruritic papulovesicular dermatitis occurring as a reaction to many endogenous and exogenous agents (Dorland, 27th ed).		02.5820
Fibrosarcoma
A sarcoma derived from deep fibrous tissue, characterized by bundles of immature proliferating fibroblasts with variable collagen formation, which tends to invade locally and metastasize by the bloodstream. (Stedman, 25th ed)		04.5180
CACH Syndrome
[description not available]		02.2510
Fusiform Aneurysm
Elongated, spindle-shaped dilation in the wall of blood vessels, usually large ARTERIES with ATHEROSCLEROSIS.		02.2510
Aneurysm
Pathological outpouching or sac-like dilatation in the wall of any blood vessel (ARTERIES or VEINS) or the heart (HEART ANEURYSM). It indicates a thin and weakened area in the wall which may later rupture. Aneurysms are classified by location, etiology, or other characteristics.		02.2510
Prolapse
The protrusion of an organ or part of an organ into a natural or artificial orifice.		02.2510
Neoplasms, Nerve Sheath
[description not available]		03.940
Nerve Sheath Neoplasms
Neoplasms which arise from nerve sheaths formed by SCHWANN CELLS in the PERIPHERAL NERVOUS SYSTEM or by OLIGODENDROCYTES in the CENTRAL NERVOUS SYSTEM. Malignant peripheral nerve sheath tumors, NEUROFIBROMA, and NEURILEMMOMA are relatively common tumors in this category.		03.940
Pemphigus Foliaceus
[description not available]		08.1340
Pemphigus
Group of chronic blistering diseases characterized histologically by ACANTHOLYSIS and blister formation within the EPIDERMIS.		08.1340
Hypophosphatemia
A condition of an abnormally low level of PHOSPHATES in the blood.		011.7112
Adrenal Cortex Cancer
[description not available]		02.2510
Adrenal Cortex Neoplasms
Tumors or cancers of the ADRENAL CORTEX.		02.2510
Uveal Neoplasms
Tumors or cancer of the UVEA.		07.33132
Aggressive Natural Killer Cell Leukemia
[description not available]		02.7930
Leukemia, Large Granular Lymphocytic
A spectrum of disorders characterized by clonal expansions of the peripheral blood LYMPHOCYTE populations known as large granular lymphocytes which contain abundant cytoplasm and azurophilic granules. Subtypes develop from either CD3-negative NATURAL KILLER CELLS or CD3-positive T-CELLS. The clinical course of both subtypes can vary from spontaneous regression to progressive, malignant disease.		02.7930
Sterility, Female
[description not available]		02.9840
Infertility, Female
Diminished or absent ability of a female to achieve conception.		02.9840
Complications, Neoplastic Pregnancy
[description not available]		07.99460
Acute Edematous Pancreatitis
[description not available]		02.6620
Pancreatitis
INFLAMMATION of the PANCREAS. Pancreatitis is classified as acute unless there are computed tomographic or endoscopic retrograde cholangiopancreatographic findings of CHRONIC PANCREATITIS (International Symposium on Acute Pancreatitis, Atlanta, 1992). The two most common forms of acute pancreatitis are ALCOHOLIC PANCREATITIS and gallstone pancreatitis.		02.6620
Central Nervous System Neoplasm
[description not available]		06.79223
Central Nervous System Neoplasms
Benign and malignant neoplastic processes that arise from or secondarily involve the brain, spinal cord, or meninges.		18.79223
Leukemic Infiltration
A pathologic change in leukemia in which leukemic cells permeate various organs at any stage of the disease. All types of leukemia show various degrees of infiltration, depending upon the type of leukemia. The degree of infiltration may vary from site to site. The liver and spleen are common sites of infiltration, the greatest appearing in myelocytic leukemia, but infiltration is seen also in the granulocytic and lymphocytic types. The kidney is also a common site and of the gastrointestinal system, the stomach and ileum are commonly involved. In lymphocytic leukemia the skin is often infiltrated. The central nervous system too is a common site.		06.68120
Cerebral Infarction, Middle Cerebral Artery
[description not available]		02.5820
Acute Ischemic Stroke
[description not available]		02.7220
Ischemic Stroke
Stroke due to BRAIN ISCHEMIA resulting in interruption or reduction of blood flow to a part of the brain. When obstruction is due to a BLOOD CLOT formed within in a cerebral blood vessel it is a thrombotic stroke. When obstruction is formed elsewhere and moved to block a cerebral blood vessel (see CEREBRAL EMBOLISM) it is referred to as embolic stroke. Wake-up stroke refers to ischemic stroke occurring during sleep while cryptogenic stroke refers to ischemic stroke of unknown origin.		02.7220
Infarction, Middle Cerebral Artery
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.		02.5820
Fasciitis
Inflammation of the fascia. There are three major types: 1, Eosinophilic fasciitis, an inflammatory reaction with eosinophilia, producing hard thickened skin with an orange-peel configuration suggestive of scleroderma and considered by some a variant of scleroderma; 2, Necrotizing fasciitis (FASCIITIS, NECROTIZING), a serious fulminating infection (usually by a beta hemolytic streptococcus) causing extensive necrosis of superficial fascia; 3, Nodular/Pseudosarcomatous /Proliferative fasciitis, characterized by a rapid growth of fibroblasts with mononuclear inflammatory cells and proliferating capillaries in soft tissue, often the forearm; it is not malignant but is sometimes mistaken for fibrosarcoma.		05.341
Benign Monoclonal Gammopathies
[description not available]		03.3350
Left Ventricular Dysfunction
[description not available]		07.5112
Ventricular Dysfunction, Left
A condition in which the LEFT VENTRICLE of the heart was functionally impaired. This condition usually leads to HEART FAILURE; MYOCARDIAL INFARCTION; and other cardiovascular complications. Diagnosis is made by measuring the diminished ejection fraction and a depressed level of motility of the left ventricular wall.		07.5112
Hypomelanosis
[description not available]		05.52151
Hypopigmentation
A condition caused by a deficiency or a loss of melanin pigmentation in the epidermis, also known as hypomelanosis. Hypopigmentation can be localized or generalized, and may result from genetic defects, trauma, inflammation, or infections.		05.52151
Thromboembolism, Venous
[description not available]		02.2510
Venous Thromboembolism
Obstruction of a vein or VEINS (embolism) by a blood clot (THROMBUS) in the blood stream.		02.2510
Abdominal Migraine
[description not available]		03.9321
Migraine Disorders
A class of disabling primary headache disorders, characterized by recurrent unilateral pulsatile headaches. The two major subtypes are common migraine (without aura) and classic migraine (with aura or neurological symptoms). (International Classification of Headache Disorders, 2nd ed. Cephalalgia 2004: suppl 1)		03.9321
Multiple Primary Neoplasms
[description not available]		08.39271
Bisphosphonate Osteonecrosis
[description not available]		02.3110
Aseptic Necrosis of Bone
[description not available]		03.7430
Osteonecrosis
Death of a bone or part of a bone, either atraumatic or posttraumatic.		03.7430
Musculoskeletal Pain
Discomfort stemming from muscles, LIGAMENTS, tendons, and bones.		09.6530
Abnormalities, Multiple
Congenital abnormalities that affect more than one organ or body structure.		03.4220
Atrophy
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.		03.5120
Hypertrophy
General increase in bulk of a part or organ due to CELL ENLARGEMENT and accumulation of FLUIDS AND SECRETIONS, not due to tumor formation, nor to an increase in the number of cells (HYPERPLASIA).		02.5320
Glaucoma
An ocular disease, occurring in many forms, having as its primary characteristics an unstable or a sustained increase in the intraocular pressure which the eye cannot withstand without damage to its structure or impairment of its function. The consequences of the increased pressure may be manifested in a variety of symptoms, depending upon type and severity, such as excavation of the optic disk, hardness of the eyeball, corneal anesthesia, reduced visual acuity, seeing of colored halos around lights, disturbed dark adaptation, visual field defects, and headaches. (Dictionary of Visual Science, 4th ed)		02.2510
Intraocular Pressure
The pressure of the fluids in the eye.		03.7630
Injuries, Radiation
[description not available]		03.4720
Allergic Alveolitis, Extrinsic
[description not available]		02.4720
Alveolitis, Extrinsic Allergic
A common interstitial lung disease caused by hypersensitivity reactions of PULMONARY ALVEOLI after inhalation of and sensitization to environmental antigens of microbial, animal, or chemical sources. The disease is characterized by lymphocytic alveolitis and granulomatous pneumonitis.		02.4720
Adenomatous Polyposis Coli, Familial
[description not available]		03.8840
Adenomatous Polyposis Coli
A polyposis syndrome due to an autosomal dominant mutation of the APC genes (GENES, APC) on CHROMOSOME 5. The syndrome is characterized by the development of hundreds of ADENOMATOUS POLYPS in the COLON and RECTUM of affected individuals by early adulthood.		03.8840
Abnormal Karyotype
A variation from the normal set of chromosomes characteristic of a species.		04.6251
Orthopedic Disorders
[description not available]		03.5720
Musculoskeletal Diseases
Diseases of the muscles and their associated ligaments and other connective tissue and of the bones and cartilage viewed collectively.		03.5720
Skin Ulcer
An ULCER of the skin and underlying tissues.		02.8430
Icterus
[description not available]		03.7130
Cachexia
General ill health, malnutrition, and weight loss, usually associated with chronic disease.		02.3110
Jaundice
A clinical manifestation of HYPERBILIRUBINEMIA, characterized by the yellowish staining of the SKIN; MUCOUS MEMBRANE; and SCLERA. Clinical jaundice usually is a sign of LIVER dysfunction.		03.7130
Destombes-Rosai-Dorfman Syndrome
[description not available]		02.5220
Histiocytosis, Sinus
Benign, non-Langerhans-cell, histiocytic proliferative disorder that primarily affects the lymph nodes. It is often referred to as sinus histiocytosis with massive lymphadenopathy.		02.5220
Cold Fingers, Hereditary
[description not available]		03.730
Raynaud Disease
An idiopathic vascular disorder characterized by bilateral Raynaud phenomenon, the abrupt onset of digital paleness or CYANOSIS in response to cold exposure or stress.		03.730
Cranial Sinus Thrombosis
[description not available]		02.3110
Infarct of the Spleen
[description not available]		02.3110
Priapism
A prolonged painful erection that may lasts hours and is not associated with sexual activity. It is seen in patients with SICKLE CELL ANEMIA, advanced malignancy, spinal trauma; and certain drug treatments.		03.7830
Anastomotic Leak
Breakdown of the connection and subsequent leakage of effluent (fluids, secretions, air) from a SURGICAL ANASTOMOSIS of the digestive, respiratory, genitourinary, and cardiovascular systems. Most common leakages are from the breakdown of suture lines in gastrointestinal or bowel anastomosis.		02.3110
Neoplasm Metastasis, Unknown Primary
[description not available]		02.7730
Symptom Cluster
[description not available]		03.0140
Syndrome
A characteristic symptom complex.		03.0140
Fibrodysplasia Ossificans Progressiva
[description not available]		02.930
Ectopic Ossification
[description not available]		02.6320
Myositis Ossificans
A disease characterized by bony deposits or the ossification of muscle tissue.		02.930
Carcinoma, Epidermoid
[description not available]		08.34372
Cancer of Mouth
[description not available]		02.8330
Carcinoma, Squamous Cell
A carcinoma derived from stratified SQUAMOUS EPITHELIAL CELLS. It may also occur in sites where glandular or columnar epithelium is normally present. (From Stedman, 25th ed)		08.34372
Mouth Neoplasms
Tumors or cancer of the MOUTH.		02.8330
Glomerulonephritis, Minimal Change
[description not available]		02.5320
Nephrosis, Lipoid
A kidney disease with no or minimal histological glomerular changes on light microscopy and with no immune deposits. It is characterized by lipid accumulation in the epithelial cells of KIDNEY TUBULES and in the URINE. Patients usually show NEPHROTIC SYNDROME indicating the presence of PROTEINURIA with accompanying EDEMA.		02.5320
Pleurisy, Tuberculous
[description not available]		02.3110
Central Nervous System Tuberculosis
[description not available]		02.3110
Muscle Contraction
A process leading to shortening and/or development of tension in muscle tissue. Muscle contraction occurs by a sliding filament mechanism whereby actin filaments slide inward among the myosin filaments.		04.15150
Muscle Relaxation
That phase of a muscle twitch during which a muscle returns to a resting position.		07.5320
Chronic Pancreatitis
[description not available]		02.3110
Pancreatitis, Chronic
INFLAMMATION of the PANCREAS that is characterized by recurring or persistent ABDOMINAL PAIN with or without STEATORRHEA or DIABETES MELLITUS. It is characterized by the irregular destruction of the pancreatic parenchyma which may be focal, segmental, or diffuse.		02.3110
Anterior Choroidal Artery Infarction
[description not available]		03.0340
Coronary Thrombosis
Coagulation of blood in any of the CORONARY VESSELS. The presence of a blood clot (THROMBUS) often leads to MYOCARDIAL INFARCTION.		02.3110
Cerebral Infarction
The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).		03.0340
Glomerulonephritis, Lupus
[description not available]		03.8940
Lupus Nephritis
Glomerulonephritis associated with autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Lupus nephritis is histologically classified into 6 classes: class I - normal glomeruli, class II - pure mesangial alterations, class III - focal segmental glomerulonephritis, class IV - diffuse glomerulonephritis, class V - diffuse membranous glomerulonephritis, and class VI - advanced sclerosing glomerulonephritis (The World Health Organization classification 1982).		08.8940
Carcinoma, Small Cell Lung
[description not available]		04.5551
Small Cell Lung Carcinoma
A form of highly malignant lung cancer that is composed of small ovoid cells (SMALL CELL CARCINOMA).		16.5551
Pyrexia
[description not available]		07.1554
Fever
An abnormal elevation of body temperature, usually as a result of a pathologic process.		07.1554
Chondrosarcoma
A slowly growing malignant neoplasm derived from cartilage cells, occurring most frequently in pelvic bones or near the ends of long bones, in middle-aged and old people. Most chondrosarcomas arise de novo, but some may develop in a preexisting benign cartilaginous lesion or in patients with ENCHONDROMATOSIS. (Stedman, 25th ed)		111.1731
Cancer of Muscle
[description not available]		02.7930
Lymph Node Metastasis
[description not available]		08.18270
Tricuspid Incompetence
[description not available]		04.8421
Melena
The black, tarry, foul-smelling FECES that contain degraded blood.		03.0610
Lymphocytopenia
[description not available]		02.7630
Lymphopenia
Reduction in the number of lymphocytes.		07.7630
Alopecia Cicatrisata
[description not available]		08.184
Alopecia
Absence of hair from areas where it is normally present.		08.184
Histiocytosis, Non-Langerhans-Cell
Group of disorders which feature accumulations of active HISTIOCYTES and LYMPHOCYTES, but where the histiocytes are not LANGERHANS CELLS. The group includes HEMOPHAGOCYTIC LYMPHOHISTIOCYTOSIS; SINUS HISTIOCYTOSIS; xanthogranuloma; reticulohistiocytoma; JUVENILE XANTHOGRANULOMA; xanthoma disseminatum; as well as the lipid storage diseases (SEA-BLUE HISTIOCYTE SYNDROME; and NIEMANN-PICK DISEASES).		03.0140
Cancer of Cecum
[description not available]		02.9840
Ascites
Accumulation or retention of free fluid within the peritoneal cavity.		09.3741
Acute Promyelocytic Leukemia
[description not available]		012.09230
Leukemia, Promyelocytic, Acute
An acute myeloid leukemia in which abnormal PROMYELOCYTES predominate. It is frequently associated with DISSEMINATED INTRAVASCULAR COAGULATION.		07.09230
Neoplasms, Skull Base
[description not available]		06.9282
Bronchial Hyperreactivity
Tendency of the smooth muscle of the tracheobronchial tree to contract more intensely in response to a given stimulus than it does in the response seen in normal individuals. This condition is present in virtually all symptomatic patients with asthma. The most prominent manifestation of this smooth muscle contraction is a decrease in airway caliber that can be readily measured in the pulmonary function laboratory.		05.6161
Atypical Chronic Myeloid Leukemia
[description not available]		09.35421
Anemia, Fanconi
[description not available]		02.4720
Fanconi Anemia
Congenital disorder affecting all bone marrow elements, resulting in ANEMIA; LEUKOPENIA; and THROMBOPENIA, and associated with cardiac, renal, and limb malformations as well as dermal pigmentary changes. Spontaneous CHROMOSOME BREAKAGE is a feature of this disease along with predisposition to LEUKEMIA. There are at least 7 complementation groups in Fanconi anemia: FANCA, FANCB, FANCC, FANCD1, FANCD2, FANCE, FANCF, FANCG, and FANCL. (from Online Mendelian Inheritance in Man, http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=227650, August 20, 2004)		02.4720
Cardiac Remodeling, Ventricular
[description not available]		03.0240
Carcinoma, Squamous Cell of Head and Neck
[description not available]		03.4220
Squamous Cell Carcinoma of Head and Neck
The most common type of head and neck carcinoma that originates from cells on the surface of the NASAL CAVITY; MOUTH; PARANASAL SINUSES, SALIVARY GLANDS, and LARYNX. Mutations in TNFRSF10B, PTEN, and ING1 genes are associated with this cancer.		03.4220
Atypical Ductal Hyperplasia
[description not available]		02.4820
Carcinoma, Intraductal, Noninfiltrating
A noninvasive (noninfiltrating) carcinoma of the breast characterized by a proliferation of malignant epithelial cells confined to the mammary ducts or lobules, without light-microscopy evidence of invasion through the basement membrane into the surrounding stroma.		02.4820
Desmoplastic Small Cell Tumor
[description not available]		03.5311
Desmoplastic Small Round Cell Tumor
A rare, aggressive soft tissue sarcoma that primarily affects adolescents and young adults. It is most commonly found in the abdomen.		08.5311
Achalasia
[description not available]		02.1510
Anus Prolapse
[description not available]		02.1510
Esophageal Achalasia
A motility disorder of the ESOPHAGUS in which the LOWER ESOPHAGEAL SPHINCTER (near the CARDIA) fails to relax resulting in functional obstruction of the esophagus, and DYSPHAGIA. Achalasia is characterized by a grossly contorted and dilated esophagus (megaesophagus).		02.1510
Colitis, Granulomatous
[description not available]		02.4820
Chronic Idiopathic Intestinal Pseudo-Obstruction
[description not available]		02.1710
Crohn Disease
A chronic transmural inflammation that may involve any part of the DIGESTIVE TRACT from MOUTH to ANUS, mostly found in the ILEUM, the CECUM, and the COLON. In Crohn disease, the inflammation, extending through the intestinal wall from the MUCOSA to the serosa, is characteristically asymmetric and segmental. Epithelioid GRANULOMAS may be seen in some patients.		02.4820
Intestinal Pseudo-Obstruction
A type of ILEUS, a functional not mechanical obstruction of the INTESTINES. This syndrome is caused by a large number of disorders involving the smooth muscles (MUSCLE, SMOOTH) or the NERVOUS SYSTEM.		02.1710
Orphan Diseases
Rare diseases that have not been well studied.		05.21100
Bladder Pain Syndrome
[description not available]		02.5220
Cystitis, Interstitial
A condition with recurring discomfort or pain in the URINARY BLADDER and the surrounding pelvic region without an identifiable disease. Severity of pain in interstitial cystitis varies greatly and often is accompanied by increased urination frequency and urgency.		02.5220
Beuren Syndrome
[description not available]		02.1510
Aortic Diseases
Pathological processes involving any part of the AORTA.		02.7330
Koch's Disease
[description not available]		03.1950
Tuberculosis
Any of the infectious diseases of man and other animals caused by species of MYCOBACTERIUM TUBERCULOSIS.		03.1950
Eye Disorders
[description not available]		05.6460
Eye Diseases
Diseases affecting the eye.		05.6460
Papulosquamous Disorders
[description not available]		02.4620
Scalp Dermatoses
Skin diseases involving the SCALP.		02.1710
Hand Dermatosis
[description not available]		02.9940
Hand Dermatoses
Skin diseases involving the HANDS.		02.9940
Nausea
An unpleasant sensation in the stomach usually accompanied by the urge to vomit. Common causes are early pregnancy, sea and motion sickness, emotional stress, intense pain, food poisoning, and various enteroviruses.		012.312210
Endotoxemia
A condition characterized by the presence of ENDOTOXINS in the blood. On lysis, the outer cell wall of gram-negative bacteria enters the systemic circulation and initiates a pathophysiologic cascade of pro-inflammatory mediators.		02.1710
Isochromosomes
Metacentric chromosomes produced during MEIOSIS or MITOSIS when the CENTROMERE splits transversely instead of longitudinally. The chromosomes produced by this abnormal division are one chromosome having the two long arms of the original chromosome, but no short arms, and the other chromosome consisting of the two short arms and no long arms. Each of these isochromosomes constitutes a simultaneous duplication and deletion.		02.1510
Signet Ring Cell Carcinoma
[description not available]		02.1510
Carcinoma, Signet Ring Cell
A poorly differentiated adenocarcinoma in which the nucleus is pressed to one side by a cytoplasmic droplet of mucus. It usually arises in the gastrointestinal system.		02.1510
T-Cell Lymphoma
[description not available]		04.470
Lymphoma, T-Cell
A group of heterogeneous lymphoid tumors representing malignant transformations of T-lymphocytes.		04.470
Vision, Diminished
[description not available]		02.830
Cardiomyopathies, Primary
[description not available]		03.1750
Cardiomyopathies
A group of diseases in which the dominant feature is the involvement of the CARDIAC MUSCLE itself. Cardiomyopathies are classified according to their predominant pathophysiological features (DILATED CARDIOMYOPATHY; HYPERTROPHIC CARDIOMYOPATHY; RESTRICTIVE CARDIOMYOPATHY) or their etiological/pathological factors (CARDIOMYOPATHY, ALCOHOLIC; ENDOCARDIAL FIBROELASTOSIS).		03.1750
EBV Infections
[description not available]		03.9240
Primary Peritonitis
[description not available]		0340
Cardiomyopathy, Restrictive
A form of CARDIAC MUSCLE disease in which the ventricular walls are excessively rigid, impeding ventricular filling. It is marked by reduced diastolic volume of either or both ventricles but normal or nearly normal systolic function. It may be idiopathic or associated with other diseases (ENDOMYOCARDIAL FIBROSIS or AMYLOIDOSIS) causing interstitial fibrosis.		02.1510
Endomyocardial Fibrosis
A condition characterized by the thickening of the ventricular ENDOCARDIUM and subendocardium (MYOCARDIUM), seen mostly in children and young adults in the TROPICAL CLIMATE. The fibrous tissue extends from the apex toward and often involves the HEART VALVES causing restrictive blood flow into the respective ventricles (CARDIOMYOPATHY, RESTRICTIVE).		03.1750
Peritonitis
INFLAMMATION of the PERITONEUM lining the ABDOMINAL CAVITY as the result of infectious, autoimmune, or chemical processes. Primary peritonitis is due to infection of the PERITONEAL CAVITY via hematogenous or lymphatic spread and without intra-abdominal source. Secondary peritonitis arises from the ABDOMINAL CAVITY itself through RUPTURE or ABSCESS of intra-abdominal organs.		0340
Epstein-Barr Virus Infections
Infection with human herpesvirus 4 (HERPESVIRUS 4, HUMAN); which may facilitate the development of various lymphoproliferative disorders. These include BURKITT LYMPHOMA (African type), INFECTIOUS MONONUCLEOSIS, and oral hairy leukoplakia (LEUKOPLAKIA, HAIRY).		03.9240
Gouty Arthritis
[description not available]		07.1510
Arthritis, Gouty
Arthritis, especially of the great toe, as a result of gout. Acute gouty arthritis often is precipitated by trauma, infection, surgery, etc. The initial attacks are usually monoarticular but later attacks are often polyarticular. Acute and chronic gouty arthritis are associated with accumulation of MONOSODIUM URATE in and around affected joints.		02.1510
Mesothelial Neoplasms
[description not available]		03.8521
Familial Waldenstrom's Macroglobulinaemia
[description not available]		02.1710
Gammapathy, Monoclonal
[description not available]		02.1710
Ileal Diseases
Pathological development in the ILEUM including the ILEOCECAL VALVE.		02.1710
Waldenstrom Macroglobulinemia
A lymphoproliferative disorder characterized by pleomorphic B-LYMPHOCYTES including PLASMA CELLS, with increased levels of monoclonal serum IMMUNOGLOBULIN M. There is lymphoplasmacytic cells infiltration into bone marrow and often other tissues, also known as lymphoplasmacytic lymphoma. Clinical features include ANEMIA; HEMORRHAGES; and hyperviscosity.		02.1710
Paraproteinemias
A group of related diseases characterized by an unbalanced or disproportionate proliferation of immunoglobulin-producing cells, usually from a single clone. These cells frequently secrete a structurally homogeneous immunoglobulin (M-component) and/or an abnormal immunoglobulin.		02.1710
Histiocytic Sarcoma
Malignant neoplasms composed of MACROPHAGES or DENDRITIC CELLS. Most histiocytic sarcomas present as localized tumor masses without a leukemic phase. Though the biological behavior of these neoplasms resemble lymphomas, their cell lineage is histiocytic not lymphoid.		02.5820
Hypertrophy, Right Ventricular
Enlargement of the RIGHT VENTRICLE of the heart. This increase in ventricular mass is often attributed to PULMONARY HYPERTENSION and is a contributor to cardiovascular morbidity and mortality.		03.680
Idiopathic Parkinson Disease
[description not available]		02.5720
Parkinson Disease
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)		02.5720
Anaphylactic Reaction
[description not available]		03.6730
Circulatory Collapse
[description not available]		02.4820
Anaphylaxis
An acute hypersensitivity reaction due to exposure to a previously encountered ANTIGEN. The reaction may include rapidly progressing URTICARIA, respiratory distress, vascular collapse, systemic SHOCK, and death.		03.6730
Shock
A pathological condition manifested by failure to perfuse or oxygenate vital organs.		02.4820
Loa loa Filariasis
[description not available]		03.0610
Loiasis
A parasitic infection caused by the nematode Loa loa. The vector in the transmission of this infection is the horsefly (Tabanus) or the deerfly or mango fly (Chrysops). The larvae may be seen just beneath the skin or passing through the conjunctiva. Eye lesions are not uncommon. The disease is generally mild and painless.		15.0610
Mouth Ulcer
[description not available]		03.1750
Adamantiades-Behcet Disease
[description not available]		02.1510
Retinal Pigment Epithelial Detachment
[description not available]		02.1510
Behcet Syndrome
Rare chronic inflammatory disease involving the small blood vessels. It is of unknown etiology and characterized by mucocutaneous ulceration in the mouth and genital region and uveitis with hypopyon. The neuro-ocular form may cause blindness and death. SYNOVITIS; THROMBOPHLEBITIS; gastrointestinal ulcerations; RETINAL VASCULITIS; and OPTIC ATROPHY may occur as well.		02.1510
Retinal Detachment
Separation of the inner layers of the retina (neural retina) from the pigment epithelium. Retinal detachment occurs more commonly in men than in women, in eyes with degenerative myopia, in aging and in aphakia. It may occur after an uncomplicated cataract extraction, but it is seen more often if vitreous humor has been lost during surgery. (Dorland, 27th ed; Newell, Ophthalmology: Principles and Concepts, 7th ed, p310-12).		02.1510
Panuveitis
Inflammation in which both the anterior and posterior segments of the uvea are involved and a specific focus is not apparent. It is often severe and extensive and a serious threat to vision. Causes include systemic diseases such as tuberculosis, sarcoidosis, and syphilis, as well as malignancies. The intermediate segment of the eye is not involved.		02.1510
Oral Ulcer
A loss of mucous substance of the mouth showing local excavation of the surface, resulting from the sloughing of inflammatory necrotic tissue. It is the result of a variety of causes, e.g., denture irritation, aphthous stomatitis (STOMATITIS, APHTHOUS); NOMA; necrotizing gingivitis (GINGIVITIS, NECROTIZING ULCERATIVE); TOOTHBRUSHING; and various irritants. (From Jablonski, Dictionary of Dentistry, 1992, p842)		03.1750
Chromosome Deletion
Actual loss of portion of a chromosome.		08.73304
Brill-Symmers Disease
[description not available]		03.6730
Lymphoma, Follicular
Malignant lymphoma in which the lymphomatous cells are clustered into identifiable nodules within the LYMPH NODES. The nodules resemble to some extent the GERMINAL CENTER of lymph node follicles and most likely represent neoplastic proliferation of lymph node-derived follicular center B-LYMPHOCYTES.		03.6730
Deficiency of GP 2b 3a Complex
[description not available]		02.1710
Bleb
[description not available]		03.0140
Neoplasms, Bone Marrow
[description not available]		04.7361
Bone Marrow Neoplasms
Neoplasms located in the bone marrow. They are differentiated from neoplasms composed of bone marrow cells, such as MULTIPLE MYELOMA. Most bone marrow neoplasms are metastatic.		04.7361
Mouth Diseases
Diseases involving the MOUTH.		05.0590
Bullous Dermatoses
[description not available]		02.7830
Leukemia, Myelogenous, Aggressive Phase
[description not available]		013.094215
Paraganglioma, Gangliocytic
[description not available]		03.3560
Paraganglioma
A neural crest tumor usually derived from the chromoreceptor tissue of a paraganglion, such as the carotid body, or medulla of the adrenal gland (usually called a chromaffinoma or pheochromocytoma). It is more common in women than in men. (Stedman, 25th ed; from Segen, Dictionary of Modern Medicine, 1992)		03.3560
Porphyria
[description not available]		02.4920
Porphyrias
A diverse group of metabolic diseases characterized by errors in the biosynthetic pathway of HEME in the LIVER, the BONE MARROW, or both. They are classified by the deficiency of specific enzymes, the tissue site of enzyme defect, or the clinical features that include neurological (acute) or cutaneous (skin lesions). Porphyrias can be hereditary or acquired as a result of toxicity to the hepatic or erythropoietic marrow tissues.		02.4920
Experimental Leukemia
[description not available]		04.39200
Cryptogenic Fibrosing Alveolitis
[description not available]		07.3651
Esophageal Reflux
[description not available]		02.4620
Gastroesophageal Reflux
Retrograde flow of gastric juice (GASTRIC ACID) and/or duodenal contents (BILE ACIDS; PANCREATIC JUICE) into the distal ESOPHAGUS, commonly due to incompetence of the LOWER ESOPHAGEAL SPHINCTER.		02.4620
Idiopathic Pulmonary Fibrosis
A common interstitial lung disease of unknown etiology, usually occurring between 50-70 years of age. Clinically, it is characterized by an insidious onset of breathlessness with exertion and a nonproductive cough, leading to progressive DYSPNEA. Pathological features show scant interstitial inflammation, patchy collagen fibrosis, prominent fibroblast proliferation foci, and microscopic honeycomb change.		19.3651
Intestinal Perforation
Opening or penetration through the wall of the INTESTINES.		03.1850
Afibrinogenemia, Congenital
[description not available]		02.5920
Afibrinogenemia
A deficiency or absence of FIBRINOGEN in the blood.		02.5920
Agenesis of Hemidiaphragm
[description not available]		02.7730
Hernias, Diaphragmatic, Congenital
Protrusion of abdominal structures into the THORAX as a result of embryologic defects in the DIAPHRAGM often present in the neonatal period. It can be isolated, syndromic, non-syndromic or be a part of chromosome abnormality. Associated pulmonary hypoplasia and PULMONARY HYPERTENSION can further complicate stabilization and surgical intervention.		02.7730
Paralysis, Legs
[description not available]		02.1710
Paraplegia
Severe or complete loss of motor function in the lower extremities and lower portions of the trunk. This condition is most often associated with SPINAL CORD DISEASES, although BRAIN DISEASES; PERIPHERAL NERVOUS SYSTEM DISEASES; NEUROMUSCULAR DISEASES; and MUSCULAR DISEASES may also cause bilateral leg weakness.		02.1710
Acne
[description not available]		02.4820
Acne Vulgaris
A chronic disorder of the pilosebaceous apparatus associated with an increase in sebum secretion. It is characterized by open comedones (blackheads), closed comedones (whiteheads), and pustular nodules. The cause is unknown, but heredity and age are predisposing factors.		02.4820
Cutaneous T-Cell Lymphoma
[description not available]		02.1710
Lymphoma, T-Cell, Cutaneous
A group of lymphomas exhibiting clonal expansion of malignant T-lymphocytes arrested at varying stages of differentiation as well as malignant infiltration of the skin. MYCOSIS FUNGOIDES; SEZARY SYNDROME; LYMPHOMATOID PAPULOSIS; and PRIMARY CUTANEOUS ANAPLASTIC LARGE CELL LYMPHOMA are the best characterized of these disorders.		02.1710
Acute Hepatic Failure
[description not available]		09.5990
Liver Failure, Acute
A form of rapid-onset LIVER FAILURE, also known as fulminant hepatic failure, caused by severe liver injury or massive loss of HEPATOCYTES. It is characterized by sudden development of liver dysfunction and JAUNDICE. Acute liver failure may progress to exhibit cerebral dysfunction even HEPATIC COMA depending on the etiology that includes hepatic ISCHEMIA, drug toxicity, malignant infiltration, and viral hepatitis such as post-transfusion HEPATITIS B and HEPATITIS C.		04.5990
Granulomatosis, Wegener's
[description not available]		03.420
Allergic Angiitis
[description not available]		03.7330
Granulomatosis with Polyangiitis
A multisystemic disease of a complex genetic background. It is characterized by inflammation of the blood vessels (VASCULITIS) leading to damage in any number of organs. The common features include granulomatous inflammation of the RESPIRATORY TRACT and KIDNEYS. Most patients have measurable autoantibodies (ANTINEUTROPHIL CYTOPLASMIC ANTIBODIES) against MYELOBLASTIN.		08.420
Churg-Strauss Syndrome
Widespread necrotizing angiitis with granulomas. Pulmonary involvement is frequent. Asthma or other respiratory infection may precede evidence of vasculitis. Eosinophilia and lung involvement differentiate this disease from POLYARTERITIS NODOSA.		08.7330
Encapsulating Peritoneal Sclerosis
[description not available]		02.5220
Blood Pressure, High
[description not available]		06.54101
Hypertension
Persistently high systemic arterial BLOOD PRESSURE. Based on multiple readings (BLOOD PRESSURE DETERMINATION), hypertension is currently defined as when SYSTOLIC PRESSURE is consistently greater than 140 mm Hg or when DIASTOLIC PRESSURE is consistently 90 mm Hg or more.		011.54101
Stenosis, Pulmonary Vein
Narrowing of the PULMONARY VEIN.		04.4811
Androgen-Independent Prostatic Cancer
[description not available]		02.8530
Prostatic Neoplasms, Castration-Resistant
Tumors or cancer of the PROSTATE which can grow in the presence of low or residual amount of androgen hormones such as TESTOSTERONE.		14.8530
Carcinoma, Lewis Lung
A carcinoma discovered by Dr. Margaret R. Lewis of the Wistar Institute in 1951. This tumor originated spontaneously as a carcinoma of the lung of a C57BL mouse. The tumor does not appear to be grossly hemorrhagic and the majority of the tumor tissue is a semifirm homogeneous mass. (From Cancer Chemother Rep 2 1972 Nov;(3)1:325) It is also called 3LL and LLC and is used as a transplantable malignancy.		02.7930
Genetic Diseases
[description not available]		03.0910
Genetic Diseases, Inborn
Diseases that are caused by genetic mutations present during embryo or fetal development, although they may be observed later in life. The mutations may be inherited from a parent's genome or they may be acquired in utero.		03.0910
Heart Disease, Ischemic
[description not available]		02.1710
Myocardial Ischemia
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).		02.1710
Bacterial Disease
[description not available]		03.3820
Bacterial Infections
Infections by bacteria, general or unspecified.		03.3820
Conjunctival Diseases
Diseases involving the CONJUNCTIVA.		02.7630
47,XX,+21
[description not available]		03.9140
Down Syndrome
A chromosome disorder associated either with an extra chromosome 21 or an effective trisomy for chromosome 21. Clinical manifestations include hypotonia, short stature, brachycephaly, upslanting palpebral fissures, epicanthus, Brushfield spots on the iris, protruding tongue, small ears, short, broad hands, fifth finger clinodactyly, Simian crease, and moderate to severe INTELLECTUAL DISABILITY. Cardiac and gastrointestinal malformations, a marked increase in the incidence of LEUKEMIA, and the early onset of ALZHEIMER DISEASE are also associated with this condition. Pathologic features include the development of NEUROFIBRILLARY TANGLES in neurons and the deposition of AMYLOID BETA-PROTEIN, similar to the pathology of ALZHEIMER DISEASE. (Menkes, Textbook of Child Neurology, 5th ed, p213)		03.9140
Impaired Glucose Tolerance
[description not available]		02.1710
Compensatory Hyperinsulinemia
A GLUCOSE-induced HYPERINSULINEMIA, a marker of insulin-resistant state. It is a mechanism to compensate for reduced sensitivity to insulin.		02.1710
Hyperinsulinism
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.		02.1710
Glucose Intolerance
A pathological state in which BLOOD GLUCOSE level is less than approximately 140 mg/100 ml of PLASMA at fasting, and above approximately 200 mg/100 ml plasma at 30-, 60-, or 90-minute during a GLUCOSE TOLERANCE TEST. This condition is seen frequently in DIABETES MELLITUS, but also occurs with other diseases and MALNUTRITION.		02.1710
Central Nervous System Disease
[description not available]		04.0850
Central Nervous System Diseases
Diseases of any component of the brain (including the cerebral hemispheres, diencephalon, brain stem, and cerebellum) or the spinal cord.		04.0850
DRESS Syndrome
[description not available]		02.5720
Cancer of the Retina
[description not available]		03.3260
Eye Cancer, Retinoblastoma
[description not available]		0340
Neoplasm Seeding
The local implantation of tumor cells by contamination of instruments and surgical equipment during and after surgical resection, resulting in local growth of the cells and tumor formation.		05.4851
Retinoblastoma
A malignant tumor arising from the nuclear layer of the retina that is the most common primary tumor of the eye in children. The tumor tends to occur in early childhood or infancy and may be present at birth. The majority are sporadic, but the condition may be transmitted as an autosomal dominant trait. Histologic features include dense cellularity, small round polygonal cells, and areas of calcification and necrosis. An abnormal pupil reflex (leukokoria); NYSTAGMUS, PATHOLOGIC; STRABISMUS; and visual loss represent common clinical characteristics of this condition. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2104)		0840
Polyarthritis
[description not available]		03.9240
Milk-Alkali Syndrome
[description not available]		03.8840
Arthritis
Acute or chronic inflammation of JOINTS.		03.9240
Hypercalcemia
Abnormally high level of calcium in the blood.		08.8840
Cancer of the Vulva
[description not available]		02.7730
Vulvar Neoplasms
Tumors or cancer of the VULVA.		02.7730
Complications, Hematologic Pregnancy
[description not available]		04.5350
Extranodal NK-T-Cell Lymphoma
[description not available]		02.1710
Ptosis, Eyelid
[description not available]		02.5520
Anti-MuSK Myasthenia Gravis
[description not available]		02.2110
Blepharoptosis
Drooping of the upper lid due to deficient development or paralysis of the levator palpebrae muscle.		02.5520
Myasthenia Gravis
A disorder of neuromuscular transmission characterized by fatigable weakness of cranial and skeletal muscles with elevated titers of ACETYLCHOLINE RECEPTORS or muscle-specific receptor tyrosine kinase (MuSK) autoantibodies. Clinical manifestations may include ocular muscle weakness (fluctuating, asymmetric, external ophthalmoplegia; diplopia; ptosis; and weakness of eye closure) and extraocular fatigable weakness of facial, bulbar, respiratory, and proximal limb muscles. The disease may remain limited to the ocular muscles (ocular myasthenia). THYMOMA is commonly associated with this condition.		02.2110
FMR1-Related Primary Ovarian Insufficiency
[description not available]		03.1750
Primary Ovarian Insufficiency
Cessation of ovarian function after MENARCHE but before the age of 40, without or with OVARIAN FOLLICLE depletion. It is characterized by the presence of OLIGOMENORRHEA or AMENORRHEA, elevated GONADOTROPINS, and low ESTRADIOL levels. It is a state of female HYPERGONADOTROPIC HYPOGONADISM. Etiologies include genetic defects, autoimmune processes, chemotherapy, radiation, and infections. The most commonly known genetic cause is the expansion of a CGG repeat to 55 to 199 copies in the 5' untranslated region in the X-linked FMR1 gene.		03.1750
Tumour Lysis Syndrome
[description not available]		04.67100
Tumor Lysis Syndrome
A syndrome resulting from cytotoxic therapy, occurring generally in aggressive, rapidly proliferating lymphoproliferative disorders. It is characterized by combinations of hyperuricemia, lactic acidosis, hyperkalemia, hyperphosphatemia and hypocalcemia.		04.67100
Respiratory Tract Diseases
Diseases involving the RESPIRATORY SYSTEM.		03.1210
Fatty Liver, Nonalcoholic
[description not available]		02.5520
Non-alcoholic Fatty Liver Disease
Fatty liver finding without excessive ALCOHOL CONSUMPTION.		02.5520
Preterm Birth
[description not available]		02.1710
Premature Birth
CHILDBIRTH before 37 weeks of PREGNANCY (259 days from the first day of the mother's last menstrual period, or 245 days after FERTILIZATION).		02.1710
Adenoma, Prostatic
[description not available]		02.5220
Prostatic Hyperplasia
Increase in constituent cells in the PROSTATE, leading to enlargement of the organ (hypertrophy) and adverse impact on the lower urinary tract function. This can be caused by increased rate of cell proliferation, reduced rate of cell death, or both.		02.5220
Chromosome Inversion
An aberration in which a chromosomal segment is deleted and reinserted in the same place but turned 180 degrees from its original orientation, so that the gene sequence for the segment is reversed with respect to that of the rest of the chromosome.		03.76100
Chromosomal Triplication
[description not available]		07.51291
Leukostasis
Abnormal intravascular leukocyte aggregation and clumping often seen in leukemia patients. The brain and lungs are the two most commonly affected organs. This acute syndrome requires aggressive cytoreductive modalities including chemotherapy and/or leukophoresis. It is differentiated from LEUKEMIC INFILTRATION which is a neoplastic process where leukemic cells invade organs.		09.3870
Rupture
Forcible or traumatic tear or break of an organ or other soft part of the body.		04.6330
Cancer of Cervix
[description not available]		05.5182
Bleeding Between Periods
[description not available]		02.2110
Uterine Cervical Neoplasms
Tumors or cancer of the UTERINE CERVIX.		05.5182
Metrorrhagia
Abnormal uterine bleeding that is not related to MENSTRUATION, usually in females without regular MENSTRUAL CYCLE. The irregular and unpredictable bleeding usually comes from a dysfunctional ENDOMETRIUM.		02.2110
Allergy, Drug
[description not available]		04.9381
Drug Hypersensitivity
Immunologically mediated adverse reactions to medicinal substances used legally or illegally.		04.9381
Cholangiocellular Carcinoma
[description not available]		04.8271
Bile Duct Cancer
[description not available]		04.9481
Bile Duct Neoplasms
Tumors or cancer of the BILE DUCTS.		04.9481
Cholangiocarcinoma
A malignant tumor arising from the epithelium of the BILE DUCTS.		04.8271
Cockayne Syndrome
A syndrome characterized by multiple system abnormalities including DWARFISM; PHOTOSENSITIVITY DISORDERS; PREMATURE AGING; and HEARING LOSS. It is caused by mutations of a number of autosomal recessive genes encoding proteins that involve transcriptional-coupled DNA REPAIR processes. Cockayne syndrome is classified by the severity and age of onset. Type I (classical; CSA) is early childhood onset in the second year of life; type II (congenital; CSB) is early onset at birth with severe symptoms; type III (xeroderma pigmentosum; XP) is late childhood onset with mild symptoms.		02.2110
Cancer of Granulosa Cells
[description not available]		02.9840
Glaucoma, Neovascular
A form of secondary glaucoma which develops as a consequence of another ocular disease and is attributed to the forming of new vessels in the angle of the anterior chamber.		03.1210
Schistosoma japonicum Infection
[description not available]		02.2110
Diffuse Large B-Cell Lymphoma
[description not available]		07.09100
Lymphoma, Large B-Cell, Diffuse
Malignant lymphoma composed of large B lymphoid cells whose nuclear size can exceed normal macrophage nuclei, or more than twice the size of a normal lymphocyte. The pattern is predominantly diffuse. Most of these lymphomas represent the malignant counterpart of B-lymphocytes at midstage in the process of differentiation.		07.09100
Auricular Fibrillation
[description not available]		02.7730
Atrial Fibrillation
Abnormal cardiac rhythm that is characterized by rapid, uncoordinated firing of electrical impulses in the upper chambers of the heart (HEART ATRIA). In such case, blood cannot be effectively pumped into the lower chambers of the heart (HEART VENTRICLES). It is caused by abnormal impulse generation.		02.7730
American Trypanosomiasis
[description not available]		02.2110
Chagas Disease
Infection with the protozoan parasite TRYPANOSOMA CRUZI, a form of TRYPANOSOMIASIS endemic in Central and South America. It is named after the Brazilian physician Carlos Chagas, who discovered the parasite. Infection by the parasite (positive serologic result only) is distinguished from the clinical manifestations that develop years later, such as destruction of PARASYMPATHETIC GANGLIA; CHAGAS CARDIOMYOPATHY; and dysfunction of the ESOPHAGUS or COLON.		02.2110
Nervous System Disorders
[description not available]		05.0631
Nervous System Diseases
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.		05.0631
Duncan Disease
[description not available]		05.661
Lymphoproliferative Disorders
Disorders characterized by proliferation of lymphoid tissue, general or unspecified.		05.661
Mucositis, Oral
[description not available]		03.4620
Stomatitis
INFLAMMATION of the soft tissues of the MOUTH, such as MUCOSA; PALATE; GINGIVA; and LIP.		03.4620
Anguilluliasis
[description not available]		02.5520
Strongyloidiasis
Infection with nematodes of the genus STRONGYLOIDES. The presence of larvae may produce pneumonitis and the presence of adult worms in the intestine could lead to moderate to severe diarrhea.		02.5520
Angor Pectoris
[description not available]		04.7821
Cerebral Ischemia
[description not available]		04.7261
Diseases, Peripheral Vascular
[description not available]		02.2110
Angina Pectoris
The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.		04.7821
Brain Ischemia
Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.		04.7261
Peripheral Vascular Diseases
Pathological processes involving any one of the BLOOD VESSELS in the vasculature outside the HEART.		02.2110
Clinically Isolated CNS Demyelinating Syndrome
[description not available]		02.2110
Demyelinating Diseases
Diseases characterized by loss or dysfunction of myelin in the central or peripheral nervous system.		02.2110
Ovarian Diseases
Pathological processes of the OVARY.		02.2110
Cells, Neoplasm Circulating
[description not available]		04.9781
Anaplastic Astrocytoma
[description not available]		05.4653
Anaplastic Oligodendroglioma
[description not available]		05.2943
Astrocytoma
Neoplasms of the brain and spinal cord derived from glial cells which vary from histologically benign forms to highly anaplastic and malignant tumors. Fibrillary astrocytomas are the most common type and may be classified in order of increasing malignancy (grades I through IV). In the first two decades of life, astrocytomas tend to originate in the cerebellar hemispheres; in adults, they most frequently arise in the cerebrum and frequently undergo malignant transformation. (From Devita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2013-7; Holland et al., Cancer Medicine, 3d ed, p1082)		05.4653
Oligodendroglioma
A relatively slow-growing glioma that is derived from oligodendrocytes and tends to occur in the cerebral hemispheres, thalamus, or lateral ventricle. They may present at any age, but are most frequent in the third to fifth decades, with an earlier incidence peak in the first decade. Histologically, these tumors are encapsulated, relatively avascular, and tend to form cysts and microcalcifications. Neoplastic cells tend to have small round nuclei surrounded by unstained nuclei. The tumors may vary from well-differentiated to highly anaplastic forms. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2052; Adams et al., Principles of Neurology, 6th ed, p655)		010.2943
Arthritides, Bacterial
[description not available]		02.2110
Nephrotic Syndrome
A condition characterized by severe PROTEINURIA, greater than 3.5 g/day in an average adult. The substantial loss of protein in the urine results in complications such as HYPOPROTEINEMIA; generalized EDEMA; HYPERTENSION; and HYPERLIPIDEMIAS. Diseases associated with nephrotic syndrome generally cause chronic kidney dysfunction.		02.2110
Degenerative Disc Disease
[description not available]		02.2110
Demyelinative Myelitis
[description not available]		02.2110
Intervertebral Disc Degeneration
Degenerative changes in the INTERVERTEBRAL DISC due to aging or structural damage, especially to the vertebral end-plates.		02.2110
Anemias, Iron-Deficiency
[description not available]		02.2110
Anemia, Iron-Deficiency
Anemia characterized by decreased or absent iron stores, low serum iron concentration, low transferrin saturation, and low hemoglobin concentration or hematocrit value. The erythrocytes are hypochromic and microcytic and the iron binding capacity is increased.		02.2110
Thrombocytopathy
[description not available]		02.7730
Blood Platelet Disorders
Disorders caused by abnormalities in platelet count or function.		02.7730
Dermatitis Exfoliativa
[description not available]		03.1350
Dermatitis, Exfoliative
The widespread involvement of the skin by a scaly, erythematous dermatitis occurring either as a secondary or reactive process to an underlying cutaneous disorder (e.g., atopic dermatitis, psoriasis, etc.), or as a primary or idiopathic disease. It is often associated with the loss of hair and nails, hyperkeratosis of the palms and soles, and pruritus. (From Dorland, 27th ed)		03.1350
Hematoma, Subdural
Accumulation of blood in the SUBDURAL SPACE between the DURA MATER and the arachnoidal layer of the MENINGES. This condition primarily occurs over the surface of a CEREBRAL HEMISPHERE, but may develop in the spinal canal (HEMATOMA, SUBDURAL, SPINAL). Subdural hematoma can be classified as the acute or the chronic form, with immediate or delayed symptom onset, respectively. Symptoms may include loss of consciousness, severe HEADACHE, and deteriorating mental status.		08.5995
Chronic Fatigue and Immune Dysfunction Syndrome
[description not available]		0310
Fatigue Syndrome, Chronic
A syndrome characterized by persistent or recurrent fatigue, diffuse musculoskeletal pain, sleep disturbances, and subjective cognitive impairment of 6 months duration or longer. Symptoms are not caused by ongoing exertion; are not relieved by rest; and result in a substantial reduction of previous levels of occupational, educational, social, or personal activities. Minor alterations of immune, neuroendocrine, and autonomic function may be associated with this syndrome. There is also considerable overlap between this condition and FIBROMYALGIA. (From Semin Neurol 1998;18(2):237-42; Ann Intern Med 1994 Dec 15;121(12): 953-9)		0310
Paronychia
An inflammatory reaction involving the folds of the skin surrounding the fingernail. It is characterized by acute or chronic purulent, tender, and painful swellings of the tissues around the nail, caused by an abscess of the nail fold. The pathogenic yeast causing paronychia is most frequently Candida albicans. Saprophytic fungi may also be involved. The causative bacteria are usually Staphylococcus, Pseudomonas aeruginosa, or Streptococcus. (Andrews' Diseases of the Skin, 8th ed, p271)		02.0810
Benign Mastocytoma
[description not available]		04.3641
Autoimmune Disease
[description not available]		012.61150
Autoimmune Diseases
Disorders that are characterized by the production of antibodies that react with host tissues or immune effector cells that are autoreactive to endogenous peptides.		012.61150
Allergic Encephalomyelitis
[description not available]		02.7730
Hepatic Veno Occlusive Disease
[description not available]		03.4220
Hepatic Veno-Occlusive Disease
Liver disease that is caused by injuries to the ENDOTHELIAL CELLS of the vessels and subendothelial EDEMA, but not by THROMBOSIS. Extracellular matrix, rich in FIBRONECTINS, is usually deposited around the HEPATIC VEINS leading to venous outflow occlusion and sinusoidal obstruction.		03.4220
Peripheral Arterial Diseases
[description not available]		04.8571
Arterial Obstructive Diseases
[description not available]		05.1660
Arterial Occlusive Diseases
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.		05.1660
Peripheral Arterial Disease
Lack of perfusion in the EXTREMITIES resulting from atherosclerosis. It is characterized by INTERMITTENT CLAUDICATION, and an ANKLE BRACHIAL INDEX of 0.9 or less.		04.8571
Chemodectoma
[description not available]		09.22110
Chondroma
A benign neoplasm derived from mesodermal cells that form cartilage. It may remain within the substance of a cartilage or bone (true chondroma or enchondroma) or may develop on the surface of a cartilage (ecchondroma or ecchondrosis). (Dorland, 27th ed; Stedman, 25th ed)		09.3120
Adenoma, beta-Cell
[description not available]		02.0810
Insulinoma
A benign tumor of the PANCREATIC BETA CELLS. Insulinoma secretes excess INSULIN resulting in HYPOGLYCEMIA.		02.0810
Rhabdomyosarcoma
A malignant solid tumor arising from mesenchymal tissues which normally differentiate to form striated muscle. It can occur in a wide variety of sites. It is divided into four distinct types: pleomorphic, predominantly in male adults; alveolar (RHABDOMYOSARCOMA, ALVEOLAR), mainly in adolescents and young adults; embryonal (RHABDOMYOSARCOMA, EMBRYONAL), predominantly in infants and children; and botryoidal, also in young children. It is one of the most frequently occurring soft tissue sarcomas and the most common in children under 15. (From Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p2186; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, pp1647-9)		07.7530
Emesis
[description not available]		08.4783
Vomiting
The forcible expulsion of the contents of the STOMACH through the MOUTH.		08.4783
Genome Instability
[description not available]		08.64161
Esophagitis
INFLAMMATION, acute or chronic, of the ESOPHAGUS caused by BACTERIA, chemicals, or TRAUMA.		02.4720
Peripheral Nerve Diseases
[description not available]		02.9940
Peripheral Nervous System Diseases
Diseases of the peripheral nerves external to the brain and spinal cord, which includes diseases of the nerve roots, ganglia, plexi, autonomic nerves, sensory nerves, and motor nerves.		02.9940
Infection
[description not available]		05.7541
Infections
Invasion of the host organism by microorganisms or their toxins or by parasites that can cause pathological conditions or diseases.		05.7541
Weight Gain
Increase in BODY WEIGHT over existing weight.		03.360
Injuries, Spinal Cord
[description not available]		03.0140
Spinal Cord Injuries
Penetrating and non-penetrating injuries to the spinal cord resulting from traumatic external forces (e.g., WOUNDS, GUNSHOT; WHIPLASH INJURIES; etc.).		03.0140
Sycosis
[description not available]		02.4920
Folliculitis
Inflammation of follicles, primarily hair follicles.		07.4920
Merkel Cell Cancer
[description not available]		07.3593
Carcinoma, Merkel Cell
A carcinoma arising from MERKEL CELLS located in the basal layer of the epidermis and occurring most commonly as a primary neuroendocrine carcinoma of the skin. Merkel cells are tactile cells of neuroectodermal origin and histologically show neurosecretory granules. The skin of the head and neck are a common site of Merkel cell carcinoma, occurring generally in elderly patients. (Holland et al., Cancer Medicine, 3d ed, p1245)		19.3593
Cytomegalic Inclusion Disease
[description not available]		02.9740
Cytomegalovirus Infections
Infection with CYTOMEGALOVIRUS, characterized by enlarged cells bearing intranuclear inclusions. Infection may be in almost any organ, but the salivary glands are the most common site in children, as are the lungs in adults.		02.9740
Cytomegalovirus
A genus of the family HERPESVIRIDAE, subfamily BETAHERPESVIRINAE, infecting the salivary glands, liver, spleen, lungs, eyes, and other organs, in which they produce characteristically enlarged cells with intranuclear inclusions. Infection with Cytomegalovirus is also seen as an opportunistic infection in AIDS.		03.360
Angiogranuloma
[description not available]		02.0810
Adenocarcinoma, Clear Cell
An adenocarcinoma characterized by the presence of varying combinations of clear and hobnail-shaped tumor cells. There are three predominant patterns described as tubulocystic, solid, and papillary. These tumors, usually located in the female reproductive organs, have been seen more frequently in young women since 1970 as a result of the association with intrauterine exposure to diethylstilbestrol. (From Holland et al., Cancer Medicine, 3d ed)		02.0810
Maculopapular Cutaneous Mastocytosis
[description not available]		02.7730
Cognition Disorders
Disorders characterized by disturbances in mental processes related to learning, thinking, reasoning, and judgment.		02.0810
Cardiac Cancer
[description not available]		04.1331
Angiosarcoma
[description not available]		04.3740
Hemangiosarcoma
A rare malignant neoplasm characterized by rapidly proliferating, extensively infiltrating, anaplastic cells derived from blood vessels and lining irregular blood-filled or lumpy spaces. (Stedman, 25th ed)		04.3740
Carcinoma, Basal Cell, Pigmented
[description not available]		04.1730
Kaposi Sarcoma
[description not available]		08.07112
Carcinoma, Basal Cell
A malignant skin neoplasm that seldom metastasizes but has potentialities for local invasion and destruction. Clinically it is divided into types: nodular, cicatricial, morphaic, and erythematoid (pagetoid). They develop on hair-bearing skin, most commonly on sun-exposed areas. Approximately 85% are found on the head and neck area and the remaining 15% on the trunk and limbs. (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1471)		04.1730
Sarcoma, Kaposi
A multicentric, malignant neoplastic vascular proliferation characterized by the development of bluish-red cutaneous nodules, usually on the lower extremities, most often on the toes or feet, and slowly increasing in size and number and spreading to more proximal areas. The tumors have endothelium-lined channels and vascular spaces admixed with variably sized aggregates of spindle-shaped cells, and often remain confined to the skin and subcutaneous tissue, but widespread visceral involvement may occur. Kaposi's sarcoma occurs spontaneously in Jewish and Italian males in Europe and the United States. An aggressive variant in young children is endemic in some areas of Africa. A third form occurs in about 0.04% of kidney transplant patients. There is also a high incidence in AIDS patients. (From Dorland, 27th ed & Holland et al., Cancer Medicine, 3d ed, pp2105-7) HHV-8 is the suspected cause.		08.07112
Bilateral Headache
[description not available]		06.6362
Headache
The symptom of PAIN in the cranial region. It may be an isolated benign occurrence or manifestation of a wide variety of HEADACHE DISORDERS.		06.6362
Abdominal Neoplasms
New abnormal growth of tissue in the ABDOMEN.		08.21143
Cancer of Gallbladder
[description not available]		03.8721
Infections, Helicobacter
[description not available]		03.1750
Gallbladder Neoplasms
Tumors or cancer of the gallbladder.		03.8721
Gastritis
Inflammation of the GASTRIC MUCOSA, a lesion observed in a number of unrelated disorders.		02.110
Helicobacter Infections
Infections with organisms of the genus HELICOBACTER, particularly, in humans, HELICOBACTER PYLORI. The clinical manifestations are focused in the stomach, usually the gastric mucosa and antrum, and the upper duodenum. This infection plays a major role in the pathogenesis of type B gastritis and peptic ulcer disease.		03.1750
Hemoperitoneum
Accumulations of blood in the PERITONEAL CAVITY due to internal HEMORRHAGE.		09.150
Neurogenic Inflammation
Inflammation caused by an injurious stimulus of peripheral neurons and resulting in release of neuropeptides which affect vascular permeability and help initiate proinflammatory and immune reactions at the site of injury.		02.0810
Allodynia
[description not available]		02.0810
Pityriasis Rubra Pilaris
A chronic skin disease characterized by small follicular papules, disseminated reddish-brown scaly patches, and often, palmoplantar hyperkeratosis. The papules are about the size of a pin and topped by a horny plug.		02.0810
Polyneuropathy, Acquired
[description not available]		02.0810
Polyneuropathies
Diseases of multiple peripheral nerves simultaneously. Polyneuropathies usually are characterized by symmetrical, bilateral distal motor and sensory impairment with a graded increase in severity distally. The pathological processes affecting peripheral nerves include degeneration of the axon, myelin or both. The various forms of polyneuropathy are categorized by the type of nerve affected (e.g., sensory, motor, or autonomic), by the distribution of nerve injury (e.g., distal vs. proximal), by nerve component primarily affected (e.g., demyelinating vs. axonal), by etiology, or by pattern of inheritance.		02.0810
Retroperitoneal Neoplasms
New abnormal growth of tissue in the RETROPERITONEAL SPACE.		07.4671
Benign Fibrous Mesothelioma
[description not available]		02.7530
Acoustic Neurinoma, Bilateral
[description not available]		02.9840
Neurofibromatosis 2
An autosomal dominant disorder characterized by a high incidence of bilateral acoustic neuromas as well as schwannomas (NEURILEMMOMA) of other cranial and peripheral nerves, and other benign intracranial tumors including meningiomas, ependymomas, spinal neurofibromas, and gliomas. The disease has been linked to mutations of the NF2 gene (GENES, NEUROFIBROMATOSIS 2) on chromosome 22 (22q12) and usually presents clinically in the first or second decade of life.		02.9840
Granuloma, Hodgkin
[description not available]		05.75120
Hodgkin Disease
A malignant disease characterized by progressive enlargement of the lymph nodes, spleen, and general lymphoid tissue. In the classical variant, giant usually multinucleate Hodgkin's and REED-STERNBERG CELLS are present; in the nodular lymphocyte predominant variant, lymphocytic and histiocytic cells are seen.		05.75120
Impotence
[description not available]		02.0810
Erectile Dysfunction
The inability in the male to have a PENILE ERECTION due to psychological or organ dysfunction.		02.0810
Budd-Chiari Syndrome
A condition in which the hepatic venous outflow is obstructed anywhere from the small HEPATIC VEINS to the junction of the INFERIOR VENA CAVA and the RIGHT ATRIUM. Usually the blockage is extrahepatic and caused by blood clots (THROMBUS) or fibrous webs. Parenchymal FIBROSIS is uncommon.		02.110
Calcinosis-Raynaud Phenomenon-Sclerodactyly-Telangiectasia
[description not available]		02.0810
Fibromatosis, Abdominal
A relatively large mass of unusually firm scarlike connective tissue resulting from active participation of fibroblasts, occurring most frequently in the abdominal muscles of women who have borne children. The fibroblasts infiltrate surrounding muscle and fascia. (Stedman, 25th ed)		03.6930
Left Ventricular Hypertrophy
[description not available]		05.341
Hypertrophy, Left Ventricular
Enlargement of the LEFT VENTRICLE of the heart. This increase in ventricular mass is attributed to sustained abnormal pressure or volume loads and is a contributor to cardiovascular morbidity and mortality.		05.341
Airway Hyper-Responsiveness
[description not available]		02.0810
Angiitis
[description not available]		04.3440
Vasculitis
Inflammation of any one of the blood vessels, including the ARTERIES; VEINS; and rest of the vasculature system in the body.		04.3440
Langerhans Cell Sarcoma
Rare malignant neoplasm of dendritic LANGERHANS CELLS exhibiting atypical cytology, frequent mitoses, and aggressive clinical behavior. They can be distinguished from other histiocytic and dendritic proliferations by immunohistochemical and ultrastructure studies. Cytologically benign proliferations of Langerhans cells are called LANGERHANS CELL HISTIOCYTOSIS.		07.110
Chloasma
[description not available]		04.2460
Melanosis
Disorders of increased melanin pigmentation that develop without preceding inflammatory disease.		09.2460
Segond Fracture
[description not available]		02.0810
Tibial Fractures
Fractures of the TIBIA.		02.0810
Depression, Endogenous
[description not available]		0310
Depressive Disorder
An affective disorder manifested by either a dysphoric mood or loss of interest or pleasure in usual activities. The mood disturbance is prominent and relatively persistent.		0310
Cancer of Digestive System
[description not available]		04.6932
Digestive System Neoplasms
Tumors or cancer of the DIGESTIVE SYSTEM.		04.6932
DDD MPGNII
[description not available]		03.4370
Glomerulonephritis, Membranoproliferative
Chronic glomerulonephritis characterized histologically by proliferation of MESANGIAL CELLS, increase in the MESANGIAL EXTRACELLULAR MATRIX, and a thickening of the glomerular capillary walls. This may appear as a primary disorder or secondary to other diseases including infections and autoimmune disease SYSTEMIC LUPUS ERYTHEMATOSUS. Various subtypes are classified by their abnormal ultrastructures and immune deposits. Hypocomplementemia is a characteristic feature of all types of MPGN.		03.4370
Neurilemoma
[description not available]		04.9580
Neurilemmoma
A neoplasm that arises from SCHWANN CELLS of the cranial, peripheral, and autonomic nerves. Clinically, these tumors may present as a cranial neuropathy, abdominal or soft tissue mass, intracranial lesion, or with spinal cord compression. Histologically, these tumors are encapsulated, highly vascular, and composed of a homogenous pattern of biphasic fusiform-shaped cells that may have a palisaded appearance. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp964-5)		16.9580
Cardiomyopathy, Hypertrophic Obstructive
[description not available]		02.0810
Cardiomyopathy, Hypertrophic
A form of CARDIAC MUSCLE disease, characterized by left and/or right ventricular hypertrophy (HYPERTROPHY, LEFT VENTRICULAR; HYPERTROPHY, RIGHT VENTRICULAR), frequent asymmetrical involvement of the HEART SEPTUM, and normal or reduced left ventricular volume. Risk factors include HYPERTENSION; AORTIC STENOSIS; and gene MUTATION; (FAMILIAL HYPERTROPHIC CARDIOMYOPATHY).		02.0810
Di Guglielmo Disease
[description not available]		04.23170
Leukemia, Erythroblastic, Acute
A myeloproliferative disorder characterized by neoplastic proliferation of erythroblastic and myeloblastic elements with atypical erythroblasts and myeloblasts in the peripheral blood.		04.23170
Vascular Diseases
Pathological processes involving any of the BLOOD VESSELS in the cardiac or peripheral circulation. They include diseases of ARTERIES; VEINS; and rest of the vasculature system in the body.		06.2471
Neutrophilic Leukemia, Chronic
[description not available]		02.7330
Leukemia, Neutrophilic, Chronic
A rare myeloproliferative disorder that is characterized by a sustained, mature neutrophilic leukocytosis. No monocytosis, EOSINOPHILIA, or basophilia is present, nor is there a PHILADELPHIA CHROMOSOME or bcr-abl fusion gene (GENES, ABL).		02.7330
Hyperoxia
An abnormal increase in the amount of oxygen in the tissues and organs.		02.7530
Allergic Reaction
[description not available]		04.1330
Hypersensitivity
Altered reactivity to an antigen, which can result in pathologic reactions upon subsequent exposure to that particular antigen.		04.1330
Osteolysis
Dissolution of bone that particularly involves the removal or loss of calcium.		08.940
Femoral Neoplasms
New abnormal growth of tissue in the FEMUR.		02.110
Cancer of Endometrium
[description not available]		04.6860
Endometrial Neoplasms
Tumors or cancer of ENDOMETRIUM, the mucous lining of the UTERUS. These neoplasms can be benign or malignant. Their classification and grading are based on the various cell types and the percent of undifferentiated cells.		16.6860
Alastrim
[description not available]		03.0410
Smallpox
An acute, highly contagious, often fatal infectious disease caused by an orthopoxvirus characterized by a biphasic febrile course and distinctive progressive skin eruptions. Vaccination has succeeded in eradicating smallpox worldwide. (Dorland, 28th ed)		03.0410
Hair Diseases
Diseases affecting the orderly growth and persistence of hair.		07.5170
Electrolytes
Substances that dissociate into two or more ions, to some extent, in water. Solutions of electrolytes thus conduct an electric current and can be decomposed by it (ELECTROLYSIS). (Grant & Hackh's Chemical Dictionary, 5th ed)		02.110
Pancytopenia
Deficiency of all three cell elements of the blood, erythrocytes, leukocytes and platelets.		012.6123
AIDS-Related Opportunistic Infections
Opportunistic infections found in patients who test positive for human immunodeficiency virus (HIV). The most common include PNEUMOCYSTIS PNEUMONIA, Kaposi's sarcoma, cryptosporidiosis, herpes simplex, toxoplasmosis, cryptococcosis, and infections with Mycobacterium avium complex, Microsporidium, and Cytomegalovirus.		05.3222
Drug-Induced Stevens Johnson Syndrome
[description not available]		03.6490
Stevens-Johnson Syndrome
Rare cutaneous eruption characterized by extensive KERATINOCYTE apoptosis resulting in skin detachment with mucosal involvement. It is often provoked by the use of drugs (e.g., antibiotics and anticonvulsants) or associated with PNEUMONIA, MYCOPLASMA. It is considered a continuum of Toxic Epidermal Necrolysis.		03.6490
CJD (Creutzfeldt-Jakob Disease)
[description not available]		02.110
Besnier-Boeck Disease
[description not available]		02.110
Creutzfeldt-Jakob Syndrome
A rare transmissible encephalopathy most prevalent between the ages of 50 and 70 years. Affected individuals may present with sleep disturbances, personality changes, ATAXIA; APHASIA, visual loss, weakness, muscle atrophy, MYOCLONUS, progressive dementia, and death within one year of disease onset. A familial form exhibiting autosomal dominant inheritance and a new variant CJD (potentially associated with ENCEPHALOPATHY, BOVINE SPONGIFORM) have been described. Pathological features include prominent cerebellar and cerebral cortical spongiform degeneration and the presence of PRIONS. (From N Engl J Med, 1998 Dec 31;339(27))		02.110
Sarcoidosis
An idiopathic systemic inflammatory granulomatous disorder comprised of epithelioid and multinucleated giant cells with little necrosis. It usually invades the lungs with fibrosis and may also involve lymph nodes, skin, liver, spleen, eyes, phalangeal bones, and parotid glands.		02.110
Asthenia
Clinical sign or symptom manifested as debility, or lack or loss of strength and energy.		03.4420
Cancer of the Thymus
[description not available]		06.63102
Thymus Neoplasms
Tumors or cancer of the THYMUS GLAND.		06.63102
Tooth Erosion
Progressive loss of the hard substance of a tooth by chemical processes that do not involve bacterial action. (Jablonski, Dictionary of Dentistry, 1992, p296)		02.110
Muscular Weakness
[description not available]		02.110
Breathlessness
[description not available]		05.9691
Dyspnea
Difficult or labored breathing.		05.9691
Muscle Weakness
A vague complaint of debility, fatigue, or exhaustion attributable to weakness of various muscles. The weakness can be characterized as subacute or chronic, often progressive, and is a manifestation of many muscle and neuromuscular diseases. (From Wyngaarden et al., Cecil Textbook of Medicine, 19th ed, p2251)		02.110
Blood Loss, Postoperative
[description not available]		02.110
Petechiae
Pinhead size (3 mm) skin discolorization due to hemorrhage.		02.110
Eyelid Diseases
Diseases involving the EYELIDS.		02.4520
Ecchymosis
Extravasation of blood into the skin, resulting in a nonelevated, rounded or irregular, blue or purplish patch, larger than a petechia.		02.110
Purpura
Purplish or brownish red discoloration, easily visible through the epidermis, caused by hemorrhage into the tissues. When the size of the discolorization is		02.110
Eosinophilic Leukemia, Acute
[description not available]		02.4820
African Sleeping Sickness
[description not available]		02.110
Trypanosomiasis, African
A disease endemic among people and animals in Central Africa. It is caused by various species of trypanosomes, particularly T. gambiense and T. rhodesiense. Its second host is the TSETSE FLY. Involvement of the central nervous system produces African sleeping sickness. Nagana is a rapidly fatal trypanosomiasis of horses and other animals.		02.110
Angiospasm, Intracranial
[description not available]		02.7830
Hemorrhage, Subarachnoid
[description not available]		03.3560
Subarachnoid Hemorrhage
Bleeding into the intracranial or spinal SUBARACHNOID SPACE, most resulting from INTRACRANIAL ANEURYSM rupture. It can occur after traumatic injuries (SUBARACHNOID HEMORRHAGE, TRAUMATIC). Clinical features include HEADACHE; NAUSEA; VOMITING, nuchal rigidity, variable neurological deficits and reduced mental status.		08.3560
Vasospasm, Intracranial
Constriction of arteries in the SKULL due to sudden, sharp, and often persistent smooth muscle contraction in blood vessels. Intracranial vasospasm results in reduced vessel lumen caliber, restricted blood flow to the brain, and BRAIN ISCHEMIA that may lead to hypoxic-ischemic brain injury (HYPOXIA-ISCHEMIA, BRAIN).		02.7830
Mesothelioma
A tumor derived from mesothelial tissue (peritoneum, pleura, pericardium). It appears as broad sheets of cells, with some regions containing spindle-shaped, sarcoma-like cells and other regions showing adenomatous patterns. Pleural mesotheliomas have been linked to exposure to asbestos. (Dorland, 27th ed)		111.3193
Right Ventricular Dysfunction
[description not available]		07.2542
Abortion, Tubal
[description not available]		02.9640
Abortion, Spontaneous
Expulsion of the product of FERTILIZATION before completing the term of GESTATION and without deliberate interference.		02.9640
Acute Biphenotypic Leukemia
[description not available]		04.3670
Leukemia, Biphenotypic, Acute
An acute leukemia exhibiting cell features characteristic of both the myeloid and lymphoid lineages and probably arising from MULTIPOTENT STEM CELLS.		17.46140
Pneumatosis Cystoides Intestinalis
A condition characterized by the presence of multiple gas-filled cysts in the intestinal wall, the submucosa and/or subserosa of the INTESTINE. The majority of the cysts are found in the JEJUNUM and the ILEUM.		02.110
Amyloid Deposits
[description not available]		02.110
Myelomonocytic Leukemia, Chronic
[description not available]		06.66230
Leukemia, Myelomonocytic, Chronic
A myelodysplastic-myeloproliferative disease characterized by monocytosis, increased monocytes in the bone marrow, variable degrees of dysplasia, but an absence of immature granulocytes in the blood.		06.66230
Rhabdomyosarcoma 2
[description not available]		02.7630
Rhabdomyosarcoma, Alveolar
A form of RHABDOMYOSARCOMA occurring mainly in adolescents and young adults, affecting muscles of the extremities, trunk, orbital region, etc. It is extremely malignant, metastasizing widely at an early stage. Few cures have been achieved and the prognosis is poor. Alveolar refers to its microscopic appearance simulating the cells of the respiratory alveolus. (Holland et al., Cancer Medicine, 3d ed, p2188)		02.7630
Coronary Artery Stenosis
[description not available]		02.110
Coronary Stenosis
Narrowing or constriction of a coronary artery.		02.110
Nerve Pain
[description not available]		02.110
Neuralgia
Intense or aching pain that occurs along the course or distribution of a peripheral or cranial nerve.		02.110
Erythema Migrans, Lingual
[description not available]		03.0110
Aphthae
[description not available]		03.4320
Maxillary Diseases
Diseases involving the MAXILLA.		03.420
Stomatitis, Aphthous
A recurrent disease of the oral mucosa of unknown etiology. It is characterized by small white ulcerative lesions, single or multiple, round or oval. Two to eight crops of lesions occur per year, lasting for 7 to 14 days and then heal without scarring. (From Jablonski's Dictionary of Dentistry, 1992, p742)		03.4320
Diffuse Cutaneous Systemic Sclerosis
[description not available]		010.481411
Scleroderma, Diffuse
A rapid onset form of SYSTEMIC SCLERODERMA with progressive widespread SKIN thickening over the arms, the legs and the trunk, resulting in stiffness and disability.		010.481411
Abdomen, Acute
A clinical syndrome with acute abdominal pain that is severe, localized, and rapid in onset. Acute abdomen may be caused by a variety of disorders, injuries, or diseases.		03.4220
ANS (Autonomic Nervous System) Diseases
[description not available]		02.110
Congestive Ophthalmopathy
[description not available]		04.2360
Graves Ophthalmopathy
An autoimmune disorder of the EYE, occurring in patients with Graves disease. Subtypes include congestive (inflammation of the orbital connective tissue), myopathic (swelling and dysfunction of the extraocular muscles), and mixed congestive-myopathic ophthalmopathy.		04.2360
HPV Infection
[description not available]		02.9940
Papillomavirus Infections
Neoplasms of the skin and mucous membranes caused by papillomaviruses. They are usually benign but some have a high risk for malignant progression.		02.9940
Skin Diseases, Vascular
Skin diseases affecting or involving the cutaneous blood vessels and generally manifested as inflammation, swelling, erythema, or necrosis in the affected area.		02.1110
Carcinoma, Neuroendocrine
A group of carcinomas which share a characteristic morphology, often being composed of clusters and trabecular sheets of round blue cells, granular chromatin, and an attenuated rim of poorly demarcated cytoplasm. Neuroendocrine tumors include carcinoids, small (oat) cell carcinomas, medullary carcinoma of the thyroid, Merkel cell tumor, cutaneous neuroendocrine carcinoma, pancreatic islet cell tumors, and pheochromocytoma. Neurosecretory granules are found within the tumor cells. (Segen, Dictionary of Modern Medicine, 1992)		02.7430
Cardiac Hypertrophy
Enlargement of the HEART due to chamber HYPERTROPHY, an increase in wall thickness without an increase in the number of cells (MYOCYTES, CARDIAC). It is the result of increase in myocyte size, mitochondrial and myofibrillar mass, as well as changes in extracellular matrix.		02.7330
Cardiomegaly
Enlargement of the HEART, usually indicated by a cardiothoracic ratio above 0.50. Heart enlargement may involve the right, the left, or both HEART VENTRICLES or HEART ATRIA. Cardiomegaly is a nonspecific symptom seen in patients with chronic systolic heart failure (HEART FAILURE) or several forms of CARDIOMYOPATHIES.		02.7330
Muscle Pain
[description not available]		04.8221
Myalgia
Painful sensation in the muscles.		04.8221
Infections, Pseudomonas
[description not available]		02.4720
Ecthyma
An ulcerative pyoderma usually caused by group A beta-hemolytic streptococcal infection at the site of minor trauma. (Dorland, 27th ed)		02.4720
Pseudomonas Infections
Infections with bacteria of the genus PSEUDOMONAS.		02.4720
Lymphoma, T Cell, Peripheral
[description not available]		05.0731
Lymphoma, T-Cell, Peripheral
A group of malignant lymphomas thought to derive from peripheral T-lymphocytes in lymph nodes and other nonlymphoid sites. They include a broad spectrum of lymphocyte morphology, but in all instances express T-cell markers admixed with epithelioid histiocytes, plasma cells, and eosinophils. Although markedly similar to large-cell immunoblastic lymphoma (LYMPHOMA, LARGE-CELL, IMMUNOBLASTIC), this group's unique features warrant separate treatment.		05.0731
Polyomavirus Infections
Infections with POLYOMAVIRUS, which are often cultured from the urine of kidney transplant patients. Excretion of BK VIRUS is associated with ureteral strictures and CYSTITIS, and that of JC VIRUS with progressive multifocal leukoencephalopathy (LEUKOENCEPHALOPATHY, PROGRESSIVE MULTIFOCAL).		03.0110
Cancer of Endocrine Gland
[description not available]		05.9733
Endocrine Gland Neoplasms
Tumors or cancer of the ENDOCRINE GLANDS.		05.9733
Monosomy
The condition in which one chromosome of a pair is missing. In a normally diploid cell it is represented symbolically as 2N-1.		04.5790
Benign Cerebellar Neoplasms
[description not available]		02.110
Acid beta-Glucosidase Deficiency
[description not available]		02.110
Gaucher Disease
An autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (GLUCOSYLCERAMIDASE) leading to intralysosomal accumulation of glycosylceramide mainly in cells of the MONONUCLEAR PHAGOCYTE SYSTEM. The characteristic Gaucher cells, glycosphingolipid-filled HISTIOCYTES, displace normal cells in BONE MARROW and visceral organs causing skeletal deterioration, hepatosplenomegaly, and organ dysfunction. There are several subtypes based on the presence and severity of neurological involvement.		02.110
Brain Swelling
[description not available]		03.3360
Brain Edema
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)		03.3360
Dermatitis, Contact, Phototoxic
[description not available]		03.3820
Acute Generalised Exanthematous Pustulosis
[description not available]		02.1110
Anaplastic Large-Cell Lymphoma
[description not available]		03.6630
Lymphoma, Large-Cell, Anaplastic
A systemic, large-cell, non-Hodgkin, malignant lymphoma characterized by cells with pleomorphic appearance and expressing the CD30 ANTIGEN. These so-called hallmark cells have lobulated and indented nuclei. This lymphoma is often mistaken for metastatic carcinoma and MALIGNANT HISTIOCYTOSIS.		03.6630
Genital Diseases, Male
Pathological processes involving the male reproductive tract (GENITALIA, MALE).		02.110
Actinic Reticuloid Syndrome
[description not available]		02.9640
Lung Injury, Ventilator-Induced
[description not available]		03.920
Adrenal Cancer
[description not available]		02.7630
Pleural Effusion, Malignant
Presence of fluid in the PLEURAL CAVITY as a complication of malignant disease. Malignant pleural effusions often contain actual malignant cells.		05.4651
Back Ache
[description not available]		02.110
Back Pain
Acute or chronic pain located in the posterior regions of the THORAX; LUMBOSACRAL REGION; or the adjacent regions.		02.110
Disease, Pulmonary
[description not available]		08.09112
Lung Diseases
Pathological processes involving any part of the LUNG.		08.09112
Acute Autoimmune Neuropathy
[description not available]		02.1110
Cranial Nerve Diseases
Disorders of one or more of the twelve cranial nerves. With the exception of the optic and olfactory nerves, this includes disorders of the brain stem nuclei from which the cranial nerves originate or terminate.		02.1110
Convergent Strabismus
[description not available]		02.1110
Flaccid Quadriplegia
[description not available]		02.4920
Esotropia
A form of ocular misalignment characterized by an excessive convergence of the visual axes, resulting in a cross-eye appearance. An example of this condition occurs when paralysis of the lateral rectus muscle causes an abnormal inward deviation of one eye on attempted gaze.		02.1110
Guillain-Barre Syndrome
An acute inflammatory autoimmune neuritis caused by T cell- mediated cellular immune response directed towards peripheral myelin. Demyelination occurs in peripheral nerves and nerve roots. The process is often preceded by a viral or bacterial infection, surgery, immunization, lymphoma, or exposure to toxins. Common clinical manifestations include progressive weakness, loss of sensation, and loss of deep tendon reflexes. Weakness of respiratory muscles and autonomic dysfunction may occur. (From Adams et al., Principles of Neurology, 6th ed, pp1312-1314)		02.1110
Cat Diseases
Diseases of the domestic cat (Felis catus or F. domesticus). This term does not include diseases of the so-called big cats such as CHEETAHS; LIONS; tigers, cougars, panthers, leopards, and other Felidae for which the heading CARNIVORA is used.		05.661
Diffuse Tenosynovial Giant Cell Tumor
[description not available]		07.3290
Synovitis, Pigmented Villonodular
Diffuse outgrowth arising from the SYNOVIAL MEMBRANE; SYNOVIAL BURSA; or TENDON sheath around the joint cavity, with extension to surrounding soft tissue. It is characterized by pigmented HEMOSIDERIN-containing MACROPHAGES; FOAM CELLS; and multinucleated GIANT CELLS. It usually occurs in the hands and feet, and around large joints, such as in the ankle and knee joints.		07.3290
Giant Cell Tumor of Bone
A bone tumor composed of cellular spindle-cell stroma containing scattered multinucleated giant cells resembling osteoclasts. The tumors range from benign to frankly malignant lesions. The tumor occurs most frequently in an end of a long tubular bone in young adults. (From Dorland, 27th ed; Stedman, 25th ed)		03.8520
Cancer of Sigmoid
[description not available]		02.110
Embolism, Pulmonary
[description not available]		02.4620
Pulmonary Embolism
Blocking of the PULMONARY ARTERY or one of its branches by an EMBOLUS.		02.4620
Deficiency Diseases
A condition produced by dietary or metabolic deficiency. The term includes all diseases caused by an insufficient supply of essential nutrients, i.e., protein (or amino acids), vitamins, and minerals. It also includes an inadequacy of calories. (From Dorland, 27th ed; Stedman, 25th ed)		02.1110
Blood Poisoning
[description not available]		03.9410
Sepsis
Systemic inflammatory response syndrome with a proven or suspected infectious etiology. When sepsis is associated with organ dysfunction distant from the site of infection, it is called severe sepsis. When sepsis is accompanied by HYPOTENSION despite adequate fluid infusion, it is called SEPTIC SHOCK.		03.9410
Adenoma, Basal Cell
[description not available]		03.6630
Adenoma
A benign epithelial tumor with a glandular organization.		03.6630
Polyploid
[description not available]		0340
Ebola Hemorrhagic Fever
[description not available]		02.1110
Communicable Diseases, Emerging
Infectious diseases that are novel in their outbreak ranges (geographic and host) or transmission mode.		02.1110
Break-Bone Fever
[description not available]		02.4920
Dengue
An acute febrile disease transmitted by the bite of AEDES mosquitoes infected with DENGUE VIRUS. It is self-limiting and characterized by fever, myalgia, headache, and rash. SEVERE DENGUE is a more virulent form of dengue.		02.4920
Hemorrhagic Fever, Ebola
A highly fatal, acute hemorrhagic fever caused by EBOLAVIRUS.		02.1110
Mucositis
An INFLAMMATION of the MUCOSA with burning or tingling sensation. It is characterized by atrophy of the squamous EPITHELIUM, vascular damage, inflammatory infiltration, and ulceration. It usually occurs at the mucous lining of the MOUTH, the GASTROINTESTINAL TRACT or the airway due to chemical irritations, CHEMOTHERAPY, or radiation therapy (RADIOTHERAPY).		03.511
Febrile Neutropenia
Fever accompanied by a significant reduction in the number of NEUTROPHILS.		03.511
Abnormalities, Drug-Induced
Congenital abnormalities caused by medicinal substances or drugs of abuse given to or taken by the mother, or to which she is inadvertently exposed during the manufacture of such substances. The concept excludes abnormalities resulting from exposure to non-medicinal chemicals in the environment.		04.8950
Mediastinal Diseases
Disorders of the mediastinum, general or unspecified.		02.1110
Esophageal Fistula
Abnormal passage communicating with the ESOPHAGUS. The most common type is TRACHEOESOPHAGEAL FISTULA between the esophagus and the TRACHEA.		02.1110
Mediastinitis
Inflammation of the mediastinum, the area between the pleural sacs.		02.1110
Cancer of Eye
[description not available]		04.3341
Fibroid
[description not available]		04.8170
Leiomyoma
A benign tumor derived from smooth muscle tissue, also known as a fibroid tumor. They rarely occur outside of the UTERUS and the GASTROINTESTINAL TRACT but can occur in the SKIN and SUBCUTANEOUS TISSUE, probably arising from the smooth muscle of small blood vessels in these tissues.		04.8170
Hepatitis
INFLAMMATION of the LIVER.		07.4620
Dysphagia
[description not available]		02.4820
Deglutition Disorders
Difficulty in SWALLOWING which may result from neuromuscular disorder or mechanical obstruction. Dysphagia is classified into two distinct types: oropharyngeal dysphagia due to malfunction of the PHARYNX and UPPER ESOPHAGEAL SPHINCTER; and esophageal dysphagia due to malfunction of the ESOPHAGUS.		02.4820
Pheochromocytoma, Extra-Adrenal
[description not available]		02.1110
Pheochromocytoma
A usually benign, well-encapsulated, lobular, vascular tumor of chromaffin tissue of the ADRENAL MEDULLA or sympathetic paraganglia. The cardinal symptom, reflecting the increased secretion of EPINEPHRINE and NOREPINEPHRINE, is HYPERTENSION, which may be persistent or intermittent. During severe attacks, there may be HEADACHE; SWEATING, palpitation, apprehension, TREMOR; PALLOR or FLUSHING of the face, NAUSEA and VOMITING, pain in the CHEST and ABDOMEN, and paresthesias of the extremities. The incidence of malignancy is as low as 5% but the pathologic distinction between benign and malignant pheochromocytomas is not clear. (Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1298)		02.1110
Bladder Neck Obstruction
[description not available]		02.1110
Chromosomal Breakage
[description not available]		03.360
Antral Vascular Ectasia
[description not available]		09.7560
Cancer of Pelvis
[description not available]		03.6730
Leukoencephalopathy Syndrome, Posterior
[description not available]		02.1110
Infarct
[description not available]		02.7330
Lung Adenocarcinoma
[description not available]		02.5220
Adenocarcinoma of Lung
A carcinoma originating in the lung and the most common lung cancer type in never-smokers. Malignant cells exhibit distinct features such as glandular epithelial, or tubular morphology. Mutations in KRAS, EGFR, BRAF, and ERBB2 genes are associated with this cancer.		07.5220
Male Genital Neoplasms
[description not available]		02.1110
Genital Neoplasms, Male
Tumor or cancer of the MALE GENITALIA.		02.1110
Dyslipidemia
[description not available]		02.5220
Clubbed Fingers
[description not available]		02.1110
Dyslipidemias
Abnormalities in the serum levels of LIPIDS, including overproduction or deficiency. Abnormal serum lipid profiles may include high total CHOLESTEROL, high TRIGLYCERIDES, low HIGH DENSITY LIPOPROTEIN CHOLESTEROL, and elevated LOW DENSITY LIPOPROTEIN CHOLESTEROL.		02.5220
Atherosclerotic Parkinsonism
[description not available]		02.1310
Parkinson Disease, Secondary
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)		02.1310
Intussusception
A form of intestinal obstruction caused by the PROLAPSE of a part of the intestine into the adjoining intestinal lumen. There are four types: colic, involving segments of the LARGE INTESTINE; enteric, involving only the SMALL INTESTINE; ileocecal, in which the ILEOCECAL VALVE prolapses into the CECUM, drawing the ILEUM along with it; and ileocolic, in which the ileum prolapses through the ileocecal valve into the COLON.		02.1110
Aspergilloses, Bronchopulmonary
[description not available]		02.1310
C gattii Infection
[description not available]		02.1310
Cryptococcosis
Fungal infection caused by genus CRYPTOCOCCUS.		02.1310
Pulmonary Aspergillosis
Infections of the respiratory tract with fungi of the genus ASPERGILLUS.		02.1310
Anxiety
Feelings or emotions of dread, apprehension, and impending disaster but not disabling as with ANXIETY DISORDERS.		02.5120
Hematoma, Subdural, Cranial
[description not available]		02.1310
Hematoma, Subdural, Intracranial
Accumulation of blood in the SUBDURAL SPACE over the CEREBRAL HEMISPHERE.		02.1310
Hyperhomocysteinemia
Condition in which the plasma levels of homocysteine and related metabolites are elevated (		02.1310
Hand-Schu00FCller-Christian Disease
[description not available]		03.1550
Granulomatosis, Lipid
[description not available]		02.9840
Histiocytosis, Langerhans-Cell
A group of disorders resulting from the abnormal proliferation of and tissue infiltration by LANGERHANS CELLS which can be detected by their characteristic Birbeck granules (X bodies), or by monoclonal antibody staining for their surface CD1 ANTIGENS. Langerhans-cell granulomatosis can involve a single organ, or can be a systemic disorder.		03.1550
Erdheim-Chester Disease
A rare form of non-Langerhans-cell histiocytosis (HISTIOCYTOSIS, NON-LANGERHANS-CELL) with onset in middle age. The systemic disease is characterized by infiltration of lipid-laden macrophages, multinucleated giant cells, an inflammatory infiltrate of lymphocytes and histiocytes in the bone marrow, and a generalized sclerosis of the long bones.		02.9840
Hyperidrosis
[description not available]		02.1310
Cheilitis
Inflammation of the lips. It is of various etiologies and degrees of pathology.		02.1310
Hyperhidrosis
Excessive sweating. In the localized type, the most frequent sites are the palms, soles, axillae, inguinal folds, and the perineal area. Its chief cause is thought to be emotional. Generalized hyperhidrosis may be induced by a hot, humid environment, by fever, or by vigorous exercise.		02.1310
Parakeratosis
Persistence of the nuclei of the keratinocytes into the stratum corneum of the skin. This is a normal state only in the epithelium of true mucous membranes in the mouth and vagina. (Dorland, 27th ed)		02.1310
Erythema Multiforme
A skin and mucous membrane disease characterized by an eruption of macules, papules, nodules, vesicles, and/or bullae with characteristic bull's-eye lesions usually occurring on the dorsal aspect of the hands and forearms.		02.1310
Giant Cell Tumors
Tumors of bone tissue or synovial or other soft tissue characterized by the presence of giant cells. The most common are giant cell tumor of tendon sheath and GIANT CELL TUMOR OF BONE.		07.1990
Endometrioma
An enlarged area of ENDOMETRIOSIS that resembles a tumor. It is usually found in the OVARY. When it is filled with old blood, it is known as a chocolate cyst.		02.4920
Peritoneal Diseases
Pathological processes involving the PERITONEUM.		02.4620
Endometriosis
A condition in which functional endometrial tissue is present outside the UTERUS. It is often confined to the PELVIS involving the OVARY, the ligaments, cul-de-sac, and the uterovesical peritoneum.		02.4920
Response Evaluation Criteria in Solid Tumors
An internationally recognized set of published rules used for evaluation of cancer treatment that define when tumors found in cancer patients improve, worsen, or remain stable during treatment. These criteria are based specifically on the response of the tumor(s) to treatment, and not on the overall health status of the patient resulting from treatment.		05.8822
Facial Asymmetry
Congenital or acquired asymmetry of the face.		02.1310
Facial Palsy
[description not available]		02.1310
Cancer of Parotid
[description not available]		02.520
Parotid Neoplasms
Tumors or cancer of the PAROTID GLAND.		02.520
Pelvic Pain
Pain in the pelvic region of genital and non-genital origin.		02.1310
Diverticulum, Meckel
[description not available]		02.1310
Hyperlipemia
[description not available]		03.8521
Hyperlipidemias
Conditions with excess LIPIDS in the blood.		03.8521
Mitral Incompetence
[description not available]		02.7430
Mitral Valve Insufficiency
Backflow of blood from the LEFT VENTRICLE into the LEFT ATRIUM due to imperfect closure of the MITRAL VALVE. This can lead to mitral valve regurgitation.		02.7430
MODS
[description not available]		02.1110
Multiple Organ Failure
A progressive condition usually characterized by combined failure of several organs such as the lungs, liver, kidney, along with some clotting mechanisms, usually postinjury or postoperative.		02.1110
Lymphocytosis
Excess of normal lymphocytes in the blood or in any effusion.		02.4720
Xanthoma
[description not available]		02.1310
Endothelioma, Lymphatic
[description not available]		02.1310
Lymphangioma
A benign tumor resulting from a congenital malformation of the lymphatic system. Lymphangioendothelioma is a type of lymphangioma in which endothelial cells are the dominant component.		02.1310
Remission, Spontaneous
A spontaneous diminution or abatement of a disease over time, without formal treatment.		02.1310
Spider Veins
[description not available]		02.1310
Telangiectasis
Permanent dilation of preexisting blood vessels (CAPILLARIES; ARTERIOLES; VENULES) creating small focal red lesions, most commonly in the skin or mucous membranes. It is characterized by the prominence of skin blood vessels, such as vascular spiders.		02.1310
Pyomyositis
An intramuscular suppuration of the large skeletal muscle groups. It is associated with INFECTION such as STAPHYLOCOCCUS AUREUS and PYODERMA. It was known as a tropical disease but is increasing among the immunocompromised (IMMUNOCOMPROMISED HOST). Symptoms include muscle pain, FEVER, and leucocytosis. It has been diagnosed by MRI SCANS.		03.4120
Glucose Metabolic Disorder
[description not available]		03.0410
Diseases of Endocrine System
[description not available]		03.420
Endocrine System Diseases
Pathological processes of the ENDOCRINE GLANDS, and diseases resulting from abnormal level of available HORMONES.		03.420
Enterocele
An intestinal HERNIA.		02.1710
Hernia
Protrusion of tissue, structure, or part of an organ through the bone, muscular tissue, or the membrane by which it is normally contained. Hernia may involve tissues such as the ABDOMINAL WALL or the respiratory DIAPHRAGM. Hernias may be internal, external, congenital, or acquired.		02.1710
Carcinoma, Papillary
A malignant neoplasm characterized by the formation of numerous, irregular, finger-like projections of fibrous stroma that is covered with a surface layer of neoplastic epithelial cells. (Stedman, 25th ed)		03.8940
Dysembryoma
[description not available]		03.0410
Struma Ovarii
A rare teratoid tumor of the ovary composed almost entirely of thyroid tissue, with large follicles containing abundant colloid. Occasionally there are symptoms of hyperthyroidism. 5-10% of struma ovarii become malignant, the only absolute criterion for which is the presence of metastasis. (Dorland, 27th ed; Segen, Dictionary of Modern Medicine, 1992)		03.0410
Teratoma
A true neoplasm composed of a number of different types of tissue, none of which is native to the area in which it occurs. It is composed of tissues that are derived from three germinal layers, the endoderm, mesoderm, and ectoderm. They are classified histologically as mature (benign) or immature (malignant). (From DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1642)		03.0410
Abnormalities, Cardiovascular
[description not available]		02.5320
Cardiovascular Abnormalities
Congenital, inherited, or acquired anomalies of the CARDIOVASCULAR SYSTEM, including the HEART and BLOOD VESSELS.		02.5320
Brain Inflammation
[description not available]		02.1310
Encephalitis
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.		02.1310
Branch Vein Occlusion
[description not available]		03.4220
Retinal Vein Occlusion
Blockage of the RETINAL VEIN. Those at high risk for this condition include patients with HYPERTENSION; DIABETES MELLITUS; ATHEROSCLEROSIS; and other CARDIOVASCULAR DISEASES.		03.4220
Capillary Leak Syndrome
A condition characterized by recurring episodes of fluid leaking from capillaries into extra-vascular compartments causing hematocrit to rise precipitously. If not treated, generalized vascular leak can lead to generalized EDEMA; SHOCK; cardiovascular collapse; and MULTIPLE ORGAN FAILURE.		08.0410
Leishmania Infection
[description not available]		02.520
Leishmaniasis
A disease caused by any of a number of species of protozoa in the genus LEISHMANIA. There are four major clinical types of this infection: cutaneous (Old and New World) (LEISHMANIASIS, CUTANEOUS), diffuse cutaneous (LEISHMANIASIS, DIFFUSE CUTANEOUS), mucocutaneous (LEISHMANIASIS, MUCOCUTANEOUS), and visceral (LEISHMANIASIS, VISCERAL).		02.520
Lymphoma of Mucosa-Associated Lymphoid Tissue
[description not available]		04.840
Lymphoma, B-Cell, Marginal Zone
Extranodal lymphoma of lymphoid tissue associated with mucosa that is in contact with exogenous antigens. Many of the sites of these lymphomas, such as the stomach, salivary gland, and thyroid, are normally devoid of lymphoid tissue. They acquire mucosa-associated lymphoid tissue (MALT) type as a result of an immunologically mediated disorder.		04.840
Actinic Keratosis
[description not available]		02.1310
Dermatomycoses
Superficial infections of the skin or its appendages by any of various fungi.		02.1310
Dermatitis Seborrheica
[description not available]		02.1310
Dermatitis, Seborrheic
A chronic inflammatory disease of the skin with unknown etiology. It is characterized by moderate ERYTHEMA, dry, moist, or greasy (SEBACEOUS GLAND) scaling and yellow crusted patches on various areas, especially the scalp, that exfoliate as dandruff. Seborrheic dermatitis is common in children and adolescents with HIV INFECTIONS.		02.1310
Keratosis, Actinic
White or pink lesions on the arms, hands, face, or scalp that arise from sun-induced DNA DAMAGE to KERATINOCYTES in exposed areas. They are considered precursor lesions to superficial SQUAMOUS CELL CARCINOMA.		02.1310
Hermanski-Pudlak Syndrome
Syndrome characterized by the triad of oculocutaneous albinism (ALBINISM, OCULOCUTANEOUS); PLATELET STORAGE POOL DEFICIENCY; and lysosomal accumulation of ceroid lipofuscin.		03.3820
Black Fever
[description not available]		02.1310
Leishmaniasis, Visceral
A chronic disease caused by LEISHMANIA DONOVANI and transmitted by the bite of several sandflies of the genera Phlebotomus and Lutzomyia. It is commonly characterized by fever, chills, vomiting, anemia, hepatosplenomegaly, leukopenia, hypergammaglobulinemia, emaciation, and an earth-gray color of the skin. The disease is classified into three main types according to geographic distribution: Indian, Mediterranean (or infantile), and African.		02.1310
Adenocystic Carcinoma
[description not available]		09.05117
Carcinoma, Adenoid Cystic
Carcinoma characterized by bands or cylinders of hyalinized or mucinous stroma separating or surrounded by nests or cords of small epithelial cells. When the cylinders occur within masses of epithelial cells, they give the tissue a perforated, sievelike, or cribriform appearance. Such tumors occur in the mammary glands, the mucous glands of the upper and lower respiratory tract, and the salivary glands. They are malignant but slow-growing, and tend to spread locally via the nerves. (Dorland, 27th ed)		09.05117
Nail Abnormalities
[description not available]		02.1510
Experimental Mammary Neoplasms
[description not available]		03.2960
Basedow Disease
[description not available]		02.1310
Graves Disease
A common form of hyperthyroidism with a diffuse hyperplastic GOITER. It is an autoimmune disorder that produces antibodies against the THYROID STIMULATING HORMONE RECEPTOR. These autoantibodies activate the TSH receptor, thereby stimulating the THYROID GLAND and hypersecretion of THYROID HORMONES. These autoantibodies can also affect the eyes (GRAVES OPHTHALMOPATHY) and the skin (Graves dermopathy).		02.1310
Cancer of Paranasal Sinus
[description not available]		02.1510
Paranasal Sinus Neoplasms
Tumors or cancer of the PARANASAL SINUSES.		02.1510
Brain Vascular Disorders
[description not available]		04.630
Cerebrovascular Disorders
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.		04.630
Chemical Dependence
[description not available]		02.1310
Substance-Related Disorders
Disorders related to substance use or abuse.		02.1310
Hematoma
A collection of blood outside the BLOOD VESSELS. Hematoma can be localized in an organ, space, or tissue.		02.5120
Parasitemia
The presence of parasites (especially malarial parasites) in the blood. (Dorland, 27th ed)		02.520
Biliary Calculi
[description not available]		02.4620
Gallstones
Solid crystalline precipitates in the BILIARY TRACT, usually formed in the GALLBLADDER, resulting in the condition of CHOLELITHIASIS. Gallstones, derived from the BILE, consist mainly of calcium, cholesterol, or bilirubin.		02.4620
Dysuria
Painful URINATION. It is often associated with infections of the lower URINARY TRACT.		02.1310
Choline Deficiency
A condition produced by a deficiency of CHOLINE in animals. Choline is known as a lipotropic agent because it has been shown to promote the transport of excess fat from the liver under certain conditions in laboratory animals. Combined deficiency of choline (included in the B vitamin complex) and all other methyl group donors causes liver cirrhosis in some animals. Unlike compounds normally considered as vitamins, choline does not serve as a cofactor in enzymatic reactions. (From Saunders Dictionary & Encyclopedia of Laboratory Medicine and Technology, 1984)		02.1310
Cafe-au-Lait Spots
Light brown pigmented macules associated with NEUROFIBROMATOSIS and Albright's syndrome (see FIBROUS DYSPLASIA, POLYOSTOTIC).		02.1510
Exomphalos
[description not available]		03.0410
Hernia, Umbilical
A HERNIA due to an imperfect closure or weakness of the umbilical ring. It appears as a skin-covered protrusion at the UMBILICUS during crying, coughing, or straining. The hernia generally consists of OMENTUM or SMALL INTESTINE. The vast majority of umbilical hernias are congenital but can be acquired due to severe abdominal distention.		03.0410
Appendiceal Cancer
[description not available]		03.6630
Appendiceal Neoplasms
Tumors or cancer of the APPENDIX.		03.6630
Glenoid Labral Tears
[description not available]		02.1510
Rotator Cuff Injuries
Injuries to the ROTATOR CUFF of the shoulder joint.		02.1510
Alogia
[description not available]		02.4920
Aphasia
A cognitive disorder marked by an impaired ability to comprehend or express language in its written or spoken form. This condition is caused by diseases which affect the language areas of the dominant hemisphere. Clinical features are used to classify the various subtypes of this condition. General categories include receptive, expressive, and mixed forms of aphasia.		02.4920
Thoracic Neoplasms
New abnormal growth of tissue in the THORAX.		05.0631
Carcinoma, Ductal, Breast
An invasive (infiltrating) CARCINOMA of the mammary ductal system (MAMMARY GLANDS) in the human BREAST.		04.6932
Breast Cancer, Male
[description not available]		03.4311
Breast Neoplasms, Male
Any neoplasms of the male breast. These occur infrequently in males in developed countries, the incidence being about 1% of that in females.		15.4311
Agranulocytosis
A decrease in the number of GRANULOCYTES; (BASOPHILS; EOSINOPHILS; and NEUTROPHILS).		02.4620
Postpartum Amenorrhea
[description not available]		02.4420
Amenorrhea
Absence of menstruation.		02.4420
Diseases of Immune System
[description not available]		03.3620
Immune System Diseases
Disorders caused by abnormal or absent immunologic mechanisms, whether humoral, cell-mediated, or both.		03.3620
Anemia, Hemolytic, Acquired
[description not available]		03.8640
Purpura, Thrombopenic
[description not available]		02.9610
Anemia, Hemolytic
A condition of inadequate circulating red blood cells (ANEMIA) or insufficient HEMOGLOBIN due to premature destruction of red blood cells (ERYTHROCYTES).		03.8640
Purpura, Thrombocytopenic
Any form of purpura in which the PLATELET COUNT is decreased. Many forms are thought to be caused by immunological mechanisms.		02.9610
Rhabdomyolysis
Necrosis or disintegration of skeletal muscle often followed by myoglobinuria.		02.4620
Cruveilhier-Baumgarten Syndrome
Liver cirrhosis with intrahepatic portal obstruction, HYPERTENSION, and patent UMBILICAL VEINS.		02.7330
Hypertension, Portal
Abnormal increase of resistance to blood flow within the hepatic PORTAL SYSTEM, frequently seen in LIVER CIRRHOSIS and conditions with obstruction of the PORTAL VEIN.		02.7330
Neurovisceral Storage Disease with Vertical Supranuclear Ophthalmoplegia
[description not available]		02.0410
Niemann-Pick Disease, Type C
An autosomal recessive lipid storage disorder that is characterized by accumulation of CHOLESTEROL and SPHINGOMYELINS in cells of the VISCERA and the CENTRAL NERVOUS SYSTEM. Type C (or C1) and type D are allelic disorders caused by mutation of the NPC1 gene, which encodes a protein that mediates intracellular cholesterol transport from LYSOSOMES. Clinical signs include hepatosplenomegaly and chronic neurological symptoms. Type D is a variant in people with a Nova Scotia ancestry.		02.0410
Endometrial Stromal Sarcoma
[description not available]		03.3520
Sarcoma, Endometrial Stromal
A highly malignant subset of neoplasms arising from the endometrial stroma. Tumors in this group infiltrate the stroma with a wide range of atypia cells and numerous mitoses. They are capable of widespread metastases (NEOPLASM METASTASIS).		03.3520
Experimental Hepatoma
[description not available]		02.9740
Epithelial Neoplasms
[description not available]		05.5344
Adolescent Gynecomastia
[description not available]		04.6860
Gynecomastia
Enlargement of the BREAST in the males, caused by an excess of ESTROGENS. Physiological gynecomastia is normally observed in NEWBORNS; ADOLESCENT; and AGING males.		04.6860
Collagen Diseases
Historically, a heterogeneous group of acute and chronic diseases, including rheumatoid arthritis, systemic lupus erythematosus, progressive systemic sclerosis, dermatomyositis, etc. This classification was based on the notion that collagen was equivalent to connective tissue, but with the present recognition of the different types of collagen and the aggregates derived from them as distinct entities, the term collagen diseases now pertains exclusively to those inherited conditions in which the primary defect is at the gene level and affects collagen biosynthesis, post-translational modification, or extracellular processing directly. (From Cecil Textbook of Medicine, 19th ed, p1494)		02.0510
Connective Tissue Disease, Mixed
[description not available]		02.4520
Hormone-Dependent Neoplasms
[description not available]		04.3441
African Lymphoma
[description not available]		04.3370
Burkitt Lymphoma
A form of undifferentiated malignant LYMPHOMA usually found in central Africa, but also reported in other parts of the world. It is commonly manifested as a large osteolytic lesion in the jaw or as an abdominal mass. B-cell antigens are expressed on the immature cells that make up the tumor in virtually all cases of Burkitt lymphoma. The Epstein-Barr virus (HERPESVIRUS 4, HUMAN) has been isolated from Burkitt lymphoma cases in Africa and it is implicated as the causative agent in these cases; however, most non-African cases are EBV-negative.		04.3370
Hepatic Failure
[description not available]		03.1350
Liver Failure
Severe inability of the LIVER to perform its normal metabolic functions, as evidenced by severe JAUNDICE and abnormal serum levels of AMMONIA; BILIRUBIN; ALKALINE PHOSPHATASE; ASPARTATE AMINOTRANSFERASE; LACTATE DEHYDROGENASES; and albumin/globulin ratio. (Blakiston's Gould Medical Dictionary, 4th ed)		08.1350
Diseases in Twins
Disorders affecting TWINS, one or both, at any age.		02.4620
Fungal Diseases
[description not available]		02.0510
Infections, Respiratory
[description not available]		02.0510
Mycoses
Diseases caused by FUNGI.		02.0510
Respiratory Tract Infections
Invasion of the host RESPIRATORY SYSTEM by microorganisms, usually leading to pathological processes or diseases.		02.0510
Bone Marrow Diseases
Diseases involving the BONE MARROW.		05.0391
Diaphragmatic Hernia
[description not available]		02.4620
Marfan Syndrome, Type I
[description not available]		02.0410
Marfan Syndrome
An autosomal dominant disorder of CONNECTIVE TISSUE with abnormal features in the heart, the eye, and the skeleton. Cardiovascular manifestations include MITRAL VALVE PROLAPSE, dilation of the AORTA, and aortic dissection. Other features include lens displacement (ectopia lentis), disproportioned long limbs and enlarged DURA MATER (dural ectasia). Marfan syndrome (type 1) is associated with mutations in the gene encoding FIBRILLIN-1 (FBN1), a major element of extracellular microfibrils of connective tissue. Mutations in the gene encoding TYPE II TGF-BETA RECEPTOR (TGFBR2) are associated with Marfan syndrome type 2.		02.0410
Cardiac Edema
[description not available]		02.0410
Edema, Cardiac
Abnormal fluid retention by the body due to impaired cardiac function or heart failure. It is usually characterized by increase in venous and capillary pressure, and swollen legs when standing. It is different from the generalized edema caused by renal dysfunction (NEPHROTIC SYNDROME).		02.0410
Foot Dermatoses
Skin diseases of the foot, general or unspecified.		02.4420
Erythema
Redness of the skin produced by congestion of the capillaries. This condition may result from a variety of disease processes.		03.2760
Allergy, Food
[description not available]		02.4620
Parasite Infections
[description not available]		04.6540
Eosinophilia, Pulmonary
[description not available]		04.8170
Food Hypersensitivity
Gastrointestinal disturbances, skin eruptions, or shock due to allergic reactions to allergens in food.		02.4620
Pulmonary Eosinophilia
A condition characterized by infiltration of the lung with EOSINOPHILS due to inflammation or other disease processes. Major eosinophilic lung diseases are the eosinophilic pneumonias caused by infections, allergens, or toxic agents.		04.8170
Muscle Tissue Neoplasms
[description not available]		02.0510
Emergencies
Situations or conditions requiring immediate intervention to avoid serious adverse results.		02.9610
Myeloproliferative-Myelodisplastic Diseases
[description not available]		02.0510
Myelodysplastic-Myeloproliferative Diseases
Clonal myeloid disorders that possess both dysplastic and proliferative features but are not properly classified as either MYELODYSPLASTIC SYNDROMES or MYELOPROLIFERATIVE DISORDERS.		02.0510
Nephrogenic Systemic Fibrosis
[description not available]		04.3741
Nephrogenic Fibrosing Dermopathy
A chronic, acquired, idiopathic, progressive eruption of the skin that occurs in the context of RENAL FAILURE. It is sometimes accompanied by systemic fibrosis. The pathogenesis seems to be multifactorial, with postulated involvement of circulating fibrocytes. There is a strong association between this disorder and the use of gadolinium-based contrast agents.		16.3741
Antidiuretic Hormone, Inappropriate Secretion
[description not available]		02.0410
Hyponatremia
Deficiency of sodium in the blood; salt depletion. (Dorland, 27th ed)		02.0410
Inappropriate ADH Syndrome
A condition of HYPONATREMIA and renal salt loss attributed to overexpansion of BODY FLUIDS resulting from sustained release of ANTIDIURETIC HORMONES which stimulates renal resorption of water. It is characterized by normal KIDNEY function, high urine OSMOLALITY, low serum osmolality, and neurological dysfunction. Etiologies include ADH-producing neoplasms, injuries or diseases involving the HYPOTHALAMUS, the PITUITARY GLAND, and the LUNG. This syndrome can also be drug-induced.		02.0410
Cryoglobulinemia
A condition characterized by the presence of abnormal quantities of CRYOGLOBULINS in the blood. Upon cold exposure, these abnormal proteins precipitate into the microvasculature leading to restricted blood flow in the exposed areas.		02.4620
Extravasation of Contrast Media
[description not available]		02.0510
Adult Optic Nerve Glioma
[description not available]		03.4311
Benign Hypothalamic Neoplasms
[description not available]		03.4311
Optic Nerve Glioma
Glial cell derived tumors arising from the optic nerve, usually presenting in childhood.		03.4311
Porphyria Cutanea Tarda
An autosomal dominant or acquired porphyria due to a deficiency of UROPORPHYRINOGEN DECARBOXYLASE in the LIVER. It is characterized by photosensitivity and cutaneous lesions with little or no neurologic symptoms. Type I is the acquired form and is strongly associated with liver diseases and hepatic toxicities caused by alcohol or estrogenic steroids. Type II is the familial form.		03.1350
Brucella Infection
[description not available]		02.0410
Angioma
A vascular anomaly due to proliferation of blood or lymphatic vessels that forms a tumor-like mass. Vessels in the angioma may or may not be dilated.		02.0410
Brucellosis
Infection caused by bacteria of the genus BRUCELLA mainly involving the MONONUCLEAR PHAGOCYTE SYSTEM. This condition is characterized by fever, weakness, malaise, and weight loss.		02.0410
Hemangioma
A vascular anomaly due to proliferation of BLOOD VESSELS that forms a tumor-like mass. The common types involve CAPILLARIES and VEINS. It can occur anywhere in the body but is most frequently noticed in the SKIN and SUBCUTANEOUS TISSUE. (from Stedman, 27th ed, 2000)		02.0410
Cancer of the Fallopian Tube
[description not available]		05.0433
Fallopian Tube Neoplasms
Benign or malignant neoplasms of the FALLOPIAN TUBES. They are uncommon. If they develop, they may be located in the wall or within the lumen as a growth attached to the wall by a stalk.		17.0433
Hematoma, Epidural, Spinal
A rare epidural hematoma in the spinal epidural space, usually due to a vascular malformation (CENTRAL NERVOUS SYSTEM VASCULAR MALFORMATIONS) or TRAUMA. Spontaneous spinal epidural hematoma is a neurologic emergency due to a rapidly evolving compressive MYELOPATHY.		02.0510
Jejunal Diseases
Pathological development in the JEJUNUM region of the SMALL INTESTINE.		02.0510
Leukemia, Lymphocytic, T Cell
[description not available]		03.6530
Leukemia, T-Cell
A malignant disease of the T-LYMPHOCYTES in the bone marrow, thymus, and/or blood.		03.6530
Secondary Hyperparathyroidism
[description not available]		010.152
Hyperparathyroidism, Secondary
Abnormally elevated PARATHYROID HORMONE secretion as a response to HYPOCALCEMIA. It is caused by chronic KIDNEY FAILURE or other abnormalities in the controls of bone and mineral metabolism, leading to various BONE DISEASES, such as RENAL OSTEODYSTROPHY.		05.152
Degenerative Diseases, Central Nervous System
[description not available]		02.0510
Dementias, Transmissible
[description not available]		02.4420
Neurodegenerative Diseases
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.		02.0510
Opportunistic Infections
An infection caused by an organism which becomes pathogenic under certain conditions, e.g., during immunosuppression.		08.8740
Peritonitis, Tuberculous
A form of PERITONITIS seen in patients with TUBERCULOSIS, characterized by lesion either as a miliary form or as a pelvic mass on the peritoneal surfaces. Most patients have ASCITES, abdominal swelling, ABDOMINAL PAIN, and other systemic symptoms such as FEVER; WEIGHT LOSS; and ANEMIA.		02.0510
Acute Hemolytic Transfusion Reaction
[description not available]		02.0510
Transfusion Reaction
Complications of BLOOD TRANSFUSION. Included adverse reactions are common allergic and febrile reactions; hemolytic (delayed and acute) reactions; and other non-hemolytic adverse reactions such as infections and adverse immune reactions related to immunocompatibility.		02.0510
Hamartoma
A focal malformation resembling a neoplasm, composed of an overgrowth of mature cells and tissues that normally occur in the affected area.		02.0510
Bright Disease
A historical classification which is no longer used. It described acute glomerulonephritis, acute nephritic syndrome, or acute nephritis. Named for Richard Bright.		02.4420
Glomerulonephritis
Inflammation of the renal glomeruli (KIDNEY GLOMERULUS) that can be classified by the type of glomerular injuries including antibody deposition, complement activation, cellular proliferation, and glomerulosclerosis. These structural and functional abnormalities usually lead to HEMATURIA; PROTEINURIA; HYPERTENSION; and RENAL INSUFFICIENCY.		02.4420
Hemorrhagic Diathesis
[description not available]		03.4311
Hemorrhagic Disorders
Spontaneous or near spontaneous bleeding caused by a defect in clotting mechanisms (BLOOD COAGULATION DISORDERS) or another abnormality causing a structural flaw in the blood vessels (HEMOSTATIC DISORDERS).		03.4311
Muscular Dystrophy, Animal
MUSCULAR DYSTROPHY that occurs in VERTEBRATE animals.		02.4520
Abscess, Hepatic
[description not available]		02.4620
Liver Abscess
Solitary or multiple collections of PUS within the liver as a result of infection by bacteria, protozoa, or other agents.		02.4620
Serositis
Inflammation of a serous membrane.		03.3720
Intestinal Diseases
Pathological processes in any segment of the INTESTINE from DUODENUM to RECTUM.		04.7621
Cancer of Nasopharynx
[description not available]		02.9740
Nasopharyngeal Neoplasms
Tumors or cancer of the NASOPHARYNX.		02.9740
Arachnoidal Cerebellar Sarcoma, Circumscribed
[description not available]		02.0510
Medulloblastoma
A malignant neoplasm that may be classified either as a glioma or as a primitive neuroectodermal tumor of childhood (see NEUROECTODERMAL TUMOR, PRIMITIVE). The tumor occurs most frequently in the first decade of life with the most typical location being the cerebellar vermis. Histologic features include a high degree of cellularity, frequent mitotic figures, and a tendency for the cells to organize into sheets or form rosettes. Medulloblastoma have a high propensity to spread throughout the craniospinal intradural axis. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, pp2060-1)		02.0510
Pneumothorax, Primary Spontaneous
[description not available]		02.0510
Pneumothorax
An accumulation of air or gas in the PLEURAL CAVITY, which may occur spontaneously or as a result of trauma or a pathological process. The gas may also be introduced deliberately during PNEUMOTHORAX, ARTIFICIAL.		02.0510
Growth Plate Fractures
[description not available]		02.0510
Becker Muscular Dystrophy
[description not available]		02.0510
Muscular Dystrophy, Duchenne
An X-linked recessive muscle disease caused by an inability to synthesize DYSTROPHIN, which is involved with maintaining the integrity of the sarcolemma. Muscle fibers undergo a process that features degeneration and regeneration. Clinical manifestations include proximal weakness in the first few years of life, pseudohypertrophy, cardiomyopathy (see MYOCARDIAL DISEASES), and an increased incidence of impaired mentation. Becker muscular dystrophy is a closely related condition featuring a later onset of disease (usually adolescence) and a slowly progressive course. (Adams et al., Principles of Neurology, 6th ed, p1415)		02.0510
Adult-Onset Still Disease
[description not available]		02.0510
Still's Disease, Adult-Onset
Systemic-onset rheumatoid arthritis in adults. It differs from classical rheumatoid arthritis in that it is more often marked by acute febrile onset, and generalized lymphadenopathy and hepatosplenomegaly are more prominent.		02.0510
Bronchial Diseases
Diseases involving the BRONCHI.		02.0510
Abnormalities, Sex Chromosome
[description not available]		02.0510
Adjuvant Arthritis
[description not available]		08.1450
Bacterial Meningitides
[description not available]		02.9610
Meningitis, Bacterial
Bacterial infections of the leptomeninges and subarachnoid space, frequently involving the cerebral cortex, cranial nerves, cerebral blood vessels, spinal cord, and nerve roots.		02.9610
Angiohemophilia
[description not available]		02.0510
von Willebrand Diseases
Group of hemorrhagic disorders in which the VON WILLEBRAND FACTOR is either quantitatively or qualitatively abnormal. They are usually inherited as an autosomal dominant trait though rare kindreds are autosomal recessive. Symptoms vary depending on severity and disease type but may include prolonged bleeding time, deficiency of factor VIII, and impaired platelet adhesion.		02.0510
Cancer of Spleen
[description not available]		03.4270
Coin Lesion, Pulmonary
[description not available]		02.0510
Deafness, Transitory
[description not available]		02.0510
Ataxia
Impairment of the ability to perform smoothly coordinated voluntary movements. This condition may affect the limbs, trunk, eyes, pharynx, larynx, and other structures. Ataxia may result from impaired sensory or motor function. Sensory ataxia may result from posterior column injury or PERIPHERAL NERVE DISEASES. Motor ataxia may be associated with CEREBELLAR DISEASES; CEREBRAL CORTEX diseases; THALAMIC DISEASES; BASAL GANGLIA DISEASES; injury to the RED NUCLEUS; and other conditions.		02.0510
Bewilderment
[description not available]		02.0510
Hearing Loss
A general term for the complete or partial loss of the ability to hear from one or both ears.		02.0510
Leukemia, Smoldering
[description not available]		03.3520
Anemia, Refractory, with Excess of Blasts
Chronic refractory anemia with granulocytopenia, and/or thrombocytopenia. Myeloblasts and progranulocytes constitute 5 to 40 percent of the nucleated marrow cells.		03.3520
Animal Mammary Carcinoma
[description not available]		02.4620
Halo Nevi
[description not available]		02.0510
Lichen Sclerosis
[description not available]		02.0510
Lichen Sclerosus et Atrophicus
A chronic inflammatory mucocutaneous disease usually affecting the female genitalia (VULVAR LICHEN SCLEROSUS) and BALANITIS XEROTICA OBLITERANS in males. It is also called white spot disease and Csillag's disease.		07.0510
Encephalopathy, Toxic
[description not available]		02.9610
Coxsackie Virus Infections
[description not available]		02.4520
Emphysema
A pathological accumulation of air in tissues or organs.		02.0510
Cancer of the Uterus
[description not available]		05.9491
Uterine Neoplasms
Tumors or cancer of the UTERUS.		17.9491
Bronchospasm, Exercise-Induced
[description not available]		02.0510
Asthma, Exercise-Induced
Asthma attacks following a period of exercise. Usually the induced attack is short-lived and regresses spontaneously. The magnitude of postexertional airway obstruction is strongly influenced by the environment in which exercise is performed (i.e. inhalation of cold air during physical exertion markedly augments the severity of the airway obstruction; conversely, warm humid air blunts or abolishes it).		02.0510
Infections, Nematomorpha
[description not available]		02.0510
Helminthiasis
Infestation with parasitic worms of the helminth class.		02.0510
Ureteral Obstruction
Blockage in any part of the URETER causing obstruction of urine flow from the kidney to the URINARY BLADDER. The obstruction may be congenital, acquired, unilateral, bilateral, complete, partial, acute, or chronic. Depending on the degree and duration of the obstruction, clinical features vary greatly such as HYDRONEPHROSIS and obstructive nephropathy.		02.4420
Infectious Diseases
[description not available]		06.4231
Communicable Diseases
An illness caused by an infectious agent or its toxins that occurs through the direct or indirect transmission of the infectious agent or its products from an infected individual or via an animal, vector or the inanimate environment to a susceptible animal or human host.		06.4231
Neoplasms, Nervous System
[description not available]		02.9710
B-K Mole Syndrome
[description not available]		02.0510
Dysplastic Nevus Syndrome
Clinically atypical nevi (usually exceeding 5 mm in diameter and having variable pigmentation and ill defined borders) with an increased risk for development of non-familial cutaneous malignant melanoma. Biopsies show melanocytic dysplasia. Nevi are clinically and histologically identical to the precursor lesions for melanoma in the B-K mole syndrome. (Stedman, 25th ed)		02.0510
Leukemia, Lymphocytic
[description not available]		05.11100
Leukemia, Lymphoid
Leukemia associated with HYPERPLASIA of the lymphoid tissues and increased numbers of circulating malignant LYMPHOCYTES and lymphoblasts.		17.11100
Embryopathies
[description not available]		02.9610
Abscess
Accumulation of purulent material in tissues, organs, or circumscribed spaces, usually associated with signs of infection.		03.3620
Central Retinal Edema, Cystoid
[description not available]		02.7330
Choked Disk
[description not available]		02.7330
Neuroretinitis
[description not available]		02.0510
Bacterial Eye Infections
[description not available]		02.0510
Bartonella henselae Infection
[description not available]		02.0510
Cat-Scratch Disease
A self-limiting bacterial infection of the regional lymph nodes caused by AFIPIA felis, a gram-negative bacterium recently identified by the Centers for Disease Control and Prevention and by BARTONELLA HENSELAE. It usually arises one or more weeks following a feline scratch, with raised inflammatory nodules at the site of the scratch being the primary symptom.		02.0510
Macular Edema
Fluid accumulation in the outer layer of the MACULA LUTEA that results from intraocular or systemic insults. It may develop in a diffuse pattern where the macula appears thickened or it may acquire the characteristic petaloid appearance referred to as cystoid macular edema. Although macular edema may be associated with various underlying conditions, it is most commonly seen following intraocular surgery, venous occlusive disease, DIABETIC RETINOPATHY, and posterior segment inflammatory disease. (From Survey of Ophthalmology 2004; 49(5) 470-90)		02.7330
Papilledema
Swelling of the OPTIC DISK, usually in association with increased intracranial pressure, characterized by hyperemia, blurring of the disk margins, microhemorrhages, blind spot enlargement, and engorgement of retinal veins. Chronic papilledema may cause OPTIC ATROPHY and visual loss. (Miller et al., Clinical Neuro-Ophthalmology, 4th ed, p175)		02.7330
Retinitis
Inflammation of the RETINA. It is rarely limited to the retina, but is commonly associated with diseases of the choroid (CHORIORETINITIS) and of the OPTIC DISK (neuroretinitis).		02.0510
Leukocytopenia
[description not available]		05.5861
Leukopenia
A decrease in the number of LEUKOCYTES in a blood sample below the normal range (LEUKOCYTE COUNT less than 4000).		05.5861
Fibrosis, Radiation
[description not available]		02.9610
Radiation Pneumonitis
Inflammation of the lung due to harmful effects of ionizing or non-ionizing radiation.		02.9610
Brain Stem Neoplasms, Primary
[description not available]		04.7521
Brain Stem Neoplasms
Benign and malignant intra-axial tumors of the MESENCEPHALON; PONS; or MEDULLA OBLONGATA of the BRAIN STEM. Primary and metastatic neoplasms may occur in this location. Clinical features include ATAXIA, cranial neuropathies (see CRANIAL NERVE DISEASES), NAUSEA, hemiparesis (see HEMIPLEGIA), and quadriparesis. Primary brain stem neoplasms are more frequent in children. Histologic subtypes include GLIOMA; HEMANGIOBLASTOMA; GANGLIOGLIOMA; and EPENDYMOMA.		04.7521
Anemia, Macrocytic
Anemia characterized by larger than normal erythrocytes, increased mean corpuscular volume (MCV) and increased mean corpuscular hemoglobin (MCH).		02.0510
Liver Abscess, Pyogenic
Single or multiple areas of PUS due to bacterial infection within the hepatic parenchyma. It can be caused by a variety of BACTERIA, local or disseminated from infections elsewhere such as in APPENDICITIS; CHOLECYSTITIS; PERITONITIS; and after LIVER TRANSPLANTATION.		02.0510
Group A Strep Infection
[description not available]		02.0510
Streptococcal Infections
Infections with bacteria of the genus STREPTOCOCCUS.		02.0510
Uremia
A clinical syndrome associated with the retention of renal waste products or uremic toxins in the blood. It is usually the result of RENAL INSUFFICIENCY. Most uremic toxins are end products of protein or nitrogen CATABOLISM, such as UREA or CREATININE. Severe uremia can lead to multiple organ dysfunctions with a constellation of symptoms.		02.0510
Cancer of Testis
[description not available]		05.8481
Testicular Neoplasms
Tumors or cancer of the TESTIS. Germ cell tumors (GERMINOMA) of the testis constitute 95% of all testicular neoplasms.		05.8481
Seminoma
A radiosensitive, malignant neoplasm of the testis, thought to be derived from primordial germ cells of the sexually undifferentiated embryonic gonad. There are three variants: classical (typical), the most common type; anaplastic; and spermatocytic. The classical seminoma is composed of fairly well differentiated sheets or cords of uniform polygonal or round cells (seminoma cells), each cell having abundant clear cytoplasm, distinct cell membranes, a centrally placed round nucleus, and one or more nucleoli. In the female, a grossly and histologically identical neoplasm, known as dysgerminoma, occurs. (Dorland, 27th ed)		02.4520
Argentaffinoma
[description not available]		04.6932
Carcinoid Tumor
A usually small, slow-growing neoplasm composed of islands of rounded, oxyphilic, or spindle-shaped cells of medium size, with moderately small vesicular nuclei, and covered by intact mucosa with a yellow cut surface. The tumor can occur anywhere in the gastrointestinal tract (and in the lungs and other sites); approximately 90% arise in the appendix. It is now established that these tumors are of neuroendocrine origin and derive from a primitive stem cell. (From Stedman, 25th ed & Holland et al., Cancer Medicine, 3d ed, p1182)		04.6932
Anomalous Ventricular Excitation Syndrome
[description not available]		02.0510
Wolff-Parkinson-White Syndrome
A form of ventricular pre-excitation characterized by a short PR interval and a long QRS interval with a delta wave. In this syndrome, atrial impulses are abnormally conducted to the HEART VENTRICLES via an ACCESSORY CONDUCTING PATHWAY that is located between the wall of the right or left atria and the ventricles, also known as a BUNDLE OF KENT. The inherited form can be caused by mutation of PRKAG2 gene encoding a gamma-2 regulatory subunit of AMP-activated protein kinase.		02.0510
Ocular Toxoplasmosis
[description not available]		02.0510
Chorioretinitis
Inflammation of the choroid in which the sensory retina becomes edematous and opaque. The inflammatory cells and exudate may burst through the sensory retina to cloud the vitreous body.		02.0510
Toxoplasmosis, Ocular
Infection caused by the protozoan parasite TOXOPLASMA in which there is extensive connective tissue proliferation, the retina surrounding the lesions remains normal, and the ocular media remain clear. Chorioretinitis may be associated with all forms of toxoplasmosis, but is usually a late sequel of congenital toxoplasmosis. The severe ocular lesions in infants may lead to blindness.		02.0510
Endothelioma, Vascular
[description not available]		02.9710
Synovioma
[description not available]		05.2641
Myxoid Liposarcoma
[description not available]		02.9710
Hemangioendothelioma
A neoplasm derived from blood vessels, characterized by numerous prominent endothelial cells that occur singly, in aggregates, and as the lining of congeries of vascular tubes or channels. Hemangioendotheliomas are relatively rare and are of intermediate malignancy (between benign hemangiomas and conventional angiosarcomas). They affect men and women about equally and rarely develop in childhood. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1866)		02.9710
Sarcoma, Synovial
A malignant neoplasm arising from tenosynovial tissue of the joints and in synovial cells of tendons and bursae. The legs are the most common site, but the tumor can occur in the abdominal wall and other trunk muscles. There are two recognized types: the monophasic (characterized by sheaths of monotonous spindle cells) and the biphasic (characterized by slit-like spaces or clefts within the tumor, lined by cuboidal or tall columnar epithelial cells). These sarcomas occur most commonly in the second and fourth decades of life. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1363)		17.2641
Liposarcoma, Myxoid
A liposarcoma containing round mesenchymal cells and a myxoid extracellular matrix in stroma.		02.9710
Infective Endocarditis
[description not available]		02.0510
Endocarditis
Inflammation of the inner lining of the heart (ENDOCARDIUM), the continuous membrane lining the four chambers and HEART VALVES. It is often caused by microorganisms including bacteria, viruses, fungi, and rickettsiae. Left untreated, endocarditis can damage heart valves and become life-threatening.		07.0510
Carcinosarcoma
A malignant neoplasm that contains elements of carcinoma and sarcoma so extensively intermixed as to indicate neoplasia of epithelial and mesenchymal tissue. (Stedman, 25th ed)		08.8321
Carcinoma, Thymic
[description not available]		05.7471
Thymoma
A neoplasm originating from thymic tissue, usually benign, and frequently encapsulated. Although it is occasionally invasive, metastases are extremely rare. It consists of any type of thymic epithelial cell as well as lymphocytes that are usually abundant. Malignant lymphomas that involve the thymus, e.g., lymphosarcoma, Hodgkin's disease (previously termed granulomatous thymoma), should not be regarded as thymoma. (From Stedman, 25th ed)		010.7471
Osteitis Fibrosa Cystica
A fibrous degeneration, cyst formation, and the presence of fibrous nodules in bone, usually due to HYPERPARATHYROIDISM.		02.0510
Hyperparathyroidism
A condition of abnormally elevated output of PARATHYROID HORMONE (or PTH) triggering responses that increase blood CALCIUM. It is characterized by HYPERCALCEMIA and BONE RESORPTION, eventually leading to bone diseases. PRIMARY HYPERPARATHYROIDISM is caused by parathyroid HYPERPLASIA or PARATHYROID NEOPLASMS. SECONDARY HYPERPARATHYROIDISM is increased PTH secretion in response to HYPOCALCEMIA, usually caused by chronic KIDNEY DISEASES.		02.0510
Ankylosing Spondylarthritis
[description not available]		02.4720
Spondylitis, Ankylosing
A chronic inflammatory condition affecting the axial joints, such as the SACROILIAC JOINT and other intervertebral or costovertebral joints. It occurs predominantly in young males and is characterized by pain and stiffness of joints (ANKYLOSIS) with inflammation at tendon insertions.		02.4720
Leukemia, Megakaryocytic
[description not available]		05.2570
Leukemia, Megakaryoblastic, Acute
An acute myeloid leukemia in which 20-30% of the bone marrow or peripheral blood cells are of megakaryocyte lineage. MYELOFIBROSIS or increased bone marrow RETICULIN is common.		05.2570
Cerebral Primitive Neuroectodermal Tumor
[description not available]		03.8221
Carcinoma, Oat Cell
[description not available]		013.08397
Neuroectodermal Tumors, Primitive
A group of malignant tumors of the nervous system that feature primitive cells with elements of neuronal and/or glial differentiation. Use of this term is limited by some authors to central nervous system tumors and others include neoplasms of similar origin which arise extracranially (i.e., NEUROECTODERMAL TUMORS, PRIMITIVE, PERIPHERAL). This term is also occasionally used as a synonym for MEDULLOBLASTOMA. In general, these tumors arise in the first decade of life and tend to be highly malignant. (From DeVita et al., Cancer: Principles and Practice of Oncology, 5th ed, p2059)		03.8221
Carcinoma, Small Cell
An anaplastic, highly malignant, and usually bronchogenic carcinoma composed of small ovoid cells with scanty neoplasm. It is characterized by a dominant, deeply basophilic nucleus, and absent or indistinct nucleoli. (From Stedman, 25th ed; Holland et al., Cancer Medicine, 3d ed, p1286-7)		013.08397
Anorectal Diseases
[description not available]		02.0510
Rectal Diseases
Pathological developments in the RECTUM region of the large intestine (INTESTINE, LARGE).		02.0510
Bilateral Wilms Tumor
[description not available]		02.0510
Wilms Tumor
A malignant kidney tumor, caused by the uncontrolled multiplication of renal stem (blastemal), stromal (STROMAL CELLS), and epithelial (EPITHELIAL CELLS) elements. However, not all three are present in every case. Several genes or chromosomal areas have been associated with Wilms tumor which is usually found in childhood as a firm lump in a child's side or ABDOMEN.		02.0510
Fibrous Tissue Neoplasms
[description not available]		02.0510
Experimental Radiation Injuries
[description not available]		02.4720
Coagulation, Disseminated Intravascular
[description not available]		02.7330
Disseminated Intravascular Coagulation
A disorder characterized by procoagulant substances entering the general circulation causing a systemic thrombotic process. The activation of the clotting mechanism may arise from any of a number of disorders. A majority of the patients manifest skin lesions, sometimes leading to PURPURA FULMINANS.		02.7330
Acne Rosacea
[description not available]		07.0610
Rosacea
A cutaneous disorder primarily of convexities of the central part of the FACE, such as FOREHEAD; CHEEK; NOSE; and CHIN. It is characterized by FLUSHING; ERYTHEMA; EDEMA; RHINOPHYMA; papules; and ocular symptoms. It may occur at any age but typically after age 30. There are various subtypes of rosacea: erythematotelangiectatic, papulopustular, phymatous, and ocular (National Rosacea Society's Expert Committee on the Classification and Staging of Rosacea, J Am Acad Dermatol 2002; 46:584-7).		07.0610
Aplasia Pure Red Cell
[description not available]		02.4520
Red-Cell Aplasia, Pure
Suppression of erythropoiesis with little or no abnormality of leukocyte or platelet production.		02.4520
Impotence, Arteriogenic
[description not available]		02.0510
Femoral Fractures
Fractures of the femur.		02.0510
Fibromatosis
[description not available]		05.5961
Fibroma
A benign tumor of fibrous or fully developed connective tissue.		05.5961
Drug Overdose
Accidental or deliberate use of a medication or street drug in excess of normal dosage.		02.7430
Rhabdoid Tumor
A rare but highly lethal childhood tumor found almost exclusively in infants. Histopathologically, it resembles RHABDOMYOSARCOMA but the tumor cells are not of myogenic origin. Although it arises primarily in the kidney, it may be found in other parts of the body. The rhabdoid cytomorphology is believed to be the expression of a very primitive malignant cell. (From Holland et al., Cancer Medicine, 3d ed, p2210)		02.0510
Arterial Diseases, Carotid
[description not available]		02.0510
Carotid Artery Diseases
Pathological conditions involving the CAROTID ARTERIES, including the common, internal, and external carotid arteries. ATHEROSCLEROSIS and TRAUMA are relatively frequent causes of carotid artery pathology.		02.0510
Neoplasms, Vascular
[description not available]		02.0510
Keloid
A sharply elevated, irregularly shaped, progressively enlarging scar resulting from formation of excessive amounts of collagen in the dermis during connective tissue repair. It is differentiated from a hypertrophic scar (CICATRIX, HYPERTROPHIC) in that the former does not spread to surrounding tissues.		02.0610
Hyperammonemia
Elevated level of AMMONIA in the blood. It is a sign of defective CATABOLISM of AMINO ACIDS or ammonia to UREA.		03.4511
Hypospermatogenesis
[description not available]		02.4420
Diplopia
A visual symptom in which a single object is perceived by the visual cortex as two objects rather than one. Disorders associated with this condition include REFRACTIVE ERRORS; STRABISMUS; OCULOMOTOR NERVE DISEASES; TROCHLEAR NERVE DISEASES; ABDUCENS NERVE DISEASES; and diseases of the BRAIN STEM and OCCIPITAL LOBE.		02.0610
Vaccinia
The cutaneous and occasional systemic reactions associated with vaccination using smallpox (variola) vaccine.		03.3620
Anterior Ischemic Optic Neuropathy
[description not available]		02.9710
Aortic Arteritis, Giant Cell
[description not available]		03.3720
Giant Cell Arteritis
A systemic autoimmune disorder that typically affects medium and large ARTERIES, usually leading to occlusive granulomatous vasculitis with transmural infiltrate containing multinucleated GIANT CELLS. The TEMPORAL ARTERY is commonly involved. This disorder appears primarily in people over the age of 50. Symptoms include FEVER; FATIGUE; HEADACHE; visual impairment; pain in the jaw and tongue; and aggravation of pain by cold temperatures. (From Adams et al., Principles of Neurology, 6th ed)		08.3720
Optic Neuropathy, Ischemic
Ischemic injury to the OPTIC NERVE which usually affects the OPTIC DISK (optic neuropathy, anterior ischemic) and less frequently the retrobulbar portion of the nerve (optic neuropathy, posterior ischemic). The injury results from occlusion of arterial blood supply which may result from TEMPORAL ARTERITIS; ATHEROSCLEROSIS; COLLAGEN DISEASES; EMBOLISM; DIABETES MELLITUS; and other conditions. The disease primarily occurs in the sixth decade or later and presents with the sudden onset of painless and usually severe monocular visual loss. Anterior ischemic optic neuropathy also features optic disk edema with microhemorrhages. The optic disk appears normal in posterior ischemic optic neuropathy. (Glaser, Neuro-Ophthalmology, 2nd ed, p135)		02.9710
Keratoacanthoma
A benign, non-neoplastic, usually self-limiting epithelial lesion closely resembling squamous cell carcinoma clinically and histopathologically. It occurs in solitary, multiple, and eruptive forms. The solitary and multiple forms occur on sunlight exposed areas and are identical histologically; they affect primarily white males. The eruptive form usually involves both sexes and appears as a generalized papular eruption.		07.0610
Oliguria
Decreased URINE output that is below the normal range. Oliguria can be defined as urine output of less than or equal to 0.5 or 1 ml/kg/hr depending on the age.		02.0710
Acoustic Neuroma
[description not available]		02.7530
Edema-Proteinuria-Hypertension Gestosis
[description not available]		02.0510
Pre-Eclampsia
A complication of PREGNANCY, characterized by a complex of symptoms including maternal HYPERTENSION and PROTEINURIA with or without pathological EDEMA. Symptoms may range between mild and severe. Pre-eclampsia usually occurs after the 20th week of gestation, but may develop before this time in the presence of trophoblastic disease.		02.0510
Cataract, Membranous
[description not available]		02.0610
Cataract
Partial or complete opacity on or in the lens or capsule of one or both eyes, impairing vision or causing blindness. The many kinds of cataract are classified by their morphology (size, shape, location) or etiology (cause and time of occurrence). (Dorland, 27th ed)		02.0610
MPTP Neurotoxicity Syndrome
[description not available]		02.0610
Aqueductal Stenosis
[description not available]		02.0510
Carbon Tetrachloride Poisoning
Poisoning that results from ingestion, injection, inhalation, or skin absorption of CARBON TETRACHLORIDE.		02.0610
Alveolar Proteinoses, Pulmonary
[description not available]		02.4320
Pulmonary Alveolar Proteinosis
A PULMONARY ALVEOLI-filling disease, characterized by dense phospholipoproteinaceous deposits in the alveoli, cough, and DYSPNEA. This disease is often related to, congenital or acquired, impaired processing of PULMONARY SURFACTANTS by alveolar macrophages, a process dependent on GRANULOCYTE-MACROPHAGE COLONY-STIMULATING FACTOR.		02.4320
Aberrant Tissue
[description not available]		02.0610
Central Hypothyroidism
[description not available]		04.3441
Pleural Diseases
Diseases involving the PLEURA.		02.0610
Hypothyroidism
A syndrome that results from abnormally low secretion of THYROID HORMONES from the THYROID GLAND, leading to a decrease in BASAL METABOLIC RATE. In its most severe form, there is accumulation of MUCOPOLYSACCHARIDES in the SKIN and EDEMA, known as MYXEDEMA. It may be primary or secondary due to other pituitary disease, or hypothalamic dysfunction.		04.3441
Cold Panniculitis
[description not available]		02.7230
Acute Coronary Syndrome
An episode of MYOCARDIAL ISCHEMIA that generally lasts longer than a transient anginal episode that ultimately may lead to MYOCARDIAL INFARCTION.		02.0610
Bladder Diseases
[description not available]		02.0610
Jaundice, Cholestatic
[description not available]		02.7330
Jaundice, Obstructive
Jaundice, the condition with yellowish staining of the skin and mucous membranes, that is due to impaired BILE flow in the BILIARY TRACT, such as INTRAHEPATIC CHOLESTASIS, or EXTRAHEPATIC CHOLESTASIS.		02.7330
Chromosomal Duplication
[description not available]		02.0610
Adnexal Diseases
Diseases of the uterine appendages (ADNEXA UTERI) including diseases involving the OVARY, the FALLOPIAN TUBES, and ligaments of the uterus (BROAD LIGAMENT; ROUND LIGAMENT).		02.0610
Neoplasms, Squamous Cell
Neoplasms of the SQUAMOUS EPITHELIAL CELLS. The concept does not refer to neoplasms located in tissue composed of squamous elements.		02.9810
Mastocytoma, Skin
A variant of cutaneous mastocytosis which occurs as a single lesion usually in infants. It is found mostly in the wrist and trunk and there is no atypical cytomorphology.		02.4820
Contracture
Prolonged shortening of the muscle or other soft tissue around a joint, preventing movement of the joint.		02.0710
Infections, Staphylococcal
[description not available]		02.0610
Staphylococcal Infections
Infections with bacteria of the genus STAPHYLOCOCCUS.		02.0610
Cochlear Hearing Loss
[description not available]		02.7430
Hearing Loss, Sensorineural
Hearing loss resulting from damage to the COCHLEA and the sensorineural elements which lie internally beyond the oval and round windows. These elements include the AUDITORY NERVE and its connections in the BRAINSTEM.		02.7430
Preleukemia
Conditions in which the abnormalities in the peripheral blood or bone marrow represent the early manifestations of acute leukemia, but in which the changes are not of sufficient magnitude or specificity to permit a diagnosis of acute leukemia by the usual clinical criteria.		02.4420
Ear Diseases
Pathological processes of the ear, the hearing, and the equilibrium system of the body.		02.0710
Facial Dermatoses
Skin diseases involving the FACE.		02.7430
Nasal Diseases
[description not available]		02.0710
Prostatic Diseases
Pathological processes involving the PROSTATE or its component tissues.		02.0610
Plica Syndrome
[description not available]		02.0710
Psoriasis Arthropathica
[description not available]		02.4420
Arthritis, Spinal
[description not available]		03.8421
Synovitis
Inflammation of the SYNOVIAL MEMBRANE.		02.0710
Arthritis, Psoriatic
A type of inflammatory arthritis associated with PSORIASIS, often involving the axial joints and the peripheral terminal interphalangeal joints. It is characterized by the presence of HLA-B27-associated SPONDYLARTHROPATHY, and the absence of rheumatoid factor.		02.4420
Malignant Hypertension
[description not available]		02.0710
Hypertension, Malignant
A condition of markedly elevated BLOOD PRESSURE with DIASTOLIC PRESSURE usually greater than 120 mm Hg. Malignant hypertension is characterized by widespread vascular damage, PAPILLEDEMA, retinopathy, HYPERTENSIVE ENCEPHALOPATHY, and renal dysfunction.		02.0710
Scrotal Hydrocele
[description not available]		03.3620
Mast-Cell Sarcoma
A unifocal malignant tumor that consists of atypical pathological MAST CELLS without systemic involvement. It causes local destructive growth in organs other than in skin or bone marrow.		04.1331
Submandibular Gland Neoplasms
New abnormal growth of tissue in the SUBMANDIBULAR GLAND.		02.9910
Cirrhoses, Experimental Liver
[description not available]		03.2960
Hypopharyngeal Cancer
[description not available]		02.4620
Cancer of the Tongue
[description not available]		02.0710
Congenital Epulides
[description not available]		02.0710
Hypopharyngeal Neoplasms
Tumors or cancer of the HYPOPHARYNX.		02.4620
Tongue Neoplasms
Tumors or cancer of the TONGUE.		02.0710
Xeroderma
[description not available]		02.0710
Dementia Praecox
[description not available]		02.0710
Ichthyosis
Any of several generalized skin disorders characterized by dryness, roughness, and scaliness, due to hypertrophy of the stratum corneum epidermis. Most are genetic, but some are acquired, developing in association with other systemic disease or genetic syndrome.		02.0710
Schizophrenia
A severe emotional disorder of psychotic depth characteristically marked by a retreat from reality with delusion formation, HALLUCINATIONS, emotional disharmony, and regressive behavior.		02.0710
Aminoaciduria, Renal
[description not available]		03.4611
Adult Fanconi Syndrome
[description not available]		03.8521
Deep Vein Thrombosis
[description not available]		02.0710
Venous Thrombosis
The formation or presence of a blood clot (THROMBUS) within a vein.		02.0710
Pain, Chronic
[description not available]		02.0710
Chronic Pain
Aching sensation that persists for more than a few months. It may or may not be associated with trauma or disease, and may persist after the initial injury has healed. Its localization, character, and timing are more vague than with acute pain.		02.0710
Cystadenocarcinoma, Serous
A malignant cystic or semicystic neoplasm. It often occurs in the ovary and usually bilaterally. The external surface is usually covered with papillary excrescences. Microscopically, the papillary patterns are predominantly epithelial overgrowths with differentiated and undifferentiated papillary serous cystadenocarcinoma cells. Psammoma bodies may be present. The tumor generally adheres to surrounding structures and produces ascites. (From Hughes, Obstetric-Gynecologic Terminology, 1972, p185)		03.8521
ALS - Amyotrophic Lateral Sclerosis
[description not available]		02.0710
Amyotrophic Lateral Sclerosis
A degenerative disorder affecting upper MOTOR NEURONS in the brain and lower motor neurons in the brain stem and SPINAL CORD. Disease onset is usually after the age of 50 and the process is usually fatal within 3 to 6 years. Clinical manifestations include progressive weakness, atrophy, FASCICULATION, hyperreflexia, DYSARTHRIA, dysphagia, and eventual paralysis of respiratory function. Pathologic features include the replacement of motor neurons with fibrous ASTROCYTES and atrophy of anterior SPINAL NERVE ROOTS and corticospinal tracts. (From Adams et al., Principles of Neurology, 6th ed, pp1089-94)		02.0710
Kidney, Polycystic
[description not available]		02.0710
Polycystic Kidney Diseases
Hereditary diseases that are characterized by the progressive expansion of a large number of tightly packed CYSTS within the KIDNEYS. They include diseases with autosomal dominant and autosomal recessive inheritance.		02.0710
Menopause
The last menstrual period. Permanent cessation of menses (MENSTRUATION) is usually defined after 6 to 12 months of AMENORRHEA in a woman over 45 years of age. In the United States, menopause generally occurs in women between 48 and 55 years of age.		03.4611
Infant, Newborn, Diseases
Diseases of newborn infants present at birth (congenital) or developing within the first month of birth. It does not include hereditary diseases not manifesting at birth or within the first 30 days of life nor does it include inborn errors of metabolism. Both HEREDITARY DISEASES and METABOLISM, INBORN ERRORS are available as general concepts.		02.0710
Chemotherapy-Induced Acral Erythema
[description not available]		02.0710
Hand-Foot Syndrome
Chemotherapy-induced dermal side effects that are associated with the use of various CYTOSTATIC AGENTS. Symptoms range from mild ERYTHEMA and/or PARESTHESIA to severe ulcerative dermatitis with debilitating pain involving typically palmoplantar and intertriginous areas. These cutaneous manifestations are sometimes accompanied by nail anomalies.		02.0710
Coronary Restenosis
Recurrent narrowing or constriction of a coronary artery following surgical procedures performed to alleviate a prior obstruction.		04.7521
Deficiency, Vitamin B 12
[description not available]		02.0710
Vitamin B 12 Deficiency
A nutritional condition produced by a deficiency of VITAMIN B 12 in the diet, characterized by megaloblastic anemia. Since vitamin B 12 is not present in plants, humans have obtained their supply from animal products, from multivitamin supplements in the form of pills, and as additives to food preparations. A wide variety of neuropsychiatric abnormalities is also seen in vitamin B 12 deficiency and appears to be due to an undefined defect involving myelin synthesis. (From Cecil Textbook of Medicine, 19th ed, p848)		02.0710
Autosomal Chromosome Disorders
[description not available]		02.0710
Penile Diseases
Pathological processes involving the PENIS or its component tissues.		02.0710
Ulcer
A lesion on the surface of the skin or a mucous surface, produced by the sloughing of inflammatory necrotic tissue.		02.0710
Clear Cell Sarcoma of Soft Tissue
[description not available]		02.9910
CCMMT
[description not available]		02.9910
Sarcoma, Clear Cell
A sarcoma of young adults occurring in the lower extremities and acral regions. It is found intimately bound to tendons as a circumscribed but unencapsulated melanin-bearing tumor of neuroectodermal origin. Clear cell sarcoma is associated with a specific t(12;22)(q13;q12) translocation.		02.9910
Complex Regional Pain Syndrome
[description not available]		02.9910
Complex Regional Pain Syndromes
Conditions characterized by pain involving an extremity or other body region, HYPERESTHESIA, and localized autonomic dysfunction following injury to soft tissue or nerve. The pain is usually associated with ERYTHEMA; SKIN TEMPERATURE changes, abnormal sudomotor activity (i.e., changes in sweating due to altered sympathetic innervation) or edema. The degree of pain and other manifestations is out of proportion to that expected from the inciting event. Two subtypes of this condition have been described: type I; (REFLEX SYMPATHETIC DYSTROPHY) and type II; (CAUSALGIA). (From Pain 1995 Oct;63(1):127-33)		02.9910
Tenosynovitis
Inflammation of the synovial lining of a tendon sheath. Causes include trauma, tendon stress, bacterial disease (gonorrhea, tuberculosis), rheumatic disease, and gout. Common sites are the hand, wrist, shoulder capsule, hip capsule, hamstring muscles, and Achilles tendon. The tendon sheaths become inflamed and painful, and accumulate fluid. Joint mobility is usually reduced.		0310
Blood Loss, Surgical
Loss of blood during a surgical procedure.		02.0710
Disease
A definite pathologic process with a characteristic set of signs and symptoms. It may affect the whole body or any of its parts, and its etiology, pathology, and prognosis may be known or unknown.		02.0710
Benign Cranial Nerve Neoplasms
[description not available]		02.0710
Pancreatic Diseases
Pathological processes of the PANCREAS.		02.9910
Amyloidosis
A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.		07.9910
Malignant Fibrohistiocytic Tumors
[description not available]		02.9910
Myxosarcoma
A sarcoma, usually a liposarcoma or malignant fibrous histiocytoma, with an abundant component of myxoid tissue resembling primitive mesenchyme containing connective tissue mucin. (Stedman, 25th ed)		02.9910
Myxoma, Nerve Sheath
[description not available]		02.9910
Histiocytoma, Malignant Fibrous
The most commonly diagnosed soft tissue sarcoma. It is a neoplasm with a fibrohistiocytic appearance found chiefly in later adult life, with peak incidence in the 7th decade.		02.9910
Solitary Fibrous Tumors
Rare neoplasms of mesenchymal origin, usually benign, and most commonly involving the PLEURA (see SOLITARY FIBROUS TUMOR, PLEURAL). They also are found in extrapleural sites.		02.9910
Anti-GBM Disease
[description not available]		02.4920
Anti-Glomerular Basement Membrane Disease
An autoimmune disease of the KIDNEY and the LUNG. It is characterized by the presence of circulating autoantibodies targeting the epitopes in the non-collagenous domains of COLLAGEN TYPE IV in the basement membranes of kidney glomeruli (KIDNEY GLOMERULUS) and lung alveoli (PULMONARY ALVEOLI), and the subsequent destruction of these basement membranes. Clinical features include pulmonary alveolar hemorrhage and glomerulonephritis.		02.4920
Craniopharyngioma, Adamantinous
[description not available]		02.0810
Craniopharyngioma
A benign pituitary-region neoplasm that originates from Rathke's pouch. The two major histologic and clinical subtypes are adamantinous (or classical) craniopharyngioma and papillary craniopharyngioma. The adamantinous form presents in children and adolescents as an expanding cystic lesion in the pituitary region. The cystic cavity is filled with a black viscous substance and histologically the tumor is composed of adamantinomatous epithelium and areas of calcification and necrosis. Papillary craniopharyngiomas occur in adults, and histologically feature a squamous epithelium with papillations. (From Joynt, Clinical Neurology, 1998, Ch14, p50)		07.0810
Leukemia, Myeloid, Acute, M4
[description not available]		02.7330
Leukemia, Myelomonocytic, Acute
A pediatric acute myeloid leukemia involving both myeloid and monocytoid precursors. At least 20% of non-erythroid cells are of monocytic origin.		02.7330
Age-Related Macular Degeneration
[description not available]		02.9910
Macular Degeneration
Degenerative changes in the RETINA usually of older adults which results in a loss of vision in the center of the visual field (the MACULA LUTEA) because of damage to the retina. It occurs in dry and wet forms.		02.9910
Cerebral Malaria
[description not available]		02.0710
Laryngeal Diseases
Pathological processes involving any part of the LARYNX which coordinates many functions such as voice production, breathing, swallowing, and coughing.		02.0810
Central Nervous System Cysticercosis
[description not available]		02.0810
Neurocysticercosis
Infection of the brain, spinal cord, or perimeningeal structures with the larval forms of the genus TAENIA (primarily T. solium in humans). Lesions formed by the organism are referred to as cysticerci. The infection may be subacute or chronic, and the severity of symptoms depends on the severity of the host immune response and the location and number of lesions. SEIZURES represent the most common clinical manifestation although focal neurologic deficits may occur. (From Joynt, Clinical Neurology, 1998, Ch27, pp46-50)		02.0810
Acute Relapsing Multiple Sclerosis
[description not available]		02.0810
Multiple Sclerosis, Relapsing-Remitting
The most common clinical variant of MULTIPLE SCLEROSIS, characterized by recurrent acute exacerbations of neurologic dysfunction followed by partial or complete recovery. Common clinical manifestations include loss of visual (see OPTIC NEURITIS), motor, sensory, or bladder function. Acute episodes of demyelination may occur at any site in the central nervous system, and commonly involve the optic nerves, spinal cord, brain stem, and cerebellum. (Adams et al., Principles of Neurology, 6th ed, pp903-914)		02.0810
Altered Level of Consciousness
[description not available]		02.0110
Mitral Stenosis
[description not available]		02.0110
Mitral Valve Stenosis
Narrowing of the passage through the MITRAL VALVE due to FIBROSIS, and CALCINOSIS in the leaflets and chordal areas. This elevates the left atrial pressure which, in turn, raises pulmonary venous and capillary pressure leading to bouts of DYSPNEA and TACHYCARDIA during physical exertion. RHEUMATIC FEVER is its primary cause.		02.0110
Intradural-Extramedullary Spinal Cord Neoplasms
[description not available]		03.6230
Spinal Cord Neoplasms
Benign and malignant neoplasms which occur within the substance of the spinal cord (intramedullary neoplasms) or in the space between the dura and spinal cord (intradural extramedullary neoplasms). The majority of intramedullary spinal tumors are primary CNS neoplasms including ASTROCYTOMA; EPENDYMOMA; and LIPOMA. Intramedullary neoplasms are often associated with SYRINGOMYELIA. The most frequent histologic types of intradural-extramedullary tumors are MENINGIOMA and NEUROFIBROMA.		03.6230
Pityriasis Rosea
A mild exanthematous inflammation of unknown etiology. It is characterized by the presence of salmon-colored maculopapular lesions. The most striking feature is the arrangement of the lesions such that the long axis is parallel to the lines of cleavage. The eruptions are usually generalized, affecting chiefly the trunk, and the course is often self-limiting.		07.4220
Viral Hepatitis, Human
[description not available]		02.0110
Hepatitis, Viral, Human
INFLAMMATION of the LIVER in humans due to infection by VIRUSES. There are several significant types of human viral hepatitis with infection caused by enteric-transmission (HEPATITIS A; HEPATITIS E) or blood transfusion (HEPATITIS B; HEPATITIS C; and HEPATITIS D).		02.0110
Hematuria
Presence of blood in the urine.		02.0110
Cystitis
Inflammation of the URINARY BLADDER, either from bacterial or non-bacterial causes. Cystitis is usually associated with painful urination (dysuria), increased frequency, urgency, and suprapubic pain.		02.4220
Refractory Anemia
[description not available]		03.6330
Anemia, Refractory
A severe sometimes chronic anemia, usually macrocytic in type, that does not respond to ordinary antianemic therapy.		03.6330
Carcinoma, Medullary
A carcinoma composed mainly of epithelial elements with little or no stroma. Medullary carcinomas of the breast constitute 5%-7% of all mammary carcinomas; medullary carcinomas of the thyroid comprise 3%-10% of all thyroid malignancies. (From Dorland, 27th ed; DeVita Jr et al., Cancer: Principles & Practice of Oncology, 3d ed, p1141; Segen, Dictionary of Modern Medicine, 1992)		06.03103
Biliary Cirrhosis
[description not available]		02.0110
Liver Cirrhosis, Biliary
FIBROSIS of the hepatic parenchyma due to obstruction of BILE flow (CHOLESTASIS) in the intrahepatic or extrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC; BILE DUCTS, EXTRAHEPATIC). Primary biliary cholangitis involves the destruction of small intra-hepatic bile ducts and decreased bile secretion. Secondary biliary cholangitis is produced by prolonged obstruction of large intrahepatic or extrahepatic bile ducts from a variety of causes.		02.0110
Mesenchymoma
A mixed mesenchymal tumor composed of two or more mesodermal cellular elements not commonly associated, not counting fibrous tissue as one of the elements. Mesenchymomas are widely distributed in the body and about 75% are malignant. (Dorland, 27th ed; Holland et al., Cancer Medicine, 3d ed, p1866)		04.6660
Chicken Pox
[description not available]		02.0110
Shingles
[description not available]		02.4320
Chickenpox
A highly contagious infectious disease caused by the varicella-zoster virus (HERPESVIRUS 3, HUMAN). It usually affects children, is spread by direct contact or respiratory route via droplet nuclei, and is characterized by the appearance on the skin and mucous membranes of successive crops of typical pruritic vesicular lesions that are easily broken and become scabbed. Chickenpox is relatively benign in children, but may be complicated by pneumonia and encephalitis in adults. (From Dorland, 27th ed)		02.0110
Herpes Zoster
An acute infectious, usually self-limited, disease believed to represent activation of latent varicella-zoster virus (HERPESVIRUS 3, HUMAN) in those who have been rendered partially immune after a previous attack of CHICKENPOX. It involves the SENSORY GANGLIA and their areas of innervation and is characterized by severe neuralgic pain along the distribution of the affected nerve and crops of clustered vesicles over the area. (From Dorland, 27th ed)		07.4320
Coronary Heart Disease
[description not available]		04.7221
Cancer, Radiation-Induced
[description not available]		02.0110
Cocarcinogenesis
The combination of two or more different factors in the production of cancer.		02.0110
Facial Neoplasms
New abnormal growth of tissue in the FACE.		02.4220
Coronary Disease
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.		04.7221
Aneuploid
[description not available]		05.5861
Joint Pain
[description not available]		03.8410
Arthralgia
Pain in the joint.		03.8410
Mycosis Fungoides
A chronic, malignant T-cell lymphoma of the skin. In the late stages, the LYMPH NODES and viscera are affected.		02.7130
Arteriosclerosis
Thickening and loss of elasticity of the walls of ARTERIES of all sizes. There are many forms classified by the types of lesions and arteries involved, such as ATHEROSCLEROSIS with fatty lesions in the ARTERIAL INTIMA of medium and large muscular arteries.		08.1250
Atypical Lipomatous Tumor
[description not available]		02.0110
Liposarcoma
A malignant tumor derived from primitive or embryonal lipoblastic cells. It may be composed of well-differentiated fat cells or may be dedifferentiated: myxoid (LIPOSARCOMA, MYXOID), round-celled, or pleomorphic, usually in association with a rich network of capillaries. Recurrences are common and dedifferentiated liposarcomas metastasize to the lungs or serosal surfaces. (From Dorland, 27th ed; Stedman, 25th ed)		07.0110
Gastric Fistula
Abnormal passage communicating with the STOMACH.		02.0110
Leukemia, Acute Monocytic
[description not available]		02.4220
Leukemia, Monocytic, Acute
An acute myeloid leukemia in which 80% or more of the leukemic cells are of monocytic lineage including monoblasts, promonocytes, and MONOCYTES.		02.4220
Epiphora
[description not available]		07.4220
Lacrimal Apparatus Diseases
Diseases of the LACRIMAL APPARATUS.		02.4220
Gangrene
Death and putrefaction of tissue usually due to a loss of blood supply.		02.9310
Pityriasis
A name originally applied to a group of skin diseases characterized by the formation of fine, branny scales, but now used only with a modifier. (Dorland, 27th ed)		02.0110
Bacterial Pneumonia
[description not available]		02.0210
Cerebral Nocardiosis
[description not available]		02.0210
Pneumonia, Bacterial
Inflammation of the lung parenchyma that is caused by bacterial infections.		02.0210
Exophthalmos
Abnormal protrusion of both eyes; may be caused by endocrine gland malfunction, malignancy, injury, or paralysis of the extrinsic muscles of the eye.		02.0110
Hyperthyroid
[description not available]		02.0110
Orbital Neoplasms
Neoplasms of the bony orbit and contents except the eyeball.		02.4320
Fibrocartilaginous Dysplasia of Bone
[description not available]		02.0110
Fibrous Dysplasia of Bone
A disease of bone marked by thinning of the cortex by fibrous tissue containing bony spicules, producing pain, disability, and gradually increasing deformity. Only one bone may be involved (FIBROUS DYSPLASIA, MONOSTOTIC) or several (FIBROUS DYSPLASIA, POLYOSTOTIC).		02.0110
Hyperthyroidism
Hypersecretion of THYROID HORMONES from the THYROID GLAND. Elevated levels of thyroid hormones increase BASAL METABOLIC RATE.		02.0110
Dehiscence, Surgical Wound
[description not available]		02.0110
Adiadochokinesis
[description not available]		02.0210
Age-Related Memory Disorders
[description not available]		02.0210
Brachial Paresis
[description not available]		02.0210
Essential Polyarteritis
[description not available]		02.0210
Central Nervous System Origin Vertigo
[description not available]		02.0210
Cerebellar Ataxia
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)		02.0210
Memory Disorders
Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.		02.0210
Vertigo
An illusion of movement, either of the external world revolving around the individual or of the individual revolving in space. Vertigo may be associated with disorders of the inner ear (EAR, INNER); VESTIBULAR NERVE; BRAINSTEM; or CEREBRAL CORTEX. Lesions in the TEMPORAL LOBE and PARIETAL LOBE may be associated with FOCAL SEIZURES that may feature vertigo as an ictal manifestation. (From Adams et al., Principles of Neurology, 6th ed, pp300-1)		02.0210
Diabetic Angiopathies
VASCULAR DISEASES that are associated with DIABETES MELLITUS.		02.0210
Colitis, Mucous
[description not available]		02.9310
Hemorrhage, Peptic Ulcer
[description not available]		02.9310
Irritable Bowel Syndrome
A disorder with chronic or recurrent colonic symptoms without a clearcut etiology. This condition is characterized by chronic or recurrent ABDOMINAL PAIN, bloating, MUCUS in FECES, and an erratic disturbance of DEFECATION.		02.9310
Polyps
Discrete abnormal tissue masses that protrude into the lumen of the DIGESTIVE TRACT or the RESPIRATORY TRACT. Polyps can be spheroidal, hemispheroidal, or irregular mound-shaped structures attached to the MUCOUS MEMBRANE of the lumen wall either by a stalk, pedunculus, or by a broad base.		02.0210
Acute Febrile Neutrophilic Dermatosis
[description not available]		02.7230
Delayed Hypersensitivity
[description not available]		02.0210
Acquired Immune Deficiency Syndrome
[description not available]		08.6330
Acquired Immunodeficiency Syndrome
An acquired defect of cellular immunity associated with infection by the human immunodeficiency virus (HIV), a CD4-positive T-lymphocyte count under 200 cells/microliter or less than 14% of total lymphocytes, and increased susceptibility to opportunistic infections and malignant neoplasms. Clinical manifestations also include emaciation (wasting) and dementia. These elements reflect criteria for AIDS as defined by the CDC in 1993.		03.6330
Cardiometabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components not only include metabolic dysfunctions of METABOLIC SYNDROME but also HYPERTENSION, and ABDOMINAL OBESITY.		02.0210
Metabolic Syndrome
A cluster of symptoms that are risk factors for CARDIOVASCULAR DISEASES and TYPE 2 DIABETES MELLITUS. The major components of metabolic syndrome include ABDOMINAL OBESITY; atherogenic DYSLIPIDEMIA; HYPERTENSION; HYPERGLYCEMIA; INSULIN RESISTANCE; a proinflammatory state; and a prothrombotic (THROMBOSIS) state.		02.0210
Cancer of Mediastinum
[description not available]		02.9310
Mediastinal Neoplasms
Tumors or cancer of the MEDIASTINUM.		02.9310
Intestinal Polyps
Discrete abnormal tissue masses that protrude into the lumen of the INTESTINE. A polyp is attached to the intestinal wall either by a stalk, pedunculus, or by a broad base.		02.0210
MEA 2a
[description not available]		02.4320
MEA 2b
[description not available]		02.4320
Pulmonary Sarcoidosis
[description not available]		02.0210
Sarcoidosis, Pulmonary
Sarcoidosis affecting predominantly the lungs, the site most frequently involved and most commonly causing morbidity and mortality in sarcoidosis. Pulmonary sarcoidosis is characterized by sharply circumscribed granulomas in the alveolar, bronchial, and vascular walls, composed of tightly packed cells derived from the mononuclear phagocyte system. The clinical symptoms when present are dyspnea upon exertion, nonproductive cough, and wheezing. (Cecil Textbook of Medicine, 19th ed, p431)		02.0210
Neuroectodermal Tumors
Malignant neoplasms arising in the neuroectoderm, the portion of the ectoderm of the early embryo that gives rise to the central and peripheral nervous systems, including some glial cells.		02.0210
Leiomyoblastoma
[description not available]		03.8120
Encephalitis, Viral
Inflammation of brain parenchymal tissue as a result of viral infection. Encephalitis may occur as primary or secondary manifestation of TOGAVIRIDAE INFECTIONS; HERPESVIRIDAE INFECTIONS; ADENOVIRIDAE INFECTIONS; FLAVIVIRIDAE INFECTIONS; BUNYAVIRIDAE INFECTIONS; PICORNAVIRIDAE INFECTIONS; PARAMYXOVIRIDAE INFECTIONS; ORTHOMYXOVIRIDAE INFECTIONS; RETROVIRIDAE INFECTIONS; and ARENAVIRIDAE INFECTIONS.		02.0210
AIDS, Simian
[description not available]		02.0210
Brain Disorders
[description not available]		02.9440
Brain Diseases
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.		02.9440
Anaplastic Ependymoma
[description not available]		02.0210
Ependymoma
Glioma derived from EPENDYMOGLIAL CELLS that tend to present as malignant intracranial tumors in children and as benign intraspinal neoplasms in adults. It may arise from any level of the ventricular system or central canal of the spinal cord. Intracranial ependymomas most frequently originate in the FOURTH VENTRICLE and histologically are densely cellular tumors which may contain ependymal tubules and perivascular pseudorosettes. Spinal ependymomas are usually benign papillary or myxopapillary tumors. (From DeVita et al., Principles and Practice of Oncology, 5th ed, p2018; Escourolle et al., Manual of Basic Neuropathology, 2nd ed, pp28-9)		02.0210
Cerebrospinal Fluid Effusion, Subdural
[description not available]		02.4320
Adenocarcinoma, Endometrioid
[description not available]		02.0210
Carcinoma, Endometrioid
An adenocarcinoma characterized by the presence of cells resembling the glandular cells of the ENDOMETRIUM. It is a common histological type of ovarian CARCINOMA and ENDOMETRIAL CARCINOMA. There is a high frequency of co-occurrence of this form of adenocarcinoma in both tissues.		02.0210
Angiitis, Central Nervous System
[description not available]		02.0210
Island Cell Tumor
[description not available]		02.9410
Adenoma, Islet Cell
A benign tumor of the pancreatic ISLET CELLS. Usually it involves the INSULIN-producing PANCREATIC BETA CELLS, as in INSULINOMA, resulting in HYPERINSULINISM.		02.9410
Cancer, Embryonal
[description not available]		04.7321
Neoplasms, Germ Cell and Embryonal
Neoplasms composed of primordial GERM CELLS of embryonic GONADS or of elements of the germ layers of the EMBRYO, MAMMALIAN. The concept does not refer to neoplasms located in the gonads or present in an embryo or FETUS.		04.7321
Alopecia Mucinosa
[description not available]		02.0210
Hidradenitis
The inflammation of a sweat gland (usually of the apocrine type). The condition can be idiopathic or occur as a result of or in association with another underlying condition. Neutrophilic eccrine hidradenitis is a relatively rare variant that has been reported in patients undergoing chemotherapy, usually for non-Hodgkin lymphomas or leukemic conditions.		07.0210
Interstitial Cell Tumor
[description not available]		02.4320
Fever of Unknown Origin
Fever in which the etiology cannot be ascertained.		02.0210
Lymphatic Diseases
Diseases of LYMPH; LYMPH NODES; or LYMPHATIC VESSELS.		02.9440
Congenital Thrombotic Thrombocytopenic Purpura
[description not available]		02.0210
Branch Retinal Artery Occlusion
[description not available]		02.0210
Purpura, Thrombotic Thrombocytopenic
An acquired, congenital, or familial disorder caused by PLATELET AGGREGATION with THROMBOSIS in terminal arterioles and capillaries. Clinical features include THROMBOCYTOPENIA; HEMOLYTIC ANEMIA; AZOTEMIA; FEVER; and thrombotic microangiopathy. The classical form also includes neurological symptoms and end-organ damage, such as RENAL FAILURE. Mutations in the ADAMTS13 PROTEIN gene have been identified in familial cases.		02.0210
Retinal Artery Occlusion
Sudden ISCHEMIA in the RETINA due to blocked blood flow through the CENTRAL RETINAL ARTERY or its branches leading to sudden complete or partial loss of vision, respectively, in the eye.		02.0210
Uveitis, Anterior
Inflammation of the anterior uvea comprising the iris, angle structures, and the ciliary body. Manifestations of this disorder include ciliary injection, exudation into the anterior chamber, iris changes, and adhesions between the iris and lens (posterior synechiae). Intraocular pressure may be increased or reduced.		02.0210
Nephritis
Inflammation of any part of the KIDNEY.		02.0210
Duodenal Reflux
[description not available]		02.0310
Hepatorenal Syndrome
Functional KIDNEY FAILURE in patients with liver disease, usually LIVER CIRRHOSIS or portal hypertension (HYPERTENSION, PORTAL), and in the absence of intrinsic renal disease or kidney abnormality. It is characterized by intense renal vasculature constriction, reduced renal blood flow, OLIGURIA, and sodium retention.		02.0210
Infections, Poxviridae
[description not available]		03.3420
Tachyarrhythmia
[description not available]		02.9410
Flushing
A transient reddening of the face that may be due to fever, certain drugs, exertion, or stress.		03.3520
Tachycardia
Abnormally rapid heartbeat, usually with a HEART RATE above 100 beats per minute for adults. Tachycardia accompanied by disturbance in the cardiac depolarization (cardiac arrhythmia) is called tachyarrhythmia.		02.9410
Mucorales Infection
[description not available]		02.0210
Mucormycosis
Infection in humans and animals caused by any fungus in the order MUCORALES (e.g., RHIZOPUS; MUCOR; CUNNINGHAMELLA; APOPHYSOMYCES; ABSIDIA; SAKSENAEA and RHIZOMUCOR) There are many clinical types associated with infection including central nervous system, lung, gastrointestinal tract, skin, orbit and paranasal sinuses. In humans, it usually occurs as an OPPORTUNISTIC INFECTION.		02.0210
Hyperplasia, Reactive Lymphoid
[description not available]		02.0210
Hepatitis, Animal
INFLAMMATION of the LIVER in non-human animals.		02.9410
Hairy Cell Leukemia
[description not available]		02.0310
Leukemia, Hairy Cell
A neoplastic disease of the lymphoreticular cells which is considered to be a rare type of chronic leukemia; it is characterized by an insidious onset, splenomegaly, anemia, granulocytopenia, thrombocytopenia, little or no lymphadenopathy, and the presence of hairy or flagellated cells in the blood and bone marrow.		02.0310
B Virus Infection
[description not available]		02.9410
Aortic Incompetence
[description not available]		02.0210
Aortic Valve Insufficiency
Pathological condition characterized by the backflow of blood from the ASCENDING AORTA back into the LEFT VENTRICLE, leading to regurgitation. It is caused by diseases of the AORTIC VALVE or its surrounding tissue (aortic root).		02.0210
Listeria Cerebritis
[description not available]		02.0210
Aspergillus Infection
[description not available]		02.4320
Fungal Lung Diseases
[description not available]		02.7230
Aspergillosis
Infections with fungi of the genus ASPERGILLUS.		02.4320
Acquired Meningocele
[description not available]		02.0310
Mediastinal Cyst
Cysts of one of the parts of the mediastinum: the superior part, containing the trachea, esophagus, thoracic duct and thymus organs; the inferior middle part, containing the pericardium; the inferior anterior part containing some lymph nodes; and the inferior posterior part, containing the thoracic duct and esophagus.		02.0310
Testicular Diseases
Pathological processes of the TESTIS.		02.0210
Chromosomal Instability
An increased tendency to acquire CHROMOSOME ABERRATIONS when various processes involved in chromosome replication, repair, or segregation are dysfunctional.		03.3520
Gastroenteritis
INFLAMMATION of any segment of the GASTROINTESTINAL TRACT from ESOPHAGUS to RECTUM. Causes of gastroenteritis are many including genetic, infection, HYPERSENSITIVITY, drug effects, and CANCER.		02.0310
Colonic Diseases
Pathological processes in the COLON region of the large intestine (INTESTINE, LARGE).		02.4320
Abnormalities, Congenital
[description not available]		02.4320
Urinary Incontinence
Involuntary loss of URINE, such as leaking of urine. It is a symptom of various underlying pathological processes. Major types of incontinence include URINARY URGE INCONTINENCE and URINARY STRESS INCONTINENCE.		02.0310
Dermatitis
Any inflammation of the skin.		03.8610
Erythermalgia
[description not available]		02.0310
Erythromelalgia
A peripheral arterial disease that is characterized by the triad of ERYTHEMA, burning PAIN, and increased SKIN TEMPERATURE of the extremities (or red, painful extremities). Erythromelalgia may be classified as primary or idiopathic, familial or non-familial. Secondary erythromelalgia is associated with other diseases, the most common being MYELOPROLIFERATIVE DISORDERS.		02.0310
Arthropathies
[description not available]		05.0850
Joint Diseases
Diseases involving the JOINTS.		05.0850
Fibromuscular Dysplasia
An idiopathic, segmental, nonatheromatous disease of the musculature of arterial walls, leading to STENOSIS of small and medium-sized arteries. There is true proliferation of SMOOTH MUSCLE CELLS and fibrous tissue. Fibromuscular dysplasia lesions are smooth stenosis and occur most often in the renal and carotid arteries. They may also occur in other peripheral arteries of the extremity.		02.0310
Arthritis, Degenerative
[description not available]		02.0310
Osteoarthritis
A progressive, degenerative joint disease, the most common form of arthritis, especially in older persons. The disease is thought to result not from the aging process but from biochemical changes and biomechanical stresses affecting articular cartilage. In the foreign literature it is often called osteoarthrosis deformans.		02.0310
Chromosomes, Ring
[description not available]		03.6430
Brachial Plexopathy
[description not available]		02.0310
Peripheral Nerve Neoplasms
[description not available]		02.4420
Peripheral Nervous System Neoplasms
Neoplasms which arise from peripheral nerve tissue. This includes NEUROFIBROMAS; SCHWANNOMAS; GRANULAR CELL TUMORS; and malignant peripheral NERVE SHEATH NEOPLASMS. (From DeVita Jr et al., Cancer: Principles and Practice of Oncology, 5th ed, pp1750-1)		02.4420
Brachial Plexus Neuropathies
Diseases of the cervical (and first thoracic) roots, nerve trunks, cords, and peripheral nerve components of the BRACHIAL PLEXUS. Clinical manifestations include regional pain, PARESTHESIA; MUSCLE WEAKNESS, and decreased sensation (HYPESTHESIA) in the upper extremity. These disorders may be associated with trauma (including BIRTH INJURIES); THORACIC OUTLET SYNDROME; NEOPLASMS; NEURITIS; RADIOTHERAPY; and other conditions. (From Adams et al., Principles of Neurology, 6th ed, pp1351-2)		02.0310
Graft Occlusion, Vascular
Obstruction of flow in biological or prosthetic vascular grafts.		02.9410
Neoplasms, Skull
[description not available]		02.0310
Curling Ulcer
Acute stress DUODENAL ULCER, usually observed in patients with extensive third-degree burns.		02.0310
Duodenal Ulcer
A PEPTIC ULCER located in the DUODENUM.		02.0310
Entomophthoramycosis
[description not available]		02.0310
Zygomycosis
Infection in humans and animals caused by fungi in the class Zygomycetes. It includes MUCORMYCOSIS and entomophthoramycosis. The latter is a tropical infection of subcutaneous tissue or paranasal sinuses caused by fungi in the order Entomophthorales. Phycomycosis, closely related to zygomycosis, describes infection with members of Phycomycetes, an obsolete classification.		02.0310
Short Bowel Syndrome
A malabsorption syndrome resulting from extensive operative resection of the SMALL INTESTINE, the absorptive region of the GASTROINTESTINAL TRACT.		03.4111
Sweat Gland Diseases
Diseases of the SWEAT GLANDS.		02.0310
Nail Fungus
[description not available]		02.0310
Onychomycosis
A fungal infection of the nail, usually caused by DERMATOPHYTES; YEASTS; or nondermatophyte MOLDS.		02.0310
Adenomatoid Tumor
A small, circumscribed, benign tumor of the genital tract, composed of small glandlike spaces lined by flattened or cuboidal mesothelium-like cells. (From Dorland, 27th ed)		02.0310
Human T-lymphotropic Virus 1 Infection
[description not available]		02.0310
HTLV-I Infections
Diseases caused by HUMAN T-LYMPHOTROPIC VIRUS 1.		02.0310
Basophilic Leukemia, Acute
[description not available]		02.0310
Leukemia, Basophilic, Acute
A rare acute myeloid leukemia in which the primary differentiation is to BASOPHILS. It is characterized by an extreme increase of immature basophilic granulated cells in the bone marrow and blood. Mature basophils are usually sparse.		02.0310
Sarcoma 180
An experimental sarcoma of mice.		02.0310
Dermatomyositis, Adult Type
[description not available]		02.0310
Dermatomyositis
A subacute or chronic inflammatory disease of muscle and skin, marked by proximal muscle weakness and a characteristic skin rash. The illness occurs with approximately equal frequency in children and adults. The skin lesions usually take the form of a purplish rash (or less often an exfoliative dermatitis) involving the nose, cheeks, forehead, upper trunk, and arms. The disease is associated with a complement mediated intramuscular microangiopathy, leading to loss of capillaries, muscle ischemia, muscle-fiber necrosis, and perifascicular atrophy. The childhood form of this disease tends to evolve into a systemic vasculitis. Dermatomyositis may occur in association with malignant neoplasms. (From Adams et al., Principles of Neurology, 6th ed, pp1405-6)		07.0310
Pemphigoid
[description not available]		02.9510
Pemphigoid, Bullous
A chronic and relatively benign subepidermal blistering disease usually of the elderly and without histopathologic acantholysis.		02.9510
Microglossia
[description not available]		02.0310
Granulomatosis, Lymphomatoid
[description not available]		02.4420
Infections, Listeria
[description not available]		02.0310
Catastrophic Illness
An acute or prolonged illness usually considered to be life-threatening or with the threat of serious residual disability. Treatment may be radical and is frequently costly.		02.0310
Water-Electrolyte Imbalance
Disturbances in the body's WATER-ELECTROLYTE BALANCE.		02.0310
Epulides
[description not available]		02.0310
Gingival Diseases
Diseases involving the GINGIVA.		02.0310
Tooth Diseases
Diseases involving the TEETH.		02.0310
Rheumatism
[description not available]		03.3520
Rheumatic Diseases
Disorders of connective tissue, especially the joints and related structures, characterized by inflammation, degeneration, or metabolic derangement.		08.3520
Cocaine Abuse
[description not available]		02.0310
Cocaine-Related Disorders
Disorders related or resulting from use of cocaine.		02.0310
Cancer of Jaw
[description not available]		02.9510
Babesia Infection
[description not available]		02.0310
Bladder, Overactive
[description not available]		02.9510
Urinary Bladder, Overactive
Symptom of overactive detrusor muscle of the URINARY BLADDER that contracts with abnormally high frequency and urgency. Overactive bladder is characterized by the frequent feeling of needing to urinate during the day, during the night, or both. URINARY INCONTINENCE may or may not be present.		02.9510
Endotoxin Shock
[description not available]		02.0310
Shock, Septic
Sepsis associated with HYPOTENSION or hypoperfusion despite adequate fluid resuscitation. Perfusion abnormalities may include but are not limited to LACTIC ACIDOSIS; OLIGURIA; or acute alteration in mental status.		02.0310
Jaw Diseases
Diseases involving the JAW.		02.9510
Neoplasms, Plasma Cell
Neoplasms associated with a proliferation of a single clone of PLASMA CELLS and characterized by the secretion of PARAPROTEINS.		02.9510
Rida
[description not available]		02.0310
Candida Infection
[description not available]		02.0410
Candidiasis
Infection with a fungus of the genus CANDIDA. It is usually a superficial infection of the moist areas of the body and is generally caused by CANDIDA ALBICANS. (Dorland, 27th ed)		02.0410
Elevated ICP (Intracranial Pressure)
[description not available]		02.0310
Intracranial Hypertension
Increased pressure within the cranial vault. This may result from several conditions, including HYDROCEPHALUS; BRAIN EDEMA; intracranial masses; severe systemic HYPERTENSION; PSEUDOTUMOR CEREBRI; and other disorders.		02.0310
Bile Duct Obstruction, Intrahepatic
[description not available]		02.0310
Cholestasis, Intrahepatic
Impairment of bile flow due to injury to the HEPATOCYTES; BILE CANALICULI; or the intrahepatic bile ducts (BILE DUCTS, INTRAHEPATIC).		02.0310
Cystadenoma, Papillary
A benign neoplasm of the ovary.		02.0310
Choroid Neoplasms
Tumors of the choroid; most common intraocular tumors are malignant melanomas of the choroid. These usually occur after puberty and increase in incidence with advancing age. Most malignant melanomas of the uveal tract develop from benign melanomas (nevi).		02.0410
Cleft Spine
[description not available]		02.0410
Keratitis, Ulcerative
[description not available]		03.4311
Corneal Ulcer
Loss of epithelial tissue from the surface of the cornea due to progressive erosion and necrosis of the tissue; usually caused by bacterial, fungal, or viral infection.		03.4311
Angioneurotic Edema
[description not available]		02.0410
Angioedema
Swelling involving the deep DERMIS, subcutaneous, or submucosal tissues, representing localized EDEMA. Angioedema often occurs in the face, lips, tongue, and larynx.		02.0410
Craniofacial Abnormalities
Congenital structural deformities, malformations, or other abnormalities of the cranium and facial bones.		02.0410
Carditis
[description not available]		07.0410
Myocarditis
Inflammatory processes of the muscular walls of the heart (MYOCARDIUM) which result in injury to the cardiac muscle cells (MYOCYTES, CARDIAC). Manifestations range from subclinical to sudden death (DEATH, SUDDEN). Myocarditis in association with cardiac dysfunction is classified as inflammatory CARDIOMYOPATHY usually caused by INFECTION, autoimmune diseases, or responses to toxic substances. Myocarditis is also a common cause of DILATED CARDIOMYOPATHY and other cardiomyopathies.		07.0410
Carcinoma, Colloid
[description not available]		02.0410
Adenocarcinoma, Mucinous
An adenocarcinoma producing mucin in significant amounts. (From Dorland, 27th ed)		02.0410
Autosomal Hemophilia A
[description not available]		0210
Hemophilia A
The classic hemophilia resulting from a deficiency of factor VIII. It is an inherited disorder of blood coagulation characterized by a permanent tendency to hemorrhage.		0210
Anoxia, Brain
[description not available]		0210
Nerve Degeneration
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.		0210
Hypercapnia
A clinical manifestation of abnormal increase in the amount of carbon dioxide in arterial blood.		0210
Tauopathies
Neurodegenerative disorders involving deposition of abnormal tau protein isoforms (TAU PROTEINS) in neurons and glial cells in the brain. Pathological aggregations of tau proteins are associated with mutation of the tau gene on chromosome 17 in patients with ALZHEIMER DISEASE; DEMENTIA; PARKINSONIAN DISORDERS; progressive supranuclear palsy (SUPRANUCLEAR PALSY, PROGRESSIVE); and corticobasal degeneration.		0210
Splenic Rupture
Rupture of the SPLEEN due to trauma or disease.		02.0110
4 Hydroxyphenylpyruvate Dioxygenase Deficiency Disease
[description not available]		02.0110
Tyrosinemias
A group of disorders which have in common elevations of tyrosine in the blood and urine secondary to an enzyme deficiency. Type I tyrosinemia features episodic weakness, self-mutilation, hepatic necrosis, renal tubular injury, and seizures and is caused by a deficiency of the enzyme fumarylacetoacetase. Type II tyrosinemia features INTELLECTUAL DISABILITY, painful corneal ulcers, and keratoses of the palms and plantar surfaces and is caused by a deficiency of the enzyme TYROSINE TRANSAMINASE. Type III tyrosinemia features INTELLECTUAL DISABILITY and is caused by a deficiency of the enzyme 4-HYDROXYPHENYLPYRUVATE DIOXYGENASE. (Menkes, Textbook of Child Neurology, 5th ed, pp42-3)		02.0110