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sulfasalazine

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Description

Sulfasalazine is a drug used to treat inflammatory bowel disease (IBD), specifically ulcerative colitis and Crohn's disease. It is a prodrug, meaning it is converted into its active form in the body. The active form of sulfasalazine, sulfapyridine, is an anti-inflammatory agent that works by inhibiting the production of inflammatory mediators. The other component of sulfasalazine, 5-aminosalicylic acid (5-ASA), is also an anti-inflammatory agent that has been shown to be effective in treating IBD. Sulfasalazine is synthesized by combining sulfapyridine with 5-ASA. It is administered orally, typically as tablets or capsules. The importance of sulfasalazine lies in its efficacy in treating IBD. Sulfasalazine is studied extensively to understand its mechanisms of action, improve its efficacy and tolerability, and identify potential new drug targets for IBD. '

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) [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

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. [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 CID5339
CHEMBL ID242373
CHEMBL ID421
CHEMBL ID100848
CHEMBL ID1206016
CHEBI ID9334
CHEBI ID94500
SCHEMBL ID18490
SCHEMBL ID4515
SCHEMBL ID4514
SCHEMBL ID1079598
SCHEMBL ID10289061
SCHEMBL ID1229516
MeSH IDM0019365

Synonyms (264)

Synonym
BIDD:GT0161
AC-20497
HMS3393J21
AB00052101-06
BRD-K10670311-001-06-4
salazopyrin
azopyrin
azulfidine
5-[p-(2-pyridylsulfamoyl)phenylazo]salicylic acid
accucol
salazopyridin
nsc-203730
salazopiridazin
salisulf
sulcolon
colo-pleon
asulfidine
5-[[p-(2-pyridylsulfamoyl)phenyl]azo]salicylic acid
reupirin
azopyrine
s.a.s. 500
4-(pyridyl-2-amidosulfonyl)-3'-carboxy-4'-hydroxyazobenzene
w-t sasp oral
5-[p-(2-pyridylsulfamyl)phenylazo]salicylic acid
salazosulfapyridin
salicylic acid, 5-[[p-(2-pyridylsulfamoyl)phenyl]azo]-
benzosulfa
sulfasalazin
nsc203730
benzoic acid, 2-hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]-
wln: t6nj bswmr dnunr dq cvq
s.a.s.-500
DIVK1C_000860
KBIO1_000860
azulfidine en
2-hydroxy-5-[(e)-{4-[(pyridin-2-ylamino)sulfonyl]phenyl}diazenyl]benzoic acid
sulphasalazine, n-
einecs 209-974-3
sasp
ccris 4713
brn 0356241
sulfazalazine
nsc 203730
salazo-sulfapyridinum
salazosulfapiridina [inn-spanish]
azulfidine en-tabs
azosulfidin
sulfasalazina [inn-spanish]
sas-500
salicylic acid, 5-((p-(2-pyridylsulfamoyl)phenyl)azo)-
si-88
hsdb 3395
salazosulfapyridinum [inn-latin]
nsc 667219
2-hydroxy-5-[[4-[(2-pyridinylamino)sulfonyl]phenyl]azo]benzoic acid
sulfasalazinum [inn-latin]
nsc-667219
SPECTRUM_000998
PRESTWICK_848
cas-599-79-1
NCGC00016518-01
PRESTWICK2_000520
BSPBIO_002888
CMAP_000018
SMP2_000059
BSPBIO_000479
BPBIO1_000527
NCGC00090903-01
MLS001424109
sulfasalazine
salicylazosulfapyridine
C07316
salazosulfapyridine
599-79-1
2-hydroxy-5-[(e)-[4-(2-pyridylsulfamoyl)phenyl]azo]benzoic acid
sulphasalazine
benzoic acid, 2-hydroxy-5-((4-((2-pyridinylamino)sulfonyl)phenyl)azo)-
nsc667219
2-hydroxy-(5-([4-(2-pyridinylamino)sulfonyl]phenyl)azo)benzoic acid
SAS ,
MLS000759399
smr000059146
DB00795
13GS ,
5-(p-(2-pyridylsulfamyl)phenylazo)salicylic acid
2-hydroxy-5-[4-(pyridin-2-ylsulfamoyl)-phenylazo]-benzoic acid
5-(4-(2-pyridylsulfamoyl)phenylazo)-2-hydroxybenzoic acid
2-hydroxy-5-((4-((2-pyridinylamino)sulfonyl)phenyl)azo)benzoic acid
5-((p-(2-pyridylsulfamoyl)phenyl)azo)salicylic acid
azulfidine (tn)
sulfasalazine (usp/inn)
salazosulfapyridine (jp17)
D00448
PRESTWICK3_000520
5-[4-(2-pyridylsulfamoyl)phenylazo]salicylic acid
NCGC00090903-03
ssz
NCGC00090903-02
KBIO2_006614
KBIO3_002794
KBIO2_007450
KBIO2_004046
KBIOSS_001478
KBIOGR_002314
KBIO2_002314
KBIOGR_000753
KBIO2_001478
KBIOSS_002316
KBIO2_004882
KBIO3_002108
SPBIO_001032
SPECTRUM3_001364
NINDS_000860
SPECTRUM2_001216
SPBIO_002400
SPECTRUM4_000347
PRESTWICK1_000520
PRESTWICK0_000520
SPECTRUM1500552
SPECTRUM5_001443
IDI1_000860
NCGC00090903-04
NCGC00090903-05
HMS2051J21
HMS2092K07
HMS2090P13
S0580
CHEMBL242373
sulfasalazina
sulfasalazinum
CHEBI:9334 ,
salazosulfapiridina
2-hydroxy-5-{[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl}benzoic acid
(3z)-6-oxo-3-[[4-(pyridin-2-ylsulfamoyl)phenyl]hydrazinylidene]cyclohexa-1,4-diene-1-carboxylic acid
salazosulfapyridinum
CHEMBL421
sulfasalazopyridine
HMS502K22
bdbm50097125
4-(pyridyl-2-amidosulfonyl)-3''-carboxy-4''-hydroxyazobenzene
HMS1921C05
HMS1569H21
AKOS002311709
A832559
5-(p-(2-pyridylsulfamoyl)phenylazo)salicylic acid
NCGC00186644-01
NCGC00090903-07
NCGC00090903-06
HMS2096H21
tox21_201239
NCGC00254313-01
tox21_300541
NCGC00258791-01
CHEMBL100848
nsc-757330
nsc757330
pharmakon1600-01500552
tox21_111037
dtxsid0021256 ,
dtxcid401256
HMS2232H07
CCG-39145
CCG-100987
unii-3xc8guz6cb
sulfasalazine [usan:usp:inn:ban]
3xc8guz6cb ,
5-22-08-00433 (beilstein handbook reference)
s.a.s.
FT-0603483
NCGC00090903-09
sulfasalazine [hsdb]
salazosulfapyridine [jan]
sulfasalazine [mi]
2-hydroxy-5-((4-((2-pyridinylamino)sulfonyl)phenyl)azo)benzoic acid [who-ip]
sulfasalazine [vandf]
sulfasalazine [usp-rs]
sulfasalazine [inn]
sulfasalazine [ep monograph]
sulfasalazine [orange book]
sulfasalazine [iarc]
sulfasalazine [usp monograph]
benzoic acid, 2-hydroxy-5-(2-(4-((2-pyridinylamino)sulfonyl)phenyl)diazenyl)-
sulfasalazinum [who-ip latin]
sulfasalazine [mart.]
sulfasalazine [usan]
sulfasalazine [who-dd]
sulfasalazine [who-ip]
EPITOPE ID:122672
S1576
2-hydroxy-5-[[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl]benzoic acid
HMS3370D16
gtpl4840
NCEXYHBECQHGNR-UHFFFAOYSA-N
AB00052101-04
DL-510
HY-14655
smr004703430
MLS006011702
NC00237
SCHEMBL18490
SCHEMBL4515
SCHEMBL4514
NCGC00090903-11
tox21_111037_1
HS-0062
SCHEMBL1079598
CHEMBL1206016
SCHEMBL10289061
SCHEMBL1229516
F2173-1125
737754-28-8
(e)-2-hydroxy-5-((4-(n-(pyridin-2-yl)sulfamoyl)phenyl)diazenyl)benzoic acid
sulphasalazine, antibiotic for culture media use only
Q-201769
5-[[4-(2-pyridylsulfamoyl)phenyl]azo]salicylic acid
NCEXYHBECQHGNR-QZQOTICOSA-N
2-hydroxy-5-((4-[(2-pyridinylamino)sulfonyl]phenyl)diazenyl)benzoic acid #
2-hydroxy-5-((4-(n-pyridin-2-ylsulfamoyl)phenyl)diazenyl)benzoic acid
AKOS025116975
AB00052101_07
AB00052101_08
bdbm50103596
mfcd00057363
AKOS026749974
SR-05000001721-3
sr-05000001721
sulfasalazine, united states pharmacopeia (usp) reference standard
CHEBI:94500
HMS3655G07
6-oxo-3-(2-[4-(n-pyridin-2-ylsulfamoyl)phenyl]hydrazono)cyclohexa-1,4-dienecarboxylic acid
6-oxo-3-((4-(pyridin-2-ylsulfamoyl)phenyl) hydrazinylidene]cyclohexa-1,4-diene-1-carboxylic acid
OQANPHBRHBJGNZ-UHFFFAOYSA-N
SR-05000001721-1
SR-05000001721-2
sulfasalazine, european pharmacopoeia (ep) reference standard
sulfasalazine, analytical standard, >=98% (hplc)
SBI-0051526.P003
2-hydroxy-5-(2-{4-[(pyridin-2-yl)sulfamoyl]phenyl}diazen-1-yl)benzoic acid
HMS3713H21
SW196979-4
(e)-2-hydroxy-5-((4-(n-pyridin-2-ylsulfamoyl)phenyl)diazenyl)benzoic acid
2-hydroxy-5-{(e)-[4-(pyridin-2-ylsulfamoyl)phenyl]diazenyl}benzoic acid
NCGC00090903-08
FT-0674746
Q27166356
6-oxo-3-[[4-(2-pyridinylsulfamoyl)phenyl]hydrazinylidene]-1-cyclohexa-1,4-dienecarboxylic acid
sulfasalazine (azulfidine)
2-hydroxy-5-((4-(n-(pyridin-2-yl)sulfamoyl)phenyl)diazenyl)benzoic acid
iwata
OQANPHBRHBJGNZ-BKUYFWCQSA-N
BCP13311
Q63398427
Q420035
BRD-K10670311-001-08-0
HMS3871J13
HMS3884E21
5-{4-[(2-pyridylideneamino)sulfonyl]phenyldiazenyl}salicylic acid
SY052318
AKOS037515748
H10652
2-hydroxy-5-[(e)-2-{4-[(pyridin-2-yl)sulfamoyl]phenyl}diazen-1-yl]benzoic acid
EN300-119546
Z1521554012
PD087097

Research Excerpts

Overview

Sulfasalazine (SAS) is an FDA-approved drug for the treatment of Crohn's disease, rheumatoid arthritis, and inflammatory bowel disease. It is a repurposed antitumor drug which inhibits the proliferation and survival of cancer cells by inhibiting the xCT cellular antioxidant system.

ExcerptReferenceRelevance
"Sulfasalazine (SAS) is an FDA-approved drug for the treatment of Crohn's disease, rheumatoid arthritis, and inflammatory bowel disease."( Iron plays a role in sulfasalazine-induced ferroptosis with autophagic flux blockage in K7M2 osteosarcoma cells.
Liu, J; Lou, C; Lv, H; Shang, P; Wang, Y; Zhen, C, 2022
)
1.76
"Sulfasalazine is a safe option in chronic therapy of rheumatoid arthritis and spondyloarthritis. "( Adverse reaction profile of sulfasalazine and its persistence in chronic therapy of rheumatoid arthritis and spondyloarthritis: A multicentric observational study.
David, R; Jayachandran, M; Koshy, V; Marwaha, V; Mithun, CB; Nair, AS; Padmanabhan, DS; Palatty, PL; Santhakumari, V; Singh, SK; Singhal, A; Suman, SK; Surendran, S; Tiwari, A; Yadav, P, 2022
)
2.46
"Sulfasalazine (SAS) is a repurposed antitumor drug which inhibits the proliferation and survival of cancer cells by inhibiting the xCT cellular antioxidant system. "( Inhibition of lung adenocarcinoma by combinations of sulfasalazine (SAS) and disulfiram-copper (DSF-Cu) in cell line models and mice.
Bagherpoor, AJ; Kassie, F; Luo, X; Seelig, D; Shameem, M, 2023
)
2.6
"Sulfasalazine (SAS) is a drug prescribed for pregnant and breastfeeding women with chronic inflammatory bowel diseases. "( Sulfasalazine exposure during pregnancy and lactation: reproductive outcomes in male rat offspring.
Aquino, ABO; Bilibio, JO; Borges, LI; Erthal, RP; Fernandes, GSA; Forcato, S; Gerardin, DCC; Guarnier, FA; Lens, HHM; Thomé, MLFL, 2023
)
3.8
"Sulfasalazine is a recognized therapy for inflammatory bowel disease and is of paramount importance for maintaining intestinal barrier homeostasis. "( Sulfasalazine maintains blood-brain barrier integrity and relieves lipopolysaccharide-induced inflammation in hCMEC/D3 cells.
Cao, Y; Chang, S, 2021
)
3.51
"Sulfasalazine is an anti-inflammatory agent commonly used in the treatment of autoimmune conditions such as inflammatory bowel disease and rheumatoid arthritis. "( Sulfasalazine-Induced Crystalluria Causing Severe Acute Kidney Injury.
Durando, M; Kim, JS; Tiu, H, 2017
)
3.34
"Sulfasalazine is a commonly used drug for the treatment of rheumatoid arthritis and inflammatory bowel disease. "( Sulfasalazine induces mitochondrial dysfunction and renal injury.
Abdoli, N; Asadi, B; Azarpira, N; Heidari, R; Khodaei, F; Mohammadzadeh, R; Najibi, A; Niknahad, H; Ommati, MM; Rasti, M; Saeedi, A; Shirazi Yeganeh, B; Taheri, V; Zarei, M, 2017
)
3.34
"Sulfasalazine is an inhibitor of xCT that is known to increase cellular oxidative stress, giving it anti-tumor potential."( Sulfasalazine, an inhibitor of the cystine-glutamate antiporter, reduces DNA damage repair and enhances radiosensitivity in murine B16F10 melanoma.
Kanai, E; Maruo, T; Nagane, M; Shibata, Y; Shimizu, T; Yamashita, T; Yoshioka, C, 2018
)
2.64
"Sulfasalazine (SSZ) is a well-known anti-inflammatory drug and also an inhibitor of the cystine-glutamate antiporter that is known to reduce intracellular glutathione (GSH) level and increase cellular oxidative stress, indicating its anti-tumor potential. "( Roles of intracellular and extracellular ROS formation in apoptosis induced by cold atmospheric helium plasma and X-irradiation in the presence of sulfasalazine.
Fujiwara, K; Imaue, S; Jawaid, P; Kondo, T; Mitsuhashi, Y; Moniruzzaman, R; Noguchi, K; Noguchi, M; Ogawa, R; Rehman, MU; Saitoh, JI; Tomihara, K; Zhao, QL, 2018
)
2.12
"Sulfasalazine is an anti-inflammatory and antioxidant medication used to treat autoimmune disease."( Sulfasalazine reduces placental secretion of antiangiogenic factors, up-regulates the secretion of placental growth factor and rescues endothelial dysfunction.
Brownfoot, FC; Cannon, P; Hannan, NJ; Hastie, R; Kaitu'u-Lino, TJ; Nguyen, V; Parry, LJ; Senadheera, S; Tong, S; Tuohey, L, 2019
)
2.68
"Sulfasalazine (SAS) is an US Food and Drug Administration (FDA)-approved drug for the treatment of Crohn disease that has been shown to inhibit the cystine/glutamate antiporter system xc- (SXC) and decrease tumor-associated seizures."( Sulfasalazine decreases mouse cortical hyperexcitability.
Alcoreza, O; Bouslog, A; Campbell, SL; Savoia, A; Sontheimer, H; Tewari, BP, 2019
)
2.68
"Sulfasalazine is a highly effective treatment for patients with antihistamine resistant CIU. "( Efficacy and safety of sulfasalazine in patients with chronic idiopathic urticaria.
Orden, RA; Saini, SS; Timble, H, 2014
)
2.16
"Sulfasalazine (SSZ) is an anti-inflammatory drug that has been used to treat inflammatory bowel disease and rheumatoid arthritis for decades. "( Sulfasalazine induces autophagic cell death in oral cancer cells via Akt and ERK pathways.
Han, HY; Jeong, SH; Kim, H; Lim, DS; Ryu, MH, 2014
)
3.29
"Sulfasalazine is a disease-modifying antirheumatic drug used in the treatment of AS."( Sulfasalazine for ankylosing spondylitis.
Chen, J; Lin, S; Liu, C, 2014
)
2.57
"Sulfasalazine (SAS) is a classic inhibitor of NF-κB."( p62 participates in the inhibition of NF-κB signaling and apoptosis induced by sulfasalazine in human glioma U251 cells.
Kang, J; Li, X; Li, Y; Liu, F; Su, J; Sun, L; Xia, M; Xu, Y, 2015
)
1.37
"Sulfasalazine (SSZ) is an anti-inflammatory drug that has been demonstrated to induce apoptosis and tumor regression through inhibition of plasma membrane cystine transporter xc(-). "( Xc- inhibitor sulfasalazine sensitizes colorectal cancer to cisplatin by a GSH-dependent mechanism.
Chen, G; Hu, Y; Huang, P; Lu, WH; Ma, MZ; Song, M; Wang, P; Wen, S; Xu, RH; Yang, J; Zhu, CF, 2015
)
2.22
"Sulfasalazine (SSZ) is a system XC- inhibitor; SSZ was applied intra-articularly to study the function of system XC- in the development of OA in rats subjected to anterior cruciate ligament transection and medial meniscectomy (ACLT + MMx)."( Sulfasalazine attenuates ACL transection and medial menisectomy-induced cartilage destruction by inhibition of cystine/glutamate antiporter.
Liu, CC; Tsai, RY; Tsai, WY; Wong, CS; Wu, JL, 2016
)
2.6
"Sulfasalazine is an anti-inflammatory and immune-modulating drug that is used in rheumatology and inflammatory bowel disease."( Promotion of Remyelination by Sulfasalazine in a Transgenic Zebrafish Model of Demyelination.
Chang, KY; Cho, SC; Ha, YW; Kim, S; Lee, DW; Lee, YI; Na, JE; Park, HC; Park, SC; Rhyu, IJ, 2015
)
1.43
"Sulfasalazine (SSA) is a common medication used for treatment of patients with AS."( Sulfasalazine Treatment Suppresses the Formation of HLA-B27 Heavy Chain Homodimer in Patients with Ankylosing Spondylitis.
Huang, HB; Huang, HL; Huang, KY; Lai, NS; Liu, SQ; Lu, MC; Yu, HC, 2015
)
2.58
"Sulfasalazine (SSZ) is an inhibitor of xCT and was shown to suppress the survival of CD44v-positive stem-like cancer cells both in vitro and in vivo."( Dose-escalation study for the targeting of CD44v
Doi, T; Einaga, Y; Fukutani, M; Hasegawa, H; Hironaka, S; Imamura, CK; Ishii, Y; Kuwata, T; Nagano, O; Nakajima, TE; Nomura, S; Ohtsu, A; Ozeki, T; Sato, A; Saya, H; Shitara, K; Takahashi, S; Tsuchihashi, K, 2017
)
1.18
"Sulfasalazine (SASP) is a drug commonly used in the treatment of inflammatory bowel diseases (IBD). "( Lipid peroxidation and antioxidant status in kidney and liver of rats treated with sulfasalazine.
Albina, ML; Alonso, V; Bellés, M; Domingo, JL; Linares, V; Sánchez, DJ; Sirvent, JJ, 2009
)
2.02
"Sulfasalazine (SAZ) is a widely used drug in inflammatory bowel disease patients but its mechanism of action is incompletely understood. "( Genomic analysis of sulfasalazine effect in experimental colitis is consistent primarily with the modulation of NF-kappaB but not PPAR-gamma signaling.
González, R; López-Posadas, R; Martínez-Augustin, O; Sánchez de Medina, F; Suárez, MD; Zarzuelo, A, 2009
)
2.12
"Sulfasalazine is a combination of sulfapyridine and 5-aminosalicylic acid and is used as a first-line treatment in inflammatory bowel disease."( Reversal of refractory sulfasalazine-related renal failure after treatment with corticosteroids.
Alivanis, P; Aperis, G; Arvanitis, A; Karvouniaris, N; Lambrianou, F; Paliouras, C; Zervos, A, 2010
)
2.11
"Sulfasalazine is a prodrug composed by a molecule of 5-aminosalicylic acid (5-ASA) and sulfapyridine (SP), linked by an azo bond, which has been shown to be effective in the therapy of inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease, as well as of rheumatic diseases, such as rheumatoid arthritis and ankylosing spondylitis. "( Scavenging of reactive oxygen and nitrogen species by the prodrug sulfasalazine and its metabolites 5-aminosalicylic acid and sulfapyridine.
Couto, D; Fernandes, E; Freitas, M; Gomes, A; Lima, JL; Ribeiro, D, 2010
)
2.04
"Sulfasalazine (SASP) is a drug commonly used in the treatment of inflammatory bowel diseases (IBD) such as ulcerative colitis and Crohn's disease (CD) and rheumatoid arthritis (RA). "( Oxidative stress as a mechanism underlying sulfasalazine-induced toxicity.
Alonso, V; Domingo, JL; Linares, V, 2011
)
2.07
"Sulfasalazine (SLZ) is a synthetic nonsteroidal anti-inflammatory drug used mainly for the treatment of an inflammatory bowel and other diseases. "( Controlled release of sulfasalazine release from "smart" pectin gel microspheres under physiological simulated fluids.
Castro, GR; Costas, L; López, AG; Mechetti, M; Pera, LM, 2012
)
2.14
"Sulfasalazine (SSZ) is a drug used in inflammatory bowel disease, whose precise mechanism of action remains to be clarified. "( Dissociated ROS production and ceramide generation in sulfasalazine-induced cell death in Raw 264.7 cells.
Assi, K; Gómez-Muñoz, A; Huang, S; O'Brien, L; Salh, B; Steinbrecher, U, 2002
)
2.01
"Sulfasalazine (SASP) is a novel, potent inhibitor of cellular cystine uptake mediated by the x(c)- cystine/glutamate antiporter. "( In vitro studies on the lymphoma growth-inhibitory activity of sulfasalazine.
Gout, PW; Robertson, MC; Simms, CR, 2003
)
2
"Sulfasalazine is a successful therapeutic option for cutaneous LP, constituting an alternative to corticosteroids and retinoids."( Successful treatment of lichen planus with sulfasalazine in 20 patients.
Bauzá, A; España, A; Gil, P; Lloret, P; Vázquez Doval, FJ, 2005
)
2.03
"Sulfasalazine (SFZ) is a synthetic anti-inflammatory comprising an aminosalicylate, 5-amino salicylic acid (5-ASA), linked to an antibiotic, sulfapyridine (SPY)."( Novel sulfasalazine analogues with enhanced NF-kB inhibitory and apoptosis promoting activity.
Ganesan, A; Habens, F; Mann, DA; Oakley, F; Packham, G; Srinivasan, N, 2005
)
1.53
"Sulfasalazine is a potent inhibitor of GCDCA induced hepatocyte apoptosis in vitro and in the intact liver."( Sulfasalazine reduces bile acid induced apoptosis in human hepatoma cells and perfused rat livers.
Bauchmuller, K; Bernt, C; Beuers, U; Fickert, P; Fuchsbichler, A; Rust, C; Vennegeerts, T, 2006
)
3.22
"Sulfasalazine is an antibiotic used in the treatment of inflammatory bowel diseases. "( Immunochemical method for sulfasalazine determination in human plasma.
Gallego-Iglesias, E; Maquieira, A; Pastor-Navarro, N; Puchades, R, 2007
)
2.08
"Sulfasalazine is a well established disease-modifying anti-rheumatic drug commonly used in the treatment of rheumatic disorders and inflammatory bowel disease. "( Sulfasalazine-induced immune thrombocytopenia.
Biasi, D; Cantarini, L; Fioravanti, A; Galeazzi, M; Tinazzi, I, 2007
)
3.23
"Sulfasalazine is a potent antiinflammatory drug used in the treatment of ulcerative colitis. "( Inhibition of platelet thromboxane synthetase by sulfasalazine.
Lobos, E; Stenson, WF, 1983
)
1.96
"Sulfasalazine is a two-part molecule that depends on bacterial cleavage in the colon to deliver locally acting 5-aminosalicylate, whose mechanism of action may relate to inhibition of prostaglandin synthesis."( Drug therapy of inflammatory bowel disease.
Peppercorn, MA; Sack, DM,
)
0.85
"Sulfasalazine is an effective treatment for rheumatoid arthritis (RA), producing improvements in disease parameters similar to those seen with penicillamine, hydroxychloroquine or oral or parenteral gold in comparative clinical trials."( Sulfasalazine. A review of its pharmacological properties and therapeutic efficacy in the treatment of rheumatoid arthritis.
Faulds, D; Noble, S; Rains, CP, 1995
)
2.46
"Sulfasalazine is an efficient treatment for rheumatoid arthritis (RA), but its mode of action is not known. "( Variation in the serum IgA concentration and the production of IgA in vitro in rheumatoid arthritis treated by sulfasalazine.
Anaya, JM; Bologna, C; Jorgensen, C; Reme, T; Sany, J, 1993
)
1.94
"Sulfasalazine is an effective treatment in some inflammatory diseases that exhibit mast cell (MC) hyperplasia. "( Inhibitory effects of sulfasalazine and its metabolites on histamine release and TNF-alpha production by mast cells.
Befus, AD; Bissonnette, EY; Enciso, JA, 1996
)
2.05
"Sulfasalazine is a prodrug which is enzymatically split in the bowel to form sulfapyridine (the principal active metabolite) and 5-aminosalicylic acid."( Disease-modifying antirheumatic drugs. Potential effects in older patients.
Furst, DE; Gardner, G, 1995
)
1.01
"Sulfasalazine is an effective agent for chronic discoid lupus erythematosus (CDLE) but the response to treatment is considerably variable between patients and is also unpredictable. "( NAT2 genotyping and efficacy of sulfasalazine in patients with chronic discoid lupus erythematosus.
Broly, F; Delaporte, E; Lo-Guidice, JM; Marez, D; Piette, F; Sabbagh, N, 1997
)
2.02
"Sulfasalazine (SSZ) is an anti-rheumatic drug that has been used to treat chronic arthritis. "( High toxicity of sulfasalazine in adult-onset Still's disease.
Bae, SC; Jun, JB; Jung, JH; Jung, SS; Kim, SY; Kim, TH; Lee, IH; Yoo, DH,
)
1.91
"Sulfasalazine (SSZ) is a commonly used drug in the treatment of inflammatory diseases such as rheumatoid arthritis and Crohn's disease. "( The antiinflammatory drug sulfasalazine inhibits tumor necrosis factor alpha expression in macrophages by inducing apoptosis.
Ganga, A; Rodenburg, RJ; van de Putte, LB; van Lent, PL; van Venrooij, WJ, 2000
)
2.05
"Sulfasalazine is an inhibitor of their synthesis in the mucosa."( Sulfasalazine decreases acute gastrointestinal complications due to pelvic radiotherapy.
Dursun, A; Egehan, I; Kilic, D; Ozenirler, S,
)
2.3
"Sulfasalazine is a widely used anti-inflammatory agent in the treatment of inflammatory bowel disease and several rheumatological disorders. "( Is it Crohn's disease? A severe systemic granulomatous reaction to sulfasalazine in patient with rheumatoid arthritis.
Fontana, RJ; Greenson, J; Haftel, HM; Quallich, LG, 2001
)
1.99
"Sulfasalazine has proven to be an effective agent in the therapy of inflammatory bowel disease (IBD). "( Effects of sulfasalazine on selected lymphocyte subpopulations in vivo and in vitro.
Charland, C; Field, CE; Thayer, WR, 1979
)
2.09
"Sulfasalazine is an important therapeutic agent in the management of chronic inflammatory bowel disease (CIBD). "( Sulfasalazine desensitization in children and adolescents with chronic inflammatory bowel disease.
Tolia, V, 1992
)
3.17
"Sulfasalazine appears to be an effective second line agent for the treatment of psoriatic arthritis."( Sulfasalazine therapy in psoriatic arthritis: clinical and immunologic response.
Harrington, TM; Newman, ED; Perruquet, JL, 1991
)
2.45
"Sulfasalazine continues to be a common treatment for active Crohn's disease. "( The role of mesalazine in Crohn's disease.
Hanauer, SB, 1990
)
1.72
"Sulfasalazine is a safe and effective drug in the short term treatment of AS."( Meta-analysis of sulfasalazine in ankylosing spondylitis.
Atra, E; Ferraz, MB; Goldsmith, CH; Tugwell, P, 1990
)
1.34
"Sulfasalazine is a potent inhibitor of superoxide production and granule enzyme release by stimulated neutrophils, and modulation of these responses may contribute to its anti-inflammatory properties. "( Inhibition of neutrophil degranulation and superoxide production by sulfasalazine. Comparison with 5-aminosalicylic acid, sulfapyridine and olsalazine.
Neal, TM; Vissers, MC; Winterbourn, CC, 1987
)
1.95
"Sulfasalazine is an effective drug for maintaining remission in ulcerative colitis, but its use may be precluded by side effects. "( Treatment of ulcerative colitis with oral 5-aminosalicylic acid including patients with adverse reactions to sulfasalazine.
Greenberg, GR; Habal, FM, 1988
)
1.93

Effects

Sulfasalazine (SSZ), which has an arylamine sulfonamide structure, is an anti-inflammatory drug used in the treatment of many rheumatic diseases. It has a relatively short lag time until its onset of action and is often considered to be among the more efficacious traditional DMARDs.

Sulfasalazine (SASP) has been widely used in treatment of rheumatoid arthritis and spondyloarthritis. It has been identified as a candidate molecule to be investigated as an intervention to treat preterm pre-eclampsia during pregnancy.

ExcerptReferenceRelevance
"Sulfasalazine (SSZ), which has an arylamine sulfonamide structure, is an anti-inflammatory drug used in the treatment of many rheumatic diseases. "( Sulfasalazine-Related Hypersensitivity Reactions in Patients With Rheumatic Diseases.
Cildag, S; Senturk, T, 2017
)
3.34
"Sulfasalazine has a relatively short lag time until its onset of action and is often considered to be among the more efficacious traditional DMARDs."( Sulfasalazine: a review of its use in the management of rheumatoid arthritis.
Croom, KF; Plosker, GL, 2005
)
2.49
"Sulfasalazine has a fairly rapid onset of clinical effects and modulates immune function."( Disease-modifying antirheumatic drugs, including methotrexate, sulfasalazine, gold, antimalarials, and D-penicillamine.
Brooks, P; Conaghan, PG, 1993
)
1.25
"Sulfasalazine, which has an effect in the acute exacerbations of ankylosing spondylitis, is probably also effective in chronic reactive arthritis."( Are antibiotics of any use in reactive arthritis?
Leirisalo-Repo, M, 1993
)
1.01
"Sulfasalazine has a beneficial effect on articular activity by controlling gut inflammation, but it cannot prevent evolution to overt IBD."( Long-term evolution of gut inflammation in patients with spondyloarthropathy.
Cuvelier, C; De Vos, M; Elewaut, A; Mielants, H; Veys, E, 1996
)
1.02
"Sulfasalazine apparently has a direct immunosuppressive effect on B cells."( Effect of sulfasalazine on B cells.
Dohi, Y; Imai, F; Ishibashi, T; Suzuki, T,
)
1.26
"Sulfasalazine (SASP) has evident anti-inflammatory effects and pharmacological functions on autoimmune disease."( Sulfasalazine exacerbates angiotensin II-induced cardiac remodelling by activating Akt signal pathway.
Bai, Y; Chen, C; Gao, Z; Jiang, X; Meng, Y; Zhang, X; Zheng, C, 2022
)
2.89
"Sulfasalazine has been widely used in treatment of rheumatoid arthritis and spondyloarthritis. "( Adverse reaction profile of sulfasalazine and its persistence in chronic therapy of rheumatoid arthritis and spondyloarthritis: A multicentric observational study.
David, R; Jayachandran, M; Koshy, V; Marwaha, V; Mithun, CB; Nair, AS; Padmanabhan, DS; Palatty, PL; Santhakumari, V; Singh, SK; Singhal, A; Suman, SK; Surendran, S; Tiwari, A; Yadav, P, 2022
)
2.46
"Sulfasalazine has been identified as a candidate molecule to be investigated as an intervention to treat preterm pre-eclampsia during pregnancy. "( An LC-MS/MS method for the simultaneous quantitation of sulfasalazine and sulfapyridine in human placenta.
Brownfoot, F; Cluver, C; Decloedt, E; Kellermann, T; Louw, V, 2023
)
2.6
"Sulfasalazine has potential to treat or prevent preeclampsia and warrants investigation in clinical trials."( Sulfasalazine reduces placental secretion of antiangiogenic factors, up-regulates the secretion of placental growth factor and rescues endothelial dysfunction.
Brownfoot, FC; Cannon, P; Hannan, NJ; Hastie, R; Kaitu'u-Lino, TJ; Nguyen, V; Parry, LJ; Senadheera, S; Tong, S; Tuohey, L, 2019
)
2.68
"Sulfasalazine (SASP) has been shown to inhibit NF-κB and reduce lipopolysaccharide-induced cytokine concentrations in fetal membrane explants and reduce the rate of Escherichia coli-induced preterm labour in mice."( Sulfasalazine augments a pro-inflammatory response in interleukin-1β-stimulated amniocytes and myocytes.
Bennett, PR; Boyce, EJ; Lee, YS; MacIntyre, DA; Rasheed, ZB; Sykes, L; Teoh, TG; Thomson, KR, 2015
)
2.58
"Sulfasalazine has long been used for the treatment of rheumatoid arthritis and is often chosen as a first-line treatment. "( Sulfasalazine induced immune thrombocytopenia in a patient with rheumatoid arthritis.
Carlucci, F; Narayan, N; Rigby, S, 2017
)
3.34
"Sulfasalazine has proved effective in acute pouchitis therapy."( Sulfasalazine in Prevention of Pouchitis After Proctocolectomy with Ileal Pouch-Anal Anastomosis for Ulcerative Colitis.
Bazzoli, F; Belluzzi, A; Digby, RJ; Festi, D; Liverani, E; Poggioli, G; Rosati, G; Sartini, A; Scaioli, E; Ugolini, G, 2017
)
2.62
"Sulfasalazine (SSZ), which has an arylamine sulfonamide structure, is an anti-inflammatory drug used in the treatment of many rheumatic diseases. "( Sulfasalazine-Related Hypersensitivity Reactions in Patients With Rheumatic Diseases.
Cildag, S; Senturk, T, 2017
)
3.34
"Sulfasalazine has been reported to show success in the treatment of persistent cases of alopecia areata."( Treatment of persistent alopecia areata with sulfasalazine.
Mahd, AA; Rashidi, T, 2008
)
1.33
"Oral sulfasalazine has been reported to be effective in patients with idiopathic cutaneous lichen planus (LP)."( Efficacy of sulfasalazine in the treatment of generalized lichen planus: randomized double-blinded clinical trial on 52 patients.
Ayoobi, A; Cheraghian, B; Feily, A; Mapar, MA; Omidian, M, 2010
)
1.25
"Sulfasalazine has modest efficacy compared to placebo and is inferior to corticosteroids for the treatment of mild to moderately active Crohn's disease. "( Aminosalicylates for induction of remission or response in Crohn's disease.
Hanauer, S; Lim, WC, 2010
)
1.8
"Sulfasalazine has demonstrated modest efficacy when Crohn's disease is confined to the colon."( Review article: mild to moderate Crohn's disease--defining the basis for a new treatment algorithm.
Feagan, BG; Sandborn, WJ, 2003
)
1.04
"Sulfasalazine (SASP) has been reported to depress the fertility in men and experimental male animals, but the fundamental mechanisms of infertility caused by SASP are still unknown. "( Effects of sulfasalazine on sperm acrosome reaction and gene expression in the male reproductive organs of rats.
Adachi, T; Fukushima, T; Hamada, Y; Horii, I; Horimoto, M; Kato, M; Komiyama, M; Mori, C, 2005
)
2.16
"Sulfasalazine has a relatively short lag time until its onset of action and is often considered to be among the more efficacious traditional DMARDs."( Sulfasalazine: a review of its use in the management of rheumatoid arthritis.
Croom, KF; Plosker, GL, 2005
)
2.49
"Sulfasalazine has more frequent side effects than olsalazine, balsalazide, and mesalamine formulations."( Treatment of ulcerative colitis with oral mesalamine: advances in drug formulation, efficacy expectations and dose response, compliance, and chemoprevention.
Sandborn, WJ, 2006
)
1.06
"Oral sulfasalazine has been found useful in treating this condition and is often used for prolonged therapy to prevent relapses."( Ulcerative colitis and its treatment.
Jacknowitz, AI, 1980
)
0.72
"Sulfasalazine, which has been used for treatment of ulcerative colitis in man, caused a dose-dependent and reversible reduction in fertility of the male rat. "( Antifertility effect of sulfasalazine in the male rat.
Pholpramool, C; Srikhao, A, 1983
)
2.02
"Sulfasalazine (SASP) has often been reported to cause serious blood disorders, particularly agranulocytosis; however, little quantitative information is available to estimate the risk or to identify possible modifiers of the risk. "( The risk of sulfasalazine- and mesalazine-associated blood disorders.
Dean, AD; Jick, H; Myers, MW,
)
1.95
"Sulfasalazine has a fairly rapid onset of clinical effects and modulates immune function."( Disease-modifying antirheumatic drugs, including methotrexate, sulfasalazine, gold, antimalarials, and D-penicillamine.
Brooks, P; Conaghan, PG, 1993
)
1.25
"Sulfasalazine, which has an effect in the acute exacerbations of ankylosing spondylitis, is probably also effective in chronic reactive arthritis."( Are antibiotics of any use in reactive arthritis?
Leirisalo-Repo, M, 1993
)
1.01
"Sulfasalazine has recently gained wide acceptance in the treatment of rheumatoid arthritis, and beneficial effects have also been noted in ankylosing spondylitis and reactive arthritis."( Sulfasalazine therapy for psoriatic arthritis: a double blind, placebo controlled trial.
Ellis, CN; Grober, JS; Gupta, AK; Hamilton, TA; McCune, WJ; Siegel, MT; Voorhees, JJ, 1995
)
2.46
"Sulfasalazine has a beneficial effect on articular activity by controlling gut inflammation, but it cannot prevent evolution to overt IBD."( Long-term evolution of gut inflammation in patients with spondyloarthropathy.
Cuvelier, C; De Vos, M; Elewaut, A; Mielants, H; Veys, E, 1996
)
1.02
"Sulfasalazine has proven to be effective in such cases, leading to improvement in clinical and laboratory indices of disease activity."( Current guidelines for the drug treatment of ankylosing spondylitis.
Toussirot, E; Wendling, D, 1998
)
1.02
"Sulfasalazine (SSZ) has regulatory approval for treatment of inflammatory bowel disease in children and adults, and for use as a slow acting agent in adult rheumatoid arthritis (RA). "( Sulfasalazine for the management of juvenile rheumatoid arthritis.
Brooks, CD, 2001
)
3.2
"4). Sulfasalazine has been known to suppress certain inflammatory responses of the immune system, including the production of cytokines such as tumor necrosis factor and interleukins 1 and 2; and to be a scavenger of superoxide radicals thought to provoke HIV by affecting the long terminal repeat of the virus."( Sulfasalazine: arthritis drug increases CD4 count?
Smith, D, 1995
)
2.21
"Sulfasalazine has no clinically relevant benefit in patients with ankylosing spondylitis. "( [Sulfasalazine in ankylosing spondylitis: a prospective, randomized, double-blind placebo-controlled study and comparison with other controlled studies].
Droste, U; Gromnica-Ihle, E; Milleck, D; Schmidt, WA; Wierth, S, 2002
)
2.67
"Sulfasalazine (SSZ) has recently been shown to be effective for the management of juvenile rheumatoid arthritis (JRA). "( Sulfasalazine therapy for juvenile rheumatoid arthritis.
Chen, CC; Chiang, BL; Lin, YT; Yang, YH, 2002
)
3.2
"Sulfasalazine, therefore, has certain properties of an antifolate drug."( Inhibition of folate enzymes by sulfasalazine.
Dhar, GJ; Rosenberg, IH; Selhub, J, 1978
)
1.26
"Sulfasalazine has proven to be an effective agent in the therapy of inflammatory bowel disease (IBD). "( Effects of sulfasalazine on selected lymphocyte subpopulations in vivo and in vitro.
Charland, C; Field, CE; Thayer, WR, 1979
)
2.09
"Sulfasalazine has been the most widely prescribed drug for patients with inflammatory bowel disease. "( [Therapeutic efficacy of 5-ASA molecules in idiopathic intestinal inflammatory diseases: critical review].
Van Gossum, A,
)
1.57
"Sulfasalazine has been used for many years in the management of ulcerative colitis. "( Mesalamine in ulcerative colitis.
Fitzgerald, JM; Marsh, TD, 1991
)
1.72
"Sulfasalazine has not been uniformly effective in preventing relapse in Crohn's disease, although many clinicians continue its use in patients who respond initially."( Risk-benefit assessment of drugs used in the treatment of inflammatory bowel disease.
Hanauer, SB; Stathopoulos, G,
)
0.85
"Sulfasalazine apparently has a direct immunosuppressive effect on B cells."( Effect of sulfasalazine on B cells.
Dohi, Y; Imai, F; Ishibashi, T; Suzuki, T,
)
1.26
"Sulfasalazine has been evaluated by several groups of investigators in ankylosing spondylitis and psoriatic arthritis."( Medical and surgical treatment of seronegative spondyloarthropathies.
Kozin, F, 1991
)
1
"Sulfasalazine therapy has been shown effective in rheumatoid arthritis and ankylosing spondylitis. "( Sulfasalazine therapy in psoriatic arthritis: clinical and immunologic response.
Harrington, TM; Newman, ED; Perruquet, JL, 1991
)
3.17
"Sulfasalazine has been widely used in the treatment of inflammatory bowel disease. "( Sulfasalazine-induced pulmonary disease.
Barwick, KW; DeLuca, VA; Dobuler, K; Moseley, RH, 1985
)
3.15
"Sulfasalazine has been associated with bronchopulmonary complications of inflammatory bowel disease (IBD) in adults. "( Desquamative interstitial pneumonitis complicating inflammatory bowel disease of childhood.
Fechner, RE; Sutphen, JL; Teague, WG, 1985
)
1.71
"Sulfasalazine has been reported to induce pulmonary eosinophilia and hypersensitivity with symptoms of dyspnea and fever. "( Bronchoalveolar lavage in acute hypersensitivity pneumonitis caused by sulfasalazine.
Pauwels, R; Valcke, Y; Van der Straeten, M, 1987
)
1.95
"Sulfasalazine has been used for a decade in the United Kingdom for treating rheumatoid arthritis. "( Adverse reactions to sulfasalazine: the British experience.
Dacre, JE; Scott, DL, 1988
)
2.04
"Sulfasalazine (SASP) has been used for many years as a disease-modifying agent in inflammatory bowel disease and in rheumatoid arthritis. "( The enhancing effect of cyclosporine A and sulfasalazine on the prevention of rejection in rat cardiac allografts.
Gerdin, B; Tufveson, G; Wanders, A, 1988
)
1.98

Actions

Sulfasalazine (SF) promotes remyelination and improves the outcome of multiple sclerosis (MS) patients. It can cause analytical interference in some assays for urinary normetanephrine and result in spuriously elevated levels, leading to misdiagnosis of phaeochromocytoma.

ExcerptReferenceRelevance
"Sulfasalazine can cause analytical interference in some assays for urinary normetanephrine and result in spuriously elevated levels, leading to misdiagnosis of phaeochromocytoma."( Sulfasalazine as a cause of false-positive elevation of urinary normetanephrine in patients with adrenal mass and suspected phaeochromocytoma: a diagnostic challenge.
Balasubramanian, S; Debono, M; Rab, E; Zuling, ET, 2023
)
3.07
"Sulfasalazine (SF) promotes remyelination and improves the outcome of multiple sclerosis (MS) patients. "( Sulfasalazine alters microglia phenotype by competing endogenous RNA effect of miR-136-5p and long non-coding RNA HOTAIR in cuprizone-induced demyelination.
Chen, H; Chen, X; Duan, C; Li, Y; Liu, X; Liu, Y; Yang, J; Yue, J; Zhou, X, 2018
)
3.37
"Sulfasalazine is known to inhibit nuclear factor kappa-light-chain-enhancer of activated B cells (NFkB) and upregulate heme-oxygenase 1 (HO-1) thus we explored the effect of these transcription factors on sFlt-1 secretion from human cytotrophoblasts."( Sulfasalazine reduces placental secretion of antiangiogenic factors, up-regulates the secretion of placental growth factor and rescues endothelial dysfunction.
Brownfoot, FC; Cannon, P; Hannan, NJ; Hastie, R; Kaitu'u-Lino, TJ; Nguyen, V; Parry, LJ; Senadheera, S; Tong, S; Tuohey, L, 2019
)
2.68
"Sulfasalazine was used to inhibit the nuclear factor-kappaB (NFkappaB) pathway and SP600125, a chemical inhibitor of the c-Jun N-terminal kinase, was used as an inhibitor of the activator protein-1 (AP-1) pathway."( Differential involvement of nuclear factor-kappaB and activator protein-1 pathways in the interleukin-1beta-mediated decrease of deiodinase type 1 and thyroid hormone receptor beta1 mRNA.
Boelen, A; Kwakkel, J; Wiersinga, WM, 2006
)
1.06
"Sulfasalazine may enhance the inhibitory proliferation and apoptosis effect on BxPC-3 cells induced by 5-FU, which is closely related to synergistically the cell cycle arrested in G0/G1-phase."( Effects of 5-fluouracil combined with sulfasalazine on human pancreatic carcinoma cell line BxPC-3 proliferation and apoptosis in vitro.
Guo, KJ; Guo, RX; He, SG; Huang, Z, 2007
)
2.05
"Sulfasalazine was used because of its inhibitory effect on B cells."( [Sulfasalazine therapy for hypergammaglobulinemia in patients with Sjögren's syndrome].
Dohi, Y; Imai, F; Ishibashi, T; Ohno, S; Suzuki, T; Tanaka, M, 1994
)
1.92
"Sulfasalazine appears to inhibit binding of NKCF to the target cell whereas sulfapyridine predominantly inhibits early post-binding events."( Inhibition of cytotoxicity by sulfasalazine. II. Sulfasalazine and sulfapyridine inhibit different stages of the NK and NKCF lytic processes.
Kane, MG; MacDermott, RP; Niederlehner, A; Shanahan, F; Stenson, WF; Targan, S, 1986
)
1.28
"Sulfasalazine may cause reversible male infertility, but it is entirely safe for use during pregnancy and lactation."( The safety of sulfasalazine: the gastroenterologists' experience.
Sachar, DB, 1988
)
1.36

Treatment

Treatment with sulfasalazine, etanercept, adalimumab, infliximab, and methotrexate gave no long-lasting remission. Treatment with doxantrazole, quercetin, or nedocromil did not increase the histamine concentration or the mast cell number in the colon.

ExcerptReferenceRelevance
"Sulfasalazine treatment significantly decreased intracellular glutathione levels and induced apoptosis when combined with cisplatin in USC cell lines."( Impact of the glutathione synthesis pathway on sulfasalazine-treated endometrial cancer.
Nagase, S; Ohta, T; Seino, M; Sendo, K, 2022
)
1.7
"Sulfasalazine-treated wild-type mice and xCT knockout mice were analyzed."( Cystine/Glutamate Antiporter (xCT) Is Required for Chief Cell Plasticity After Gastric Injury.
Choi, E; Engevik, AC; Goldenring, JR; Massion, PP; Meyer, AR; Mills, JC; Willet, SG; Williams, JA; Zou, Y, 2019
)
1.24
"Sulfasalazine treatment with temozolomide plus radiotherapy for newly diagnosed primary GBM is associated with a high rate of discontinuation due to hematologic toxic effects. "( Sulfasalazine and temozolomide with radiation therapy for newly diagnosed glioblastoma.
Nagatani, K; Nawashiro, H; Osada, H; Otani, N; Takeuchi, S; Wada, K,
)
3.02
"Sulfasalazine treatment also increased inosine levels in sciatic nerves of diabetic rats."( Sulfasalazine blocks the development of tactile allodynia in diabetic rats.
Berti-Mattera, LN; Kern, TS; Mitchell, R; Nemet, I; Siegel, RE, 2008
)
2.51
"Sulfasalazine and FTY720 treatment did not prevent body weight loss or reduce clinical scores of diarrhea or intestinal gross pathology, when compared with vehicle treatment. "( Pharmacologic evaluation of sulfasalazine, FTY720, and anti-IL-12/23p40 in a TNBS-induced Crohn's disease model.
Benson, EL; Heuvelman, DM; Masferrer, JL; Radi, ZA, 2011
)
2.11
"Sulfasalazine treatment was not found effective on enthesal abnormalities of IRD patients."( The effects of sulfasalazine treatment on enthesal abnormalities of inflammatory rheumatic diseases.
Duyur Cakit, B; Erdem, HR; Genc, H; Kacar, M; Nacir, B; Saracoglu, M, 2007
)
1.41
"Sulfasalazine treated patients also showed significant improvements in cutaneous involvement."( Sulfasalazine therapy for psoriatic arthritis: a double blind, placebo controlled trial.
Ellis, CN; Grober, JS; Gupta, AK; Hamilton, TA; McCune, WJ; Siegel, MT; Voorhees, JJ, 1995
)
2.46
"Sulfasalazine treatment decreased ICAM-1 and VCAM-1 protein expression."( Sulfasalazine inhibits reperfusion injury and prolongs allograft survival in rat cardiac transplants.
Feeley, BT; Hoyt, EG; Park, AK; Robbins, RC, 1999
)
2.47
"Sulfasalazine treatment showed no significant protective effect on the development of colorectal dysplasia or cancer in patients with ulcerative colitis."( Proximal colorectal dysplasia or cancer in ulcerative colitis. The impact of primary sclerosing cholangitis and sulfasalazine: results from a 20-year surveillance study.
Broomé, U; Lindberg, BU; Persson, B, 2001
)
1.24
"The sulfasalazine-treated guinea pigs showed a significantly better clinical outcome, as well as a significantly lower histological inflammation score compared with 19 controls."( Suppression of experimental autoimmune encephalomyelitis by sulfasalazine.
Hoffmann, G; Neu, I; Prosiegel, M; Ruhenstroth-Bauer, G; Vogl, S; Wildfeuer, A, 1990
)
1
"Treatment with sulfasalazine, etanercept, adalimumab, infliximab, and methotrexate gave no long-lasting remission."( Tofacitinib for the treatment of inflammatory bowel disease-associated arthritis: two case reports.
Haq, SA; Momen Majumder, MS; Rasker, JJ, 2023
)
1.25
"Treatment with sulfasalazine, low dose of natrexone or their combination resulted in significant improvement of all measured parameters compared with enteritis group."( Evaluation of therapeutic effect of low dose naltrexone in experimentally-induced Crohn's disease in rats.
Abdel-Salam, LO; Kamel, MM; Khattab, A; Osman, AS; Tawfik, DI; Tolba, HM, 2016
)
0.77
"Treatment with sulfasalazine, doxantrazole, quercetin, or nedocromil did not increase the histamine concentration or the mast cell number in the colon on day 26, thereby showing absence of degranulation of these cells."( Relationship between mast cells and the colitis with relapse induced by trinitrobenzesulphonic acid in Wistar rats.
de Oliveira, DM; Di Stasi, LC; Gomes, JC; Luchini, AC; Pellizzon, CH, 2009
)
0.69
"Cotreatment with sulfasalazine, which inhibited nuclear translocation of NF-kappaB p65, had a rapid and marked inhibitory effect on the rate of cytokine accumulation in the maternal compartment, with lesser but significant effects observed in the fetal compartment."( Prevention of inflammatory activation of human gestational membranes in an ex vivo model using a pharmacological NF-kappaB inhibitor.
Keelan, JA; Khan, S; Mitchell, MD; Yosaatmadja, F, 2009
)
0.68
"Treatment with Sulfasalazine with and without methotrexate produced good response in 71.4 % and 12.5% respectively."( Post-chikungunya chronic arthritis--our experience with DMARDs over two year follow up.
Ganu, AS; Ganu, MA, 2011
)
0.71
"Treatment with sulfasalazine correlated positively with BMD at 3 of the 5 measured bone sites."( Bone mineral density in men with rheumatoid arthritis is associated with erosive disease and sulfasalazine treatment but not with sex hormones.
Hafström, I; Tengstrand, B, 2002
)
0.87
"Treatment with sulfasalazine normalized these alterations."( Increased jejunal secretory IgA and IgM in ankylosing spondylitis: normalization after treatment with sulfasalazine.
Brandtzaeg, P; Feltelius, N; Hällgren, R; Hvatum, M; Knutson, L, 1994
)
0.84
"Treatment with sulfasalazine and prednisone resulted in a clinical remission after seven weeks."( [Clostridium difficile in early childhood ulcerative pancolitis].
Hoppen, T; Keller, KM; Rister, M; Stolte, M, 1993
)
0.63
"Treatment with sulfasalazine markedly decreased the number of leukocytes that accumulated in the inflamed (carrageenan, 2 mg/ml) air pouch."( The anti-inflammatory mechanism of sulfasalazine is related to adenosine release at inflamed sites.
Buckley, MT; Carlin, G; Cronstein, BN; Gadangi, P; Levin, RI; Longaker, M; Montesinos, MC; Naime, D; Recht, PA, 1996
)
0.91
"Treatment with sulfasalazine prior to LPS also decreased reperfusion injury compared to LPS and saline groups."( Sulfasalazine inhibits reperfusion injury and prolongs allograft survival in rat cardiac transplants.
Feeley, BT; Hoyt, EG; Park, AK; Robbins, RC, 1999
)
2.09
"Treatment with sulfasalazine is an effective method to decrease reperfusion injury and prolong allograft survival in a rat cardiac transplantation model."( Sulfasalazine inhibits reperfusion injury and prolongs allograft survival in rat cardiac transplants.
Feeley, BT; Hoyt, EG; Park, AK; Robbins, RC, 1999
)
2.1
"Drug treatment with sulfasalazine or 5-aminosalicylic acid improved enteritis score."( Chronic intrajejunal TNBS application in TNBS-sensitized rats: a new model of chronic inflammatory bowel diseases.
Selve, N, 1992
)
0.6

Toxicity

Sulfasalazine may cause reversible male infertility, but it is entirely safe for use during pregnancy and lactation. Adverse events requiring the withdrawal of therapy seem to occur less frequently with balsalazide, mesalamine, and olsalazine.

ExcerptReferenceRelevance
" A possible reversible toxic effect of salicylazosulfapyridine on semen quality is discussed."( Reversible toxic effect of salicylazosulfapyridine on semen quality.
Toth, A, 1979
)
0.26
" In both treatment groups, three patients dropped out because of adverse effects."( Relapse-preventing effect and safety of sulfasalazine and olsalazine in patients with ulcerative colitis in remission: a prospective, double-blind, randomized multicenter study. The Ulcerative Colitis Multicenter Study Group.
Rijk, MC; van Lier, HJ; van Tongeren, JH, 1992
)
0.55
" Severe toxic side-effects in three of the four patients entered required discontinuation of the trial."( Toxicity of sulfasalazine in systemic juvenile chronic arthritis.
Cats, A; Hertzberger-ten Cate, R,
)
0.51
" The role of metabolites in sulphasalazine-mediated toxicity has been investigated in vitro by the use of human red blood cells and mononuclear leucocytes as target cells, with methaemoglobin formation and cytotoxicity respectively, being the defined toxic end-points."( Direct and metabolism-dependent toxicity of sulphasalazine and its principal metabolites towards human erythrocytes and leucocytes.
Breckenridge, AM; Coleman, MD; Hussain, F; Park, BK; Pirmohamed, M, 1991
)
0.28
"5%) had adverse effects that led to discontinuation of therapy in 14 (11."( Relationship between the acetylator phenotype, plasma sulfapyridine levels and adverse effects during treatment with salicylazosulfapyridine in patients with chronic bowel diseases.
Levy, M; Rachmilewitz, D; Rahav, G; Zylber-Katz, E, 1990
)
0.28
" Forty-seven (14%) of 331 patients receiving mesalazine reported adverse events, whereas 33 (23%) of 144 patients receiving sulphasalazine and 23 (19%) of 123 patients receiving placebo reported adverse effects."( Mesalazine: a global safety evaluation.
Brimblecombe, R, 1990
)
0.28
" However, its safety profile is far superior, and very long-term treatment with sulphasalazine is a safe option for treatment of rheumatoid arthritis."( Sulphasalazine: a safe, effective agent for prolonged control of rheumatoid arthritis. A comparison with sodium aurothiomalate.
Amos, RS; Bax, DE, 1985
)
0.27
" The incidence and nature of adverse effects occurring in 774 patients with rheumatoid arthritis treated with sulphasalazine for periods ranging from one to 11 years were therefore noted."( Sulphasalazine for rheumatoid arthritis: toxicity in 774 patients monitored for one to 11 years.
Amos, RS; Bax, DE; Capell, HA; McConkey, B; Pullar, T; Situnayake, D, 1986
)
0.27
"The side effect profile of sulphasalazine was documented in 200 patients with inflammatory joint disease treated with the drug for at least 1 year."( Side effect profile of 200 patients with inflammatory arthritides treated with sulphasalazine.
Bacon, PA; Farr, M; Scott, DG, 1986
)
0.27
" Sulfasalazine may cause reversible male infertility, but it is entirely safe for use during pregnancy and lactation."( The safety of sulfasalazine: the gastroenterologists' experience.
Sachar, DB, 1988
)
1.55
" This suggests that, at least in some patients, the adverse effects of sulfasalazine are due to 5-aminosalicylic acid rather than sulfapyridine."( Adverse effects with oral 5-aminosalicyclic acid.
Fardy, JM; Lloyd, DA; Reynolds, RP, 1988
)
0.51
" The serum concentrations of the parent drug and its sulphapyridine-metabolites were determined and the adverse effects were recorded."( Acetylator phenotype and adverse effects of sulphasalazine in healthy subjects.
Evans, DA; Schröder, H, 1972
)
0.25
" In both instances there was an interval of three weeks between receiving the drug for the first time and the onset of the toxic reaction."( Combined hepatotoxicity and neurotoxicity following sulphasalazine administration.
Gibson, GE; Rowland, R; Smith, MD, 1982
)
0.26
" Adverse events occurred in 64% of all patients (highest 85% in AS and lowest 50% in ulcerative colitis, CU)."( Side effects of sulphasalazine in patients with rheumatic diseases or inflammatory bowel disease.
Laasila, K; Leirisalo-Repo, M, 1994
)
0.29
" Serious or fatal adverse reactions were not observed."( Toxicity of sulphasalazine in rheumatoid arthritis. Possible protective effect of rheumatoid factors and corticosteroids.
Gran, JT; Myklebust, G, 1993
)
0.29
"The disease RA itself is assumed to be a risk factor for the occurrence of adverse drug reactions during sulphasalazine therapy."( Rheumatoid arthritis: a risk factor for sulphasalazine toxicity? A meta-analysis.
Van 'T Hof, MA; Van De Putte, LB; Van Riel, PL; Wijnands, MJ, 1993
)
0.29
" Serious sulphasalazine-related adverse reactions are rare and their outcome is generally favourable within a few weeks after drug withdrawal."( Sulphasalazine-related life-threatening side effects: is N-acetylcysteine of therapeutic value?
De Bandt, M; Gabay, C; Palazzo, E,
)
0.13
"We investigated the adverse effects of sulfasalazine in the treatment of inflammatory bowel disease in Japan."( Adverse effects of sulfasalazine and treatment of ulcerative colitis with mesalazine.
Munakata, A; Nakajima, H; Yoshida, Y, 1995
)
0.89
" The frequency and nature of adverse effects and changes in clinical and laboratory parameters of disease activity were measured after three and six months."( Low dose desensitisation does not reduce the toxicity of sulphasalazine in rheumatoid arthritis.
Capell, HA; Hunter, JA; Madhok, R; McInnes, IB; Murphy, EA; Porter, D; Pullar, T; Thomson, EA, 1996
)
0.29
" There was no significant difference between actively and placebo desensitised patients as regards the incidence or profile of adverse effects (toxicity)."( Low dose desensitisation does not reduce the toxicity of sulphasalazine in rheumatoid arthritis.
Capell, HA; Hunter, JA; Madhok, R; McInnes, IB; Murphy, EA; Porter, D; Pullar, T; Thomson, EA, 1996
)
0.29
" Pericarditis as a side effect induced by sulfasalazine or 5-aminosalicylic acid, drugs used in the therapy of these diseases, was first described only 7 years ago."( [Pericarditis in chronic inflammatory bowel disease: underlying disease or side effects of therapy? Clinical problem solving].
Krähenbühl, S; Kupferschmidt, H; Langenegger, T, 1996
)
0.56
" The proportion of adverse events was lowest in group 1 (14%) and highest in groups 3 and 4 (25%)."( Toxicity profile of dual methotrexate combinations with gold, hydroxychloroquine, sulphasalazine and minocycline in rheumatoid arthritis patients.
Caspi, D; Elkayam, O; Segal, R; Yaron, M; Zhukovsky, G, 1997
)
0.3
" Adverse events occurred in 25."( [Sulfasalazine: side effects and duration of therapy in patients with rheumatoid arthritis].
Cervini, C; Lamanna, G; Mundo, A; Pedone, V,
)
1.04
" Most common adverse events with leflunomide were diarrhoea (17%), nausea (10%), alopecia (8%), and rash (10%)."( Efficacy and safety of leflunomide compared with placebo and sulphasalazine in active rheumatoid arthritis: a double-blind, randomised, multicentre trial. European Leflunomide Study Group.
Kalden, JR; Kvien, TK; Larsen, A; Loew-Friedrich, I; Oed, C; Rosenburg, R; Rozman, B; Scott, DL; Smolen, JS, 1999
)
0.3
" These potential adverse effects of SSZ should be considered when it is used to treat chronic arthritides with systemic symptoms."( High toxicity of sulfasalazine in adult-onset Still's disease.
Bae, SC; Jun, JB; Jung, JH; Jung, SS; Kim, SY; Kim, TH; Lee, IH; Yoo, DH,
)
0.47
" Longterm safety assessment is difficult for a number of reasons: there are relatively few trials that have followed patients beyond 5 years and the use of a combination of DMARD therapy with nonsteroidal antiinflammatory drugs and corticosteroids complicates the assessment of an observed adverse event with a particular drug."( Disease modifying antirheumatic drugs: longterm safety issues.
Capell, HA, 2001
)
0.31
" This side effect has seldom been reported in the literature."( [Sulfasalazine neurotoxicity].
Chadenat, ML; Dechy, H; Dorra, M; Dupont, C; Morelon, S; Raffin-Sanson, ML; Rouveix, E, 2001
)
1.22
"5-aminosalicylates are extensively prescribed for the treatment of ulcerative colitis but have a wide range of described adverse effects."( Sulphasalazine and mesalazine: serious adverse reactions re-evaluated on the basis of suspected adverse reaction reports to the Committee on Safety of Medicines.
Langman, MJ; Ransford, RA, 2002
)
0.31
"To determine whether serious adverse effect profiles differ for sulphasalazine and mesalazine."( Sulphasalazine and mesalazine: serious adverse reactions re-evaluated on the basis of suspected adverse reaction reports to the Committee on Safety of Medicines.
Langman, MJ; Ransford, RA, 2002
)
0.31
"Analysis of suspected serious adverse reactions reported to the Committee on Safety of Medicines of the UK in 1991-1998."( Sulphasalazine and mesalazine: serious adverse reactions re-evaluated on the basis of suspected adverse reaction reports to the Committee on Safety of Medicines.
Langman, MJ; Ransford, RA, 2002
)
0.31
"To evaluate rates on the adverse side effect and discontinuation of second-line drugs frequently used in the treatment of rheumatoid arthritis (RA)."( [Retrospective study of adverse events in patients with rheumatoid arthritis treated with second-line drugs].
Jiang, L; Ni, L; Zhao, N, 2002
)
0.31
" Sulfasalazine users reported adverse events including upper abdominal trouble (39."( [Retrospective study of adverse events in patients with rheumatoid arthritis treated with second-line drugs].
Jiang, L; Ni, L; Zhao, N, 2002
)
1.22
"Serious adverse events may occur from the use of disease modifying antirheumatic drugs (DMARDs) used to treat rheumatoid arthritis."( Monitoring and assessing the safety of disease-modifying antirheumatic drugs: a West Midlands experience.
Bevan, J; Homer, D; Jobanputra, P; Maggs, F, 2002
)
0.31
"Forty-four serious adverse events associated with DMARD use were reported between December 1999 and October 2001."( Monitoring and assessing the safety of disease-modifying antirheumatic drugs: a West Midlands experience.
Bevan, J; Homer, D; Jobanputra, P; Maggs, F, 2002
)
0.31
"We have successfully implemented a regional system for identifying potential drug-related serious adverse events."( Monitoring and assessing the safety of disease-modifying antirheumatic drugs: a West Midlands experience.
Bevan, J; Homer, D; Jobanputra, P; Maggs, F, 2002
)
0.31
" We examine whether there was a correlation between diplotype configurations (combinations of 2 haplotypes for a subject) at the NAT2 gene and the adverse effects of SSZ used for the treatment of rheumatoid arthritis (RA)."( Adverse effects of sulfasalazine in patients with rheumatoid arthritis are associated with diplotype configuration at the N-acetyltransferase 2 gene.
Kamatani, N; Kitamura, Y; Matsuda, Y; Nakajima, H; Saito, M; Saito, T; Tanaka, E; Taniguchi, A; Urano, W; Yamanaka, H, 2002
)
0.64
"1%) had experienced adverse effects from SSZ, the most common being allergic reactions including rash and fever."( Adverse effects of sulfasalazine in patients with rheumatoid arthritis are associated with diplotype configuration at the N-acetyltransferase 2 gene.
Kamatani, N; Kitamura, Y; Matsuda, Y; Nakajima, H; Saito, M; Saito, T; Tanaka, E; Taniguchi, A; Urano, W; Yamanaka, H, 2002
)
0.64
"Genotyping the NAT2 gene followed by estimation of diplotype configuration before administration of SSZ is likely to reduce the frequency of adverse effects in Japanese patients with RA."( Adverse effects of sulfasalazine in patients with rheumatoid arthritis are associated with diplotype configuration at the N-acetyltransferase 2 gene.
Kamatani, N; Kitamura, Y; Matsuda, Y; Nakajima, H; Saito, M; Saito, T; Tanaka, E; Taniguchi, A; Urano, W; Yamanaka, H, 2002
)
0.64
" Adverse events requiring the withdrawal of therapy seem to occur less frequently with balsalazide, mesalamine, and olsalazine compared with sulfasalazine."( The short- and long-term safety of 5-aminosalicylate products in the treatment of ulcerative colitis.
Baker, DE; Kane, S, 2004
)
0.53
"5 million adverse drug reaction (ADR) reports for 8620 drugs/biologics that are listed for 1191 Coding Symbols for Thesaurus of Adverse Reaction (COSTAR) terms of adverse effects."( Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
Benz, RD; Contrera, JF; Kruhlak, NL; Matthews, EJ; Weaver, JL, 2004
)
0.32
" No statistically significant difference was noted in the incidence of adverse reactions between iguratimod and salazosulfapyridine."( Efficacy and safety of iguratimod compared with placebo and salazosulfapyridine in active rheumatoid arthritis: a controlled, multicenter, double-blind, parallel-group study.
Abe, T; Hara, M; Hashimoto, H; Hoshi, K; Irimajiri, S; Matsui, N; Mizushima, Y; Nakano, S; Nobunaga, M; Sugawara, S; Yoshino, S, 2007
)
0.34
" The aim of the present study was to investigate associations of the genotypes of NAT2 with inflammatory bowel disease (IBD), and with adverse effects of SASP, which is used as the first-line treatment of IBD."( N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease.
Chen, B; Chen, M; Guo, Q; Hu, Z; Li, J; Xia, B; Ye, M, 2007
)
0.34
" Sixty-eight patients with IBD treated with SASP were followed, and their adverse reactions were recorded."( N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease.
Chen, B; Chen, M; Guo, Q; Hu, Z; Li, J; Xia, B; Ye, M, 2007
)
0.34
"Eleven patients (16%) experienced adverse effects from SASP, including nine cases of sulfapyridine (SP) dose-related adverse effects and two cases of hypersensitivity (skin rash)."( N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease.
Chen, B; Chen, M; Guo, Q; Hu, Z; Li, J; Xia, B; Ye, M, 2007
)
0.34
"The NAT2 gene polymorphism was not associated with susceptibility to IBD in Chinese populations, but the NAT2 slow acetylator genotypes were significantly associated with SP dose-related adverse effects of SASP in the treatment of IBD."( N-acetyltransferase 2 slow acetylator genotype associated with adverse effects of sulphasalazine in the treatment of inflammatory bowel disease.
Chen, B; Chen, M; Guo, Q; Hu, Z; Li, J; Xia, B; Ye, M, 2007
)
0.34
" Efficacy was assessed by the numbers of patients withdrawn for lack of effect; toxicity by withdrawals for adverse events."( A systematic review and meta-analysis of efficacy and toxicity of disease modifying anti-rheumatic drugs and biological agents for psoriatic arthritis.
Choy, EH; Ravindran, V; Scott, DL, 2008
)
0.35
"Spontaneous reporting systems for adverse drug reactions (ADRs) are handicapped by under-reporting and limited detail on individual cases."( Hepatotoxicity associated with sulfasalazine in inflammatory arthritis: A case series from a local surveillance of serious adverse events.
Amarasena, R; Bowman, S; Filer, A; Homer, D; Jobanputra, P; Jubb, R; Maggs, F; Rankin, E; Raza, K, 2008
)
0.63
"To assess the incidence and severity of disease modifying antirheumatic drug (DMARD)-induced adverse effects (AE) in patients with rheumatoid arthritis (RA) taking/not taking glucocorticoids (GC)."( Low-dose prednisolone in rheumatoid arthritis: adverse effects of various disease modifying antirheumatic drugs.
Arnold, S; Baerwald, CG; Häntzschel, H; Malysheva, OA; Pierer, M; Wagner, U; Wahle, M, 2008
)
0.35
" Commonly reported adverse events occurring in the etanercept groups were injection site reactions and pharyngitis/laryngitis (p<0."( Efficacy, safety and patient-reported outcomes of combination etanercept and sulfasalazine versus etanercept alone in patients with rheumatoid arthritis: a double-blind randomised 2-year study.
Codreanu, C; Combe, B; Fatenejad, S; Fiocco, U; Gaubitz, M; Geusens, PP; Khandker, R; Kvien, TK; Pavelka, K; Sambrook, PN; Singh, A; Smolen, JS; Wajdula, J, 2009
)
0.58
"Initial remission targeted therapy with the FIN-RACo DMARD combination in early RA is safe for kidneys and does not induce more short- or long-term renal complications compared to traditional therapy with a single DMARD."( Renal safety of initial combination versus single DMARD therapy in patients with early rheumatoid arthritis: an 11-year experience from the FIN-RACo Trial.
Hannonen, PJ; Kaipiainen-Seppänen, OA; Karjalainen, AH; Karstila, KL; Korpela, MM; Leirisalo-Repo, M; Möttönen, TT; Mustonen, JT; Rantalaiho, VM,
)
0.13
" An understanding of structure-activity relationships (SARs) of chemicals can make a significant contribution to the identification of potential toxic effects early in the drug development process and aid in avoiding such problems."( Developing structure-activity relationships for the prediction of hepatotoxicity.
Fisk, L; Greene, N; Naven, RT; Note, RR; Patel, ML; Pelletier, DJ, 2010
)
0.36
"This paper gives an overview of recent research about SASP and its main adverse effects, highlighting the mechanisms underlying them."( Oxidative stress as a mechanism underlying sulfasalazine-induced toxicity.
Alonso, V; Domingo, JL; Linares, V, 2011
)
0.63
"Although SASP and 5-aminosalicylic acid also scavenge ROS, which may account for some of their anti-inflammatory properties, the reaction with ROS may also generate toxic free radicals; hence, the ability of other antioxidants to suppress the toxicity of SASP in vivo."( Oxidative stress as a mechanism underlying sulfasalazine-induced toxicity.
Alonso, V; Domingo, JL; Linares, V, 2011
)
0.63
" There was no significant difference between the two groups in the incidence of adverse events."( Efficacy and safety of additional use of tacrolimus in patients with early rheumatoid arthritis with inadequate response to DMARDs--a multicenter, double-blind, parallel-group trial.
Kawai, S; Miyasaka, N; Takeuchi, T; Tanaka, Y; Yamamoto, K, 2011
)
0.37
" Serious adverse events rarely occurred, and the rate of serious adverse events did not differ between groups."( Clinical efficacy and safety of etanercept versus sulfasalazine in patients with ankylosing spondylitis: a randomized, double-blind trial.
Braun, J; Burgos-Vargas, R; Freundlich, B; Huang, F; Koenig, AS; van der Horst-Bruinsma, IE; Vlahos, B, 2011
)
0.62
" We collected clinical information, including patient background, treatment efficacy (evaluated using the DAS score), and adverse events observed."( Single-center, retrospective analysis of efficacy and safety of tacrolimus as a second-line DMARD in combination therapy and the risk factors contributing to adverse events in 115 patients with rheumatoid arthritis.
Amano, H; Kageyama, M; Kempe, K; Kusaoi, M; Matsudaira, R; Matsushita, M; Morimoto, S; Nawata, M; Ogasawara, M; Onuma, S; Sekiya, F; Tada, K; Takasaki, Y; Tamura, N; Toyama, S; Yamaji, K, 2012
)
0.38
"Toxicogenomics, based on the temporal effects of drugs on gene expression, is able to predict toxic effects earlier than traditional technologies by analyzing changes in genomic biomarkers that could precede subsequent protein translation and initiation of histological organ damage."( High-density real-time PCR-based in vivo toxicogenomic screen to predict organ-specific toxicity.
Bito, T; Fabian, G; Farago, N; Feher, LZ; Katona, RL; Kitajka, K; Kulin, S; Nagy, LI; Puskas, LG; Tiszlavicz, L; Tubak, V, 2011
)
0.37
" We examined the possibility that concurrent blockade of free radicals and prostaglandin E(2) (PGE(2))-mediated inflammation might constitute a safe and effective therapeutic approach to ALS."( Concurrent blockade of free radical and microsomal prostaglandin E synthase-1-mediated PGE2 production improves safety and efficacy in a mouse model of amyotrophic lateral sclerosis.
Cho, W; Gwag, BJ; Im, DS; Lee, JH; Lee, JK; Lee, YA; Lee, YB; Shin, JH; Springer, JE; Yun, BS, 2012
)
0.38
" There is a lack of information describing the degree and duration of sulfasalazine's efficacy, the frequency and nature of adverse reactions, and the appropriate safety monitoring parameters."( Efficacy and safety of sulfasalazine in patients with chronic idiopathic urticaria.
Orden, RA; Saini, SS; Timble, H, 2014
)
0.95
" The frequency of adverse events leading to an alteration of sulfasalazine treatment supports the need for close monitoring of these patients."( Efficacy and safety of sulfasalazine in patients with chronic idiopathic urticaria.
Orden, RA; Saini, SS; Timble, H, 2014
)
0.95
" However, its use is associated with a high rate of adverse effects (AEs) which can be cutaneous, hematological, renal, hepatic, gastrointestinal or neurological."( [Adverse effects of sulfasalazine: discussion of mechanism and role of sulfonamide structure].
Affes, H; Atheymen, R; Hammami, S; Ksouda, K; Mnif, L; Sahnoun, Z; Tahri, N; Zeghal, KM,
)
0.45
" Toxicity was defined by cessation of SSA due to adverse effects and response as remission after 12 months of treatment."( Pharmacogenomics of NAT2 and ABCG2 influence the toxicity and efficacy of sulphasalazine containing DMARD regimens in early rheumatoid arthritis.
Alotaibi, N; Cleland, LG; O'Doherty, C; Proudman, SM; Sorich, MJ; Suppiah, V; Wiese, MD, 2014
)
0.4
" Cessation of at least one of MTX, SSZ or HCQ occurred because of an adverse event in 38%, remission in 7% and incomplete response in 28% of patients."( Safety and retention of combination triple disease-modifying anti-rheumatic drugs in new-onset rheumatoid arthritis.
Cummins, L; Duggan, E; Katikireddi, VS; Pahau, H; Shankaranarayana, S; Su, KY; Thomas, R; Videm, V, 2015
)
0.42
" Most of these adverse effects were mild, did not require discontinuation of the medication, and resolved after stopping the medication or decreasing the dose."( The Comparative Safety of Multiple Alternative Agents in Refractory Chronic Urticaria Patients.
Khan, DA; Seth, S,
)
0.13
"The use of alternative agents for the treatment of chronic urticaria angioedema is generally safe when proper laboratory and clinical monitoring is observed."( The Comparative Safety of Multiple Alternative Agents in Refractory Chronic Urticaria Patients.
Khan, DA; Seth, S,
)
0.13
"The main aim of this study was to examine the differences between triple therapy (T: SSZ and HCQ added to MTX) and etanercept (E) added to MTX with regard to the infectious and gastrointestinal (GI) adverse events (AEs) reported in The Rheumatoid Arthritis Comparison of Active Therapies Trial."( Rheumatoid arthritis triple therapy compared with etanercept: difference in infectious and gastrointestinal adverse events.
Brophy, MT; Chang, BH; Hannagan, K; O'Dell, JR; Quach, LT; Soe Thwin, S, 2017
)
0.46
" Adverse events [AEs] in pre-specified categories and serious AEs were recorded at least every 6 months of the 5-year observation period."( Five-year Safety Data From ENCORE, a European Observational Safety Registry for Adults With Crohn's Disease Treated With Infliximab [Remicade®] or Conventional Therapy.
Boice, J; Colombel, JF; Cornillie, F; D'Haens, G; Ghosh, S; Hommes, DW; Huang, Z; Huyck, S; Lindgren, S; Panes, J; Prantera, C; Reinisch, W, 2017
)
0.46
" Adverse events (AEs) were reported in 114/122 (93."( Sirukumab in rheumatoid arthritis refractory to sulfasalazine or methotrexate: a randomized phase 3 safety and efficacy study in Japanese patients.
Harigai, M; Hsu, B; Kato, Y; Nakano, T; Takeuchi, T; Tamamura, R; Tanaka, Y; Ukyo, Y; Yamanaka, H, 2018
)
0.74
"Despite NUDT15 variants showing significant association with thiopurine-induced adverse events (AEs) in Asians, it remains unclear which variants of NUDT15 or whether additional genetic variants should be tested to predict AEs."( NUDT15 codon 139 is the best pharmacogenetic marker for predicting thiopurine-induced severe adverse events in Japanese patients with inflammatory bowel disease: a multicenter study.
Andoh, A; Araki, H; Endo, K; Hanai, H; Hiraoka, S; Hisamatsu, T; Hokari, R; Ikeya, K; Ishiguro, Y; Kakuta, Y; Kawai, Y; Kinouchi, Y; Kobayashi, T; Masamune, A; Matsumoto, T; Miura, M; Mizuno, S; Moroi, R; Motoya, S; Naganuma, M; Nagasaki, M; Naito, T; Nakagawa, S; Nakagawa, T; Nakamura, S; Nakase, H; Nishida, A; Okamoto, D; Onodera, K; Sakuraba, H; Sasaki, M; Shiga, H; Shimosegawa, T; Shinozaki, M; Suzuki, Y; Takagawa, T; Takahara, M; Toyonaga, T; Yanai, S, 2018
)
0.48
" Data were extracted for ACR20/50, HAQ-DI, SF-36 and adverse/serious adverse events after 16-24 weeks."( Efficacy and safety of systemic treatments in psoriatic arthritis: a systematic review, meta-analysis and GRADE evaluation.
Dressler, C; Eisert, L; Nast, A; Pham, PA, 2019
)
0.51
" Adverse events were reported in 58 (62%) of 93 patients in the upadacitinib group versus 52 (55%) of 94 in the placebo group."( Efficacy and safety of upadacitinib in patients with active ankylosing spondylitis (SELECT-AXIS 1): a multicentre, randomised, double-blind, placebo-controlled, phase 2/3 trial.
Chu, AD; Deodhar, A; Everding, A; Kim, TH; Kishimoto, M; Maksymowych, WP; Pangan, AL; Sieper, J; Song, IH; Sui, Y; van den Bosch, F; van der Heijde, D; Wang, X, 2019
)
0.51
" Secondary outcomes will include the incremental cost per reducing 1 case of relapse; patient reported intolerance to the treatment; adverse events; change of mean disease activity measured by DAS28, clinical disease activity index (CDAI) and simplified disease activity index (SDAI); the proportion of modified Sharp score increase < 0."( The efficacy, safety and cost-effectiveness of hydroxychloroquine, sulfasalazine, methotrexate triple therapy in preventing relapse among patients with rheumatoid arthritis achieving clinical remission or low disease activity: the study protocol of a rand
Ji, P; Wu, Y; Yan, X; Yang, L; Zhang, Z; Zhao, J; Zhou, W, 2021
)
0.86
" Adverse event rates were similar (QCHS granules 38."( Randomised clinical trial: Efficacy and safety of Qing-Chang-Hua-Shi granules in a multicenter, randomized, and double-blind clinical trial of patients with moderately active ulcerative colitis.
Chen, S; Chen, Y; Cheng, J; Gu, P; Gu, Q; Hu, J; Ke, X; Liu, Y; Ren, S; Shen, H; Shen, Z; Tang, Z; Xie, J; Zhang, L; Zhang, S; Zhao, W; Zheng, K; Zhu, L; Zou, J, 2021
)
0.62
" Safety was evaluated from treatment-emergent adverse events (TEAEs)."( Efficacy and safety of tildrakizumab in patients with active psoriatic arthritis: results of a randomised, double-blind, placebo-controlled, multiple-dose, 52-week phase IIb study.
Chohan, S; Chou, RC; Fructuoso, FJG; Gottlieb, A; Luggen, ME; Mease, PJ; Mendelsohn, AM; Rahman, P; Raychaudhuri, SP; Rozzo, SJ, 2021
)
0.62
" Four (8%) developed nonserious adverse reactions and switched to 5-aminosalicylates (5-ASA) by 1 year."( Efficacy and Safety of Sulfasalazine Suspension in Children With Ulcerative Colitis.
Bousvaros, A; Chan, C; Liu, E; Mansuri, I; Rufo, PA; Wang, S, 2023
)
1.22
"SZ suspension is a safe and effective treatment for UC in children with difficulty swallowing a pill."( Efficacy and Safety of Sulfasalazine Suspension in Children With Ulcerative Colitis.
Bousvaros, A; Chan, C; Liu, E; Mansuri, I; Rufo, PA; Wang, S, 2023
)
1.22

Pharmacokinetics

The pharmacokinetic disposition of sulfasalazine and its metabolites was studied in 8 young and 12 elderly patients with active rheumatoid arthritis. Negligible release of drug upto 5h and delayed Tmax in case of guar-gum coated sulf asalazine spheroids with or without probiotics clearly indicated successful formulation of colon targeted spheroid.

ExcerptReferenceRelevance
"The pharmacokinetic disposition of sulfasalazine and its metabolites was studied in 8 young and 12 elderly patients with active rheumatoid arthritis."( The effect of age and acetylator phenotype on the pharmacokinetics of sulfasalazine in patients with rheumatoid arthritis.
McDermott, BJ; Roberts, SD; Taggart, AJ, 1992
)
0.79
" Sulphasalazine itself is poorly absorbed (3 to 12%) and its elimination half-life of about 5 to 10 hours is probably affected by the absorption process."( Clinical pharmacokinetics of sulphasalazine, its metabolites and other prodrugs of 5-aminosalicylic acid.
Klotz, U,
)
0.13
" The elimination half-life of sulphasalazine was prolonged in the elderly whilst renal clearance was increased in slow acetylators at 'steady-state'."( The pharmacokinetics of sulphasalazine in young and elderly patients with rheumatoid arthritis.
Ahnfelt, NO; Delargy, M; Elborn, S; Forbes, J; McDermott, B; Roberts, SD; Taggart, AJ, 1987
)
0.27
" Pharmacokinetic factors may partially explain these clinical observations."( Clinical pharmacokinetics of slow-acting antirheumatic drugs.
Tett, SE, 1993
)
0.29
" Coadministration of zileuton did not significantly affect the area under the plasma concentration-time curve, the maximum (Cmax) or minimum (Cmin) plasma concentration and the time to Cmax of SASP, SP or ASP."( The influence of multiple oral doses of zileuton on the steady-state pharmacokinetics of sulfasalazine and its metabolites, sulfapyridine and N-acetylsulfapyridine.
Awni, WM; Braeckman, RA; Dubé, LM; Granneman, GR; Locke, CS, 1995
)
0.51
" The influence of sulphasalazine (SASP) on the pharmacokinetics of low dose methotrexate (MTX) and the relation between pharmacokinetic variables and clinical response was studied in 15 patients with active rheumatoid arthritis despite > 6 months of SASP treatment."( Combination of methotrexate and sulphasalazine in patients with rheumatoid arthritis: pharmacokinetic analysis and relationship to clinical response.
Haagsma, CJ; Russel, FG; Van de Putte, LB; Van Riel, PL; Vree, TB, 1996
)
0.29
", a three-compartment pharmacokinetic model, including biliary excretion, and an indirect mechanistically based pharmacodynamic model."( Pharmacokinetic-pharmacodynamic modeling of the immunomodulating agent susalimod and experimentally induced tumor necrosis factor-alpha levels in the mouse.
Gozzi, P; Grönberg, A; Påhlman, I; Palmér, L; Persson, S, 1999
)
0.3
"A pharmacokinetic model of colon-specific drug delivery developed in a previous study has been validated by use of 5-aminosalicylic acid (5-ASA) as a model anti-inflammatory drug."( Validation of a pharmacokinetic model of colon-specific drug delivery and the therapeutic effects of chitosan capsules containing 5-aminosalicylic acid on 2,4,6-trinitrobenzenesulphonic acid-induced colitis in rats.
Fujita, T; Muranishi, S; Odoriba, T; Okabe, S; Terabe, A; Tozaki, H; Yamamoto, A, 1999
)
0.3
" We investigated the effects of genetic polymorphism of NAT2 on pharmacokinetic profiles of SASP and its two metabolites, sulfapyridine (SP) and N-acetylsufapyridine (AcSP)."( Effects of NAT2 polymorphism on SASP pharmacokinetics in Chinese population.
Cao, XM; Li, JH; Liu, CG; Ma, JJ; Sun, SL; Yao, X, 2009
)
0.35
" After taking 1000mg SASP tablets, the plasma concentrations of SASP, SP and AcSP were measured with HPLC method and pharmacokinetic parameters were calculated by using the computing program 3P97."( Effects of NAT2 polymorphism on SASP pharmacokinetics in Chinese population.
Cao, XM; Li, JH; Liu, CG; Ma, JJ; Sun, SL; Yao, X, 2009
)
0.35
"The AUC(0)(-)(72) and Cmax of SP in m/m subjects were significantly higher than those in w/m and w/w subjects, with the values of 172."( Effects of NAT2 polymorphism on SASP pharmacokinetics in Chinese population.
Cao, XM; Li, JH; Liu, CG; Ma, JJ; Sun, SL; Yao, X, 2009
)
0.35
"Transporter gene knockout rats are practically advantageous over murine models for pharmacokinetic and excretion studies, but their phenotypic characterization is lacking."( Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
Bao, JQ; Bedwell, DW; Higgins, JW; Zamek-Gliszczynski, MJ, 2012
)
0.6
"This study was designed to characterize breast cancer resistance protein (Bcrp) knockout Abcg2(-/-) rats and assess the effect of ATP-binding cassette subfamily G member 2 (Abcg2) deletion on the excretion and pharmacokinetic properties of probe substrates."( Deletion of Abcg2 has differential effects on excretion and pharmacokinetics of probe substrates in rats.
Be, X; Colletti, AE; Huang, L; Jin, L; Langley, M; Ling, Y; Roberts, J; Tchaparian, EH; Wong, BK, 2012
)
0.38
"This study deciphers the pharmacokinetic parameters of guar gum based colon targeted spheroids of sulfasalazine with co-administration of probiotics in experimental rats."( In-vitro and In-vivo Pharmacokinetic Evaluation of Guar Gum-Eudragit® S100 Based Colon-targeted Spheroids of Sulfasalazine Co-administered with Probiotics.
Bawa, P; Ghai, D; Gulati, M; Kumar, B; Maharshi, P; Malik, AH; Mohanta, S; Pandey, NK; Rajesh, SY; Rathee, H; Sharma, A; Sharma, P; Singh, SK; Vaidya, Y; Yadav, AK, 2018
)
0.91
" Negligible release of drug upto 5h and delayed Tmax in case of guar-gum coated sulfasalazine spheroids with or without probiotics clearly indicated successful formulation of colon targeted spheroids."( In-vitro and In-vivo Pharmacokinetic Evaluation of Guar Gum-Eudragit® S100 Based Colon-targeted Spheroids of Sulfasalazine Co-administered with Probiotics.
Bawa, P; Ghai, D; Gulati, M; Kumar, B; Maharshi, P; Malik, AH; Mohanta, S; Pandey, NK; Rajesh, SY; Rathee, H; Sharma, A; Sharma, P; Singh, SK; Vaidya, Y; Yadav, AK, 2018
)
0.92
" This is the first report on pharmacokinetic study of a colon targeted delivery system co-administered with probiotics."( In-vitro and In-vivo Pharmacokinetic Evaluation of Guar Gum-Eudragit® S100 Based Colon-targeted Spheroids of Sulfasalazine Co-administered with Probiotics.
Bawa, P; Ghai, D; Gulati, M; Kumar, B; Maharshi, P; Malik, AH; Mohanta, S; Pandey, NK; Rajesh, SY; Rathee, H; Sharma, A; Sharma, P; Singh, SK; Vaidya, Y; Yadav, AK, 2018
)
0.69

Compound-Compound Interactions

To evaluate the efficacy and adverse reaction of total glucosides of paeony (TGP) combined with sulfasalazine (SSZ) in the treatment of ankylosing spondylitis (AS) To assess the therapeutic effect of ozone therapy combined with Sulfasalazines (SASP) for patients with ulcerative colitis (UC)

ExcerptReferenceRelevance
" Treatment with MTX alone (n = 12) or combined with SASP (n = 14), resulted in significant reductions of circulating IL-6 and sIL-2R but did not alter IL-1 beta, TNF alpha or IL-1RA concentrations."( Effect of methotrexate alone or in combination with sulphasalazine on the production and circulating concentrations of cytokines and their antagonists. Longitudinal evaluation in patients with rheumatoid arthritis.
Barrera, P; Boerbooms, AM; Borm, GF; Haagsma, CJ; Van de Putte, LB; Van der Meer, JW; Van Riel, PL, 1995
)
0.29
" In this study we determined the activity and toxicity of melphalan in combination with another GST-activity inhibitor, sulfasalazine, an agent used to treat ulcerative colitis."( Activity of melphalan in combination with the glutathione transferase inhibitor sulfasalazine.
Awasthi, S; Awasthi, YC; Fields, L; Gupta, V; Jacobs, S; Jani, JP; Levitt, M; Singh, SV; Sreevardhan, M; Xu, BH, 1995
)
0.73
" Open non-randomised uncontrolled studies have shown that antimalarials combined with cytotoxic agents are effective but highly toxic."( The use of antimalarials in combination with other disease modifying agents in RA--the British experience.
Capell, HA; Duncan, MR, 1996
)
0.29
"To prospectively determine the efficacy and safety of etanercept in combination with sulfasalazine (SSZ), hydroxychloroquine (HCQ), and gold in the treatment of rheumatoid arthritis (RA)."( Etanercept in combination with sulfasalazine, hydroxychloroquine, or gold in the treatment of rheumatoid arthritis.
Blakely, K; Fernandez, A; Haire, C; Leff, R; O'Dell, JR; Palmer, W; Petersen, K; Schned, E, 2006
)
0.84
"This study is the first to prospectively evaluate the safety of etanercept in combination with SSZ, HCQ, and gold in patients with RA."( Etanercept in combination with sulfasalazine, hydroxychloroquine, or gold in the treatment of rheumatoid arthritis.
Blakely, K; Fernandez, A; Haire, C; Leff, R; O'Dell, JR; Palmer, W; Petersen, K; Schned, E, 2006
)
0.62
"To evaluate the efficacy and adverse reaction of total glucosides of paeony (TGP) combined with sulfasalazine (SSZ) in the treatment of ankylosing spondylitis (AS)."( [Clinical observation on total glucosides of paeony combined with sulfasalazine in treatment of ankylosing spondylitis].
Bian, H; Wang, JP; Wang, SL, 2007
)
0.79
"TGP treatment combined with SSZ shows favorable effect on AS with less and milder adverse reaction."( [Clinical observation on total glucosides of paeony combined with sulfasalazine in treatment of ankylosing spondylitis].
Bian, H; Wang, JP; Wang, SL, 2007
)
0.58
"The study showed that green tea alone and in combination with sulfasalazine reduced inflammatory changes induced by tri nitro benzene sulfonic acid in rats."( Comparative evaluation of different doses of green tea extract alone and in combination with sulfasalazine in experimentally induced inflammatory bowel disease in rats.
Byrav, DS; Chakrabarti, A; Khanduja, KL; Medhi, B; Vaiphei, K, 2011
)
0.83
"To assess the therapeutic effect of ozone therapy combined with sulfasalazine sulfasalazine delivered via a colon therapy system in the treatment of distal ulcerative colitis."( [Ozone therapy combined with sulfasalazine delivered via a colon therapy system for treatment of ulcerative colitis].
Geng, Y; Liang, ZH; Ma, Q; Peng, LQ; Wang, W, 2010
)
0.89
"Ozone therapy combined with sulfasalazine delivered via a colon therapy system is feasible and effective for treatment of ulcerative colitis."( [Ozone therapy combined with sulfasalazine delivered via a colon therapy system for treatment of ulcerative colitis].
Geng, Y; Liang, ZH; Ma, Q; Peng, LQ; Wang, W, 2010
)
0.95
" Since clinical efficacy studies in rheumatoid arthritis are conducted on a background of methotrexate therapy, it is necessary to assess the potential of rheumatoid arthritis candidate drugs to perpetrate a drug-drug interaction (DDI) with methotrexate during development."( In vitro risk assessment of AZD9056 perpetrating a transporter-mediated drug-drug interaction with methotrexate.
Butters, C; Elsby, R; Fox, L; Layton, M; Sharma, P; Smith, V; Stresser, D; Surry, D, 2011
)
0.37
"The hepatic organic anion transporting polypeptides (OATPs) influence the pharmacokinetics of several drug classes and are involved in many clinical drug-drug interactions."( Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
Artursson, P; Haglund, U; Karlgren, M; Kimoto, E; Lai, Y; Norinder, U; Vildhede, A; Wisniewski, JR, 2012
)
0.38
" The underlying mechanism for TL-118-treatment success was associated with hepatic perfusion attenuation resulting from reduced nitric-oxide (NO) serum levels as elucidated by using hemodynamic response imaging (HRI, a functional MRI combined with hypercapnia and hyperoxia)."( Improved efficacy of a novel anti-angiogenic drug combination (TL-118) against colorectal-cancer liver metastases; MRI monitoring in mice.
Abramovitch, R; Corchia, N; Edrei, Y; Gross, E, 2012
)
0.38
" The present study aimed to investigate the effect of different doses of pioglitazone alone and in combination with sulfasalazine in TNBS (trinitrobenzenesulfonic acid)-induced inflammatory bowel disease (IBD) in rats."( Comparative evaluation of different doses of PPAR-γ agonist alone and in combination with sulfasalazine in experimentally induced inflammatory bowel disease in rats.
Byrav D S, P; Chakrabarti, A; Khanduja, KL; Medhi, B; Prakash, A; Vaiphei, K, 2013
)
0.82
"To observe the clinical effect and safety of Sulfasalazine (SASP) combined with ZHUANG medicine mediated thread moxibustion (ZMMTM) for patients with mild and moderate ulcerative colitis (UC)."( [Observation on clinical effect of ZHUANG medicine mediated thread moxibustion combined with medication for patients with ulcerative colitis].
Chen, LS; Li, XN; Long, JX; Zhang, LC; Zhang, S; Zhong, W, 2013
)
0.65
"A total of 46 UC patients were randomly and equally divided into moxibustion group (SASP combined with ZMMTM) and SASP medication group."( [Observation on clinical effect of ZHUANG medicine mediated thread moxibustion combined with medication for patients with ulcerative colitis].
Chen, LS; Li, XN; Long, JX; Zhang, LC; Zhang, S; Zhong, W, 2013
)
0.39
"ZMMTM combined with medication is significantly superior to simple medication in relieving clinical symptoms of mild and moderate UC patients."( [Observation on clinical effect of ZHUANG medicine mediated thread moxibustion combined with medication for patients with ulcerative colitis].
Chen, LS; Li, XN; Long, JX; Zhang, LC; Zhang, S; Zhong, W, 2013
)
0.39
" TL-118, a novel drug combination has been recently developed to inhibit tumor angiogenesis."( TL-118 and gemcitabine drug combination display therapeutic efficacy in a MYCN amplified orthotopic neuroblastoma murine model--evaluation by MRI.
Abramovitch, R; Corchia, N; Dery, E; Fried, I; Gross, E; Komar-Stossel, C; Meir, K, 2014
)
0.4
"The aim of this study was to evaluate the effect of treatment with methotrexate (MTX), by itself or combined with other non-biological disease-modifying antirheumatic drugs (DMARDs) (methotrexate, MTX with prednisolone, MTX with leflunomide, MTX with chloroquine, and MTX with sulfasalazine) on clinimetric outcomes in a retrospective cohort with a 6-month follow-up and under a Treat to Target (T2T) approach."( Treatment of rheumatoid arthritis with methotrexate alone and in combination with other conventional DMARDs using the T2T strategy. A cohort study.
Castro, C; de la Hoz-Valle, J; Palomino, A; Sánchez, G; Santos-Moreno, PI; Villarreal, L, 2015
)
0.59
"To evaluate the efficacy and safety of orally administered once-daily peficitinib in combination with limited conventional synthetic disease-modifying antirheumatic drugs (csDMARDs) in patients with moderate-to-severe rheumatoid arthritis (RA)."( Peficitinib, a JAK Inhibitor, in Combination With Limited Conventional Synthetic Disease-Modifying Antirheumatic Drugs in the Treatment of Moderate-to-Severe Rheumatoid Arthritis.
Cardiel, MH; Codding, C; Garg, JP; Genovese, MC; Greenwald, M; Kivitz, AJ; Shay, K; Wang, A; Wang, X; Zubrzycka-Sienkiewicz, A, 2017
)
0.46
"In patients with moderate-to-severe RA, orally administered once-daily peficitinib in combination with limited csDMARDs resulted in a dose-dependent ACR20 response rate over 12 weeks with satisfactory tolerability."( Peficitinib, a JAK Inhibitor, in Combination With Limited Conventional Synthetic Disease-Modifying Antirheumatic Drugs in the Treatment of Moderate-to-Severe Rheumatoid Arthritis.
Cardiel, MH; Codding, C; Garg, JP; Genovese, MC; Greenwald, M; Kivitz, AJ; Shay, K; Wang, A; Wang, X; Zubrzycka-Sienkiewicz, A, 2017
)
0.46
" Chemotherapy-naïve patients with advanced non-squamous non-small-cell lung cancer were enrolled in a dose-escalation study (standard 3 + 3 design) of SASP in combination with cisplatin and pemetrexed."( Phase I study of salazosulfapyridine in combination with cisplatin and pemetrexed for advanced non-small-cell lung cancer.
Fujita, A; Harada, T; Hirai, F; Imamura, CK; Inada, M; Iwama, E; Kishimoto, J; Mushiroda, T; Nagano, O; Nakanishi, Y; Nosaki, K; Ogata, H; Okamoto, I; Otsubo, K; Ozeki, T; Sakata, S; Saya, H; Seto, T; Suina, K; Takenoyama, M; Toyokawa, G; Tsuchihashi, K, 2017
)
0.46
"Transporter-mediated drug-drug interactions (DDI) may induce adverse clinical events."( Inhibition and stimulation of the human breast cancer resistance protein as in vitro predictor of drug-drug interactions of drugs of abuse.
Maurer, HH; Meyer, MR; Wagmann, L, 2018
)
0.48
"To investigate the influences of probiotics combined with sulfasalazine (SASP) on the expression of the Wnt/β-catenin signaling pathway in rats with ulcerative colitis (UC)."( Influences of probiotics combined with sulfasalazine on rats with ulcerative colitis via the Wnt/β-catenin signaling pathway.
Dong, LN; Guo, J; Wang, JP; Wang, M, 2019
)
1.03
"We present a case of a patient with drug-induced hypersensitivity syndrome (DIHS) caused by salazosulfapyridine combined with syndrome of inappropriate secretion of antidiuretic hormone (SIADH) caused by interstitial pneumonia (IP)."( A case of drug-induced hypersensitivity syndrome induced by salazosulfapyridine combined with SIADH caused by interstitial pneumonia.
Abe, I; Hanada, H; Higashi, T; Inoue, R; Kurihara, K; Minamikawa, T; Mitsutake, T; Morinaga, Y; Nii, K; Sakamoto, K; Tsugawa, J; Ueda, Y, 2019
)
0.51
"Twenty-four patients with cold, dampness, obstructive ankylosing spondylitis were treated with sulfasalazine and sulfasalazine in combination with moxibustion for 3 weeks."( Effects of sulfasalazine combined with moxibustion methods on patients with cold-dampness obstruction type ankylosing spondylitis.
Liao, WJ; Liu, HF; Song, FJ, 2020
)
1.17

Bioavailability

When administered orally, sulfasalazine is poorly absorbed with an estimated bioavailability of 3-12%. Based on studies in wild type and abcg2-/- mice, we observed that oral curcumin increased Cmax and relative bioavailability.

ExcerptReferenceRelevance
" These changes suggest interference with the bioavailability of digoxin by SSA."( Effect of sulfasalazine on digoxin bioavailability.
Blaug, SM; Brown, DD; Cheng, FH; Guillory, JK; Juhl, RP; Summers, RW, 1976
)
0.66
" The present study aims at comparing bioavailability of salicylazosulfapyridine following oral and rectal administration to patients with the ulcerative colitis and healthy volunteers."( [Comparison of salicylazosulfapyridine bioavailability following oral and rectal administration in patients with ulcerative colitis].
Sliwiński, Z,
)
0.13
" There was a good correlation between MATAAP and the extent of bioavailability of chlorothiazide, however, there was no correlation between TFASP and the extent of bioavailability of the drug."( Gastrointestinal absorption of chlorothiazide: evaluation of a method using salicylazosulfapyridine and acetaminophen as the marker compounds for determination of the gastrointestinal transit time in the dog.
Kawazoe, Y; Mizuta, H; Ogawa, K, 1990
)
0.28
" Sulphasalazine itself is poorly absorbed (3 to 12%) and its elimination half-life of about 5 to 10 hours is probably affected by the absorption process."( Clinical pharmacokinetics of sulphasalazine, its metabolites and other prodrugs of 5-aminosalicylic acid.
Klotz, U,
)
0.13
" The results also suggest a role for human milk FBP in regulating the nutritional bioavailability of folate."( Effect of human milk folate binding protein on folate intestinal transport.
Horne, DW; Said, HM; Wagner, C, 1986
)
0.27
" 2 SASP is poorly absorbed (less than 12%) and the half-time measured in the serum, 10."( The disposition and metabolism of sulphasalazine (salicylazosulphapyridine) in man.
Aronson, JK; Azadkhan, AK; Truelove, SC, 1982
)
0.26
" There is no change in the rate of absorption of the release sulphapyridine."( Azo reduction of sulphasalazine in healthy volunteers.
Day, J; Houston, JB; Walker, J, 1982
)
0.26
" Its bioavailability is variable and may decrease by as much as 70% in the presence of food, antacids and iron salts."( Clinical pharmacokinetics of slow-acting antirheumatic drugs.
Tett, SE, 1993
)
0.29
" In both sexes, the absolute oral bioavailability of SASP ranged between 16."( Toxicokinetics of sulfasalazine (salicylazosulfapyridine) and its metabolites in B6C3F1 mice.
Bishop, JB; Mayersohn, M; Sipes, IG; Winter, SM; Zheng, W,
)
0.47
"The bioavailability of a controlled release 5-aminosalicyclic acid preparation (Pentasa) was investigated in nine healthy children after a medication period of six days (1000 mg/day) and compared with sulfasalazine (Salazopyrin) (2000 mg/day)."( Bioavailability of 5-aminosalicyclic acid from slow release 5-aminosalicyclic acid drug and sulfasalazine in normal children.
Abildgaard, K; Christensen, LA; Fallingborg, J; Hansen, SH; Jacobsen, BA; Rasmussen, HH; Rasmussen, SN, 1993
)
0.69
" The new methodology may, therefore, be used for fast bioavailability screening of virtual libraries having millions of molecules."( Fast calculation of molecular polar surface area as a sum of fragment-based contributions and its application to the prediction of drug transport properties.
Ertl, P; Rohde, B; Selzer, P, 2000
)
0.31
" Salazopyrin is variably and comparatively poorly absorbed in man."( Salicylazosulfapyridine (salazopyrin or azopyrin) in rheumatoid arthritis and experimental polyarthritis.
GARDNER, GM; KUZELL, WC, 1950
)
0.23
" When administered orally, sulfasalazine is poorly absorbed with an estimated bioavailability of 3-12%."( Breast cancer resistance protein (Bcrp/abcg2) is a major determinant of sulfasalazine absorption and elimination in the mouse.
Brayman, TG; Khan, AA; Palandra, J; Ware, JA; Yu, L; Zaher, H,
)
0.66
" Based on studies in wild type and abcg2-/- mice, we observed that oral curcumin increased Cmax and relative bioavailability of sulfasalazine by selectively inhibiting ABCG2 function."( Curcumin inhibits the activity of ABCG2/BCRP1, a multidrug resistance-linked ABC drug transporter in mice.
Ambudkar, SV; Bauer, B; Hartz, A; Shukla, S; Ware, JA; Zaher, H, 2009
)
0.56
"In two bioavailability studies performed under comparable conditions with 24 healthy subjects of both genders equally distributed, plasma levels of SP and acetylsulfapyridine (Ac-SP) were determined after oral intake of enteric coated formulations of sulfasalazine (500 mg and 1,000 mg, respectively)."( Phenotyping with sulfasalazine - time dependence and relation to NAT2 pharmacogenetics.
Anschütz, M; Blume, HH; Hippius, M; Kuhn, UD; Schmücker, K; Schug, BS, 2010
)
0.88
"Oral bioavailability (F) is a product of fraction absorbed (Fa), fraction escaping gut-wall elimination (Fg), and fraction escaping hepatic elimination (Fh)."( Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
Chang, G; El-Kattan, A; Miller, HR; Obach, RS; Rotter, C; Steyn, SJ; Troutman, MD; Varma, MV, 2010
)
0.36
"BACKGROUND AND PURPOSE An ATP-binding cassette (ABC) transporter, breast cancer resistance protein (BCRP)/ABCG2, limits oral bioavailability of sulphasalazine."( Pharmacokinetic interaction study of sulphasalazine in healthy subjects and the impact of curcumin as an in vivo inhibitor of BCRP.
Fujita, T; Fukizawa, S; Furuie, H; Ieiri, I; Inano, A; Kusuhara, H; Maeda, K; Mayahara, H; Morimoto, N; Morishita, M; Sugiyama, Y; Sumita, K; Sunagawa, A; Wu, C; Yamada, S, 2012
)
0.38
" In Mdr1a knockout rats, loperamide and paclitaxel oral bioavailability was 2- and 4-fold increased, respectively, whereas clearance was significantly reduced (40-42%), consistent with the expected 10- to 20-fold reduction in paclitaxel excretion."( Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
Bao, JQ; Bedwell, DW; Higgins, JW; Zamek-Gliszczynski, MJ, 2012
)
0.6
" This experimental system is useful for clarifying the cause of low bioavailability of various drugs."( In vivo assessment of the impact of efflux transporter on oral drug absorption using portal vein-cannulated rats.
Hashimoto, T; Konno, Y; Matsuda, Y; Nagai, M; Satsukawa, M; Taguchi, T; Yamashita, S, 2013
)
0.39
"In mice, the bioavailability changes, which corrected the effect of systemic clearance by Bcrp knockout, correlated well with the AUC changes in humans, whereas the correlation was weak when AUC changes were directly compared."( Evaluation of the usefulness of breast cancer resistance protein (BCRP) knockout mice and BCRP inhibitor-treated monkeys to estimate the clinical impact of BCRP modulation on the pharmacokinetics of BCRP substrates.
Abe, K; Hagihara-Nakagomi, R; Hirouchi, M; Imaoka, T; Izumi, T; Karibe, T; Mikkaichi, T; Okudaira, N; Watanabe, N; Yasuda, S, 2015
)
0.42
"This study suggests that pharmacokinetics studies that use the correction of the bioavailability changes in Bcrp knockout mice are effective for estimating clinical AUC changes in ABCG2 421C>A variants for BCRP substrate drugs and those studies in monkeys that use a BCRP inhibitor serve for the assessment of BCRP impact on the gastrointestinal absorption in a non-rodent model."( Evaluation of the usefulness of breast cancer resistance protein (BCRP) knockout mice and BCRP inhibitor-treated monkeys to estimate the clinical impact of BCRP modulation on the pharmacokinetics of BCRP substrates.
Abe, K; Hagihara-Nakagomi, R; Hirouchi, M; Imaoka, T; Izumi, T; Karibe, T; Mikkaichi, T; Okudaira, N; Watanabe, N; Yasuda, S, 2015
)
0.42
"The purpose was to propose two-stage single-compartment models for evaluating dissolution characteristics in distal ileum and ascending colon, under conditions simulating the bioavailability and bioequivalence studies in fasted and fed state by using the mini-paddle and the compendial flow-through apparatus (closed-loop mode)."( Two-Stage Single-Compartment Models to Evaluate Dissolution in the Lower Intestine.
Kesisoglou, F; Markopoulos, C; Reppas, C; Symillides, M; Vertzoni, M, 2015
)
0.42
" The multi-layered enteric polymer coating could potentially protect nanoparticle dissolution at gastric pH and accelerate the dissolution velocity, which would improve the drug bioavailability in the colon."( Multi-laminated metal hydroxide nanocontainers for oral-specific delivery for bioavailability improvement and treatment of inflammatory paw edema in mice.
Deng, JP; Jeng, CC; Kankala, RK; Kankala, S; Kuthati, Y; Lee, CH; Liu, CL; Lue, SI; Shih, HY; Sie, HW; Weng, CF, 2015
)
0.42
" Methotrexate has better bioavailability as injection."( [Update on Current Care Guidelines. Rheumatoid Arthritis (RA)].
, 2015
)
0.42
" Based on computational values, LLW-3-6 has physiochemical characteristics that should allow for improved bioavailability in comparison to that of celecoxib."( Celecoxib and LLW-3-6 Reduce Survival of Human Glioma Cells Independently and Synergistically with Sulfasalazine.
Winfield, LL; Yerokun, T, 2015
)
0.63
" Oral area under the plasma concentration-time curve (AUC) and bioavailability of well known BCRP (sulfasalazine and rosuvastatin), P-glycoprotein (fexofenadine, aliskiren, and talinolol), and CYP3A (midazolam) substrates were investigated in the presence and absence of inhibitors."( Curcumin as an In Vivo Selective Intestinal Breast Cancer Resistance Protein Inhibitor in Cynomolgus Monkeys.
Abe, K; Ando, O; Imaoka, T; Karibe, T, 2018
)
0.7
"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
" Although intrathecal injection of SSZ to nerve-injured mice significantly alleviated mechanical pain hypersensitivity, no significant anti- neuropathic pain effects of SSZ were detected after oral administration due to its low bioavailability and limited spinal distribution, which were associated with efflux by the xenobiotic transporter breast cancer resistance protein (BCRP)."( Sulfasalazine alleviates neuropathic pain hypersensitivity in mice through inhibition of SGK-1 in the spinal cord.
Koyanagi, S; Kusunose, N; Matsunaga, N; Ohdo, S; Yasukochi, S, 2021
)
2.06

Dosage Studied

The correlation between the NAT2 genotype and the pharmacokinetics of SP after multiple oral dosing of sulfasalazine (SASP) was examined to elucidate the effect of multiple dosing on the predictability of the phenotype. Trials were separated into five comparison groups.

ExcerptRelevanceReference
" During therapy with sulphasalazine, determination of acetylator phenotype and total sulphapyridine concentration can guide effective dosage and avoid side-effects."( Clinical pharmacokinetics of sulphasalazine.
Das, KM; Dubin, R,
)
0.13
" A single study of serum can determine acetylator phenotype in patients on sulfasalazine therapy without using any other drug for this purpose and may help ascertain dosage and assess side effects."( Acetylation polymorphism of sulfapyridine in patients with ulcerative colitis and Crohn's disease.
Das, KM; Eastwood, MA, 1975
)
0.48
"A high-speed liquid chromatographic method for analysis of sulfasalazine (salicylazosulfapyridine) in bulk powder and tablet dosage form is presented."( High-speed liquid chromatographic analysis of sulfasalazine (salicylazosulfapyridine).
Bighley, LD; McDonnell, JP, 1975
)
0.76
" Moreover, 1 drug should be used in appropriate dosage before it is assumed to be inefficient."( Ankylosing spondylitis. Current drug treatment.
Gran, JT; Husby, G, 1992
)
0.28
"One hundred and fifty patients with rheumatoid arthritis were given sulfasalazine in a daily dosage of 2 g during an open-label, multicenter, six-month trial."( [Sulfasalazine in the treatment of rheumatoid arthritis. A multicenter open study of 150 patients during 6 months].
, 1992
)
1.43
" All patients received a daily dose of 6-mercaptopurine of 50 mg; in two pediatric patients with a poor response after 2 months, the dosage was increased to 75 mg/day."( 6-mercaptopurine therapy in selected cases of corticosteroid-dependent Crohn's disease.
Greseth, JL; Perrault, J; Tremaine, WJ, 1991
)
0.28
" It was found, that following rectal administration the drug is not so readily absorbed as in oral dosage form."( [Comparison of salicylazosulfapyridine bioavailability following oral and rectal administration in patients with ulcerative colitis].
Sliwiński, Z,
)
0.13
" A reliable lengthened dosage interval is therefore possible with this particular sustained--release formulation."( Fraction of theophylline in sustained-release formulation which is absorbed from the large bowel.
Meyer, EC; Moncrieff, J; Sommers, DK; van Wyk, M, 1990
)
0.28
" We therefore assessed small intestinal and joint inflammation in patients with rheumatoid arthritis before and after three to nine months' treatment with sulphasalazine (n = 40) and other second line drugs (n = 20), while keeping the dosage of non-steroidal anti-inflammatory drug at the same level."( Treatment of non-steroidal anti-inflammatory drug induced enteropathy.
Bjarnason, I; Gumpel, JM; Hopkinson, N; Levi, AJ; Prouse, P; Smethurst, P; Zanelli, G, 1990
)
0.28
" Our data suggest that both the route of drug administration and dosing regimen employed affect the antiinflammatory potency and/or efficacy of compounds on colitis induced by acetic acid in the rat."( Antiinflammatory effects of various drugs on acetic acid induced colitis in the rat.
Bostwick, JS; Decktor, DL; Fitzpatrick, LR; Pendleton, RG; Renzetti, M, 1990
)
0.28
" In these patients, there was also a diminution of the daily dosage of nonsteroidal antiinflammatory drugs."( [Sulfasalazine in the treatment of ankylosing spondylitis].
Krajnc, I,
)
1.04
" In all 3 patients who had previously taken methotrexate, we were able to reduce the dosage, and the prednisone dosage was reduced in 2 of 3 patients who had previously taken that drug."( Combination methotrexate and sulfasalazine in the management of rheumatoid arthritis: case observations.
Neville, C; Shiroky, JB; Watts, CS, 1989
)
0.57
" The syndrome appears to be associated with high dosage and slow acetylator status."( Sulphasalazine associated pancytopenia may be caused by acute folate deficiency.
Logan, EC; Ryrie, DR; Williamson, LM, 1986
)
0.27
" When given in a dosage of 2g daily it will prevent relapses in quiescent colitis."( Sulphasalazine: a review of 40 years' experience.
Watkinson, G, 1986
)
0.27
" Despite the relationship between dose and efficacy and a good correlation between dose and serum concentrations of sulphasalazine and its metabolites, no relationship has been demonstrated between efficacy and serum concentrations of sulphasalazine or its metabolites, although there is some suggestion that higher concentrations on single dosing are achieved in patients who develop upper gastrointestinal symptoms."( Variables affecting efficacy and toxicity of sulphasalazine in rheumatoid arthritis. A review.
Capell, HA; Pullar, T, 1986
)
0.27
" Metronidazole and azathioprin are considered to be reserve drugs and can be used in the treatment of fistulae or in order to cut down the dosage of prednisolone during remission."( [Drug therapy of chronic inflammatory intestinal diseases--current status of 5-aminosalicylic acid].
Gerok, W; Schölmerich, J, 1986
)
0.27
" LST was negative before attempting desensitization and became positive when the dosage of SASP increased to 100 mg daily."( A case of salicylazosulfapyridine (Salazopyrin)-induced acute pancreatitis with positive lymphocyte stimulation test (LST).
Arakawa, H; Chiba, M; Horie, Y; Ishida, H; Masamune, O, 1987
)
0.27
"In an open, controlled study we treated 55 patients suffering of psoriatic arthritis (PsA), 29 patients suffering of Bechterew's disease (MB) and 16 patients with Reiter's syndrome with Salazopyrin at a daily dosage of 2000 mg."( [Therapy of seronegative oligoarthritis with salazopyrine].
Martini, M; Stroehmann, I; Wüstenhagen, E,
)
0.13
"The clinical pharmacokinetics of enteric-coated sulphasalazine (Salazopyrin-EN) were studied after acute and chronic dosing in 20 patients with 'active' rheumatoid arthritis."( The pharmacokinetics of sulphasalazine in young and elderly patients with rheumatoid arthritis.
Ahnfelt, NO; Delargy, M; Elborn, S; Forbes, J; McDermott, B; Roberts, SD; Taggart, AJ, 1987
)
0.27
" It prevents relapses, particularly if the dosage is increased."( Sulfasalazine: II. Some notes on the discovery and development of salazopyrin.
Svartz, N, 1988
)
1.72
"Although the incidence of side effects associated with sulfasalazine is in the range of 20%, most of the common side effects, including gastrointestinal reactions and headache, can be managed by dosage adjustment."( The safety of sulfasalazine: the gastroenterologists' experience.
Sachar, DB, 1988
)
0.88
" The aim of our work was to assess the levels of the drug in blood (SASP and SP), to correlate them with undesirable effects in any, to verify their fluctuations in the dosing interval and to investigate the extent of the excretion of the drug in the children who were studied."( [Ulcerative colitis in children. Levels of salicylazosulfapyridine and sulfapyridine during treatment].
Guastavino, E; Heffes Nahmod, L; Licastro, R; Litwin, NH, 1988
)
0.27
"Sulphasalazine (salicyl-azo-sulphapyridine) was ingested by 27 healthy subjects for five days at a dosage of 4 g daily."( Acetylator phenotype and adverse effects of sulphasalazine in healthy subjects.
Evans, DA; Schröder, H, 1972
)
0.25
" The drug was more effective than placebo in closing fistulas (31 vs 6%) and in permitting discontinuation or reduction of steroid dosage (75 vs."( Treatment of Crohn's disease with 6-mercaptopurine. A long-term, randomized, double-blind study.
Glass, JL; Korelitz, BI; Pasternack, BS; Present, DH; Sachar, DB; Wisch, N, 1980
)
0.26
" Haematological abnormalities were observed at all dosage levels, but they occurred chiefly among the patients on 4 g daily."( Optimum dose of sulphasalazine for maintenance treatment in ulcerative colitis.
Azad Khan, AK; Howes, DT; Piris, J; Truelove, SC, 1980
)
0.26
" In the fulminant form of the disease the highly dosed application of prednisolone with ease the highly dosed application of prednisolone with parenteral hypercaloric nutrition and the substitution of mineral, protein and blood losses are therapeutically in the first place."( [Ulcerative and granulomatous colitis].
Bosseckert, H, 1981
)
0.26
"Miniaturised methods have been used to construct dose-response curves for the effects of inhibitory drugs on prostaglandin synthesis using individual rectal biopsies obtained from patients with ulcerative colitis."( Inhibition of prostaglandin synthetase in human rectal mucosa.
Hawkey, CJ; Lo Casto, M, 1983
)
0.27
" A pharmacokinetic comparison of polymer and SASP showed similar deliveries of 5-ASA and metabolites to the lower bowel, blood, and urine of orally dosed rats."( A polymeric drug for treatment of inflammatory bowel disease.
Brown, JP; McGarraugh, GV; Onderdonk, AB; Parkinson, TM; Wingard, RE, 1983
)
0.27
" Plasma and urine concentrations of 5-AS and its acetylated major metabolite (AcAS) were monitored during one dosing interval."( Disposition of 5-aminosalicylic acid, the active metabolite of sulphasalazine, in man.
Fischer, C; Klotz, U; Maier, K; Stumpf, E; von Gaisberg, U, 1983
)
0.27
" The results showed that, although there were wide individual variations in levels after oral and rectal administration, with the same dosage the levels were far higher when the drug was given orally."( A comparison of serum concentrations of sulphasalazine and some of its metabolites after therapy by the oral or rectal route.
Arthur, M; Ashworth, M; Smith, PR; Turmer, AD, 1984
)
0.27
" The dose-response curve for the inhibition of binding was very similar to the dose-response curves for the inhibition of FMLP-induced neutrophil activation."( Sulfasalazine inhibition of binding of N-formyl-methionyl-leucyl-phenylalanine (FMLP) to its receptor on human neutrophils.
Mehta, J; Spilberg, I; Stenson, WF, 1984
)
1.71
" Feed was infused continuously via a nasoduodenal tube in a dosage of 2600-3200 kcal/day."( Is tube feeding with elemental diets a primary therapy of Crohn's disease?
Egger-Schödl, M; Lochs, H; Meryn, S; Pötzi, R; Schuh, R; Westphal, G, 1984
)
0.27
"Sulfasalazine, starting at 500 mg/day (with weekly incremental dosing to a total of 4 g), was administered to two patients with disabling pressure urticaria and angioedema (symptomatic daily with normal activities) who had failed all other reported therapeutic options except corticosteroids."( Chronic sulfasalazine therapy in the treatment of delayed pressure urticaria and angioedema.
Benson, P; Engler, RJ; Squire, E, 1995
)
2.17
" Twenty-three patients (17 boys and 6 girls) with juvenile spondyloarthropathy inadequately controlled by nonsteroidal antiinflammatory therapy were given sulfasalazine in an average dosage of 39 mg/kg/d."( [Treatment of juvenile spondyloarthropathies with sulfasalazine].
Job-Deslandre, C; Menkès, CJ,
)
0.58
" Consequently, sulfasalazine was given in a daily dosage of 2 grams."( [Beneficial effect of sulfasalazine in spondylarthropathy in 2 patients with HIV infection].
David, M; Mijiyawa, M,
)
0.8
" Differences found in the incidence of side effects among the various disease groups can probably be explained by patient selection, particularly with respect to age, proportion treated for the first time with sulphasalazine, and dosage used."( Rheumatoid arthritis: a risk factor for sulphasalazine toxicity? A meta-analysis.
Van 'T Hof, MA; Van De Putte, LB; Van Riel, PL; Wijnands, MJ, 1993
)
0.29
" The tissue level of 5-ASA had a significant correlation to the dosage of 5-ASA."( [Localization of salazopyrin in colonic mucosa patients with ulcerative colitis].
Fukushima, R; Kashima, K; Kitano, A; Nakagawa, M; Nakamura, S; Obayashi, M; Okabe, H; Tabata, A; Tomobuchi, M; Yasuda, K, 1993
)
0.29
" Four patients with connective tissue diseases were treated with salazopyrin in desensitisation doses, as management with full dosage had previously been followed by a skin rash."( [Salazopyrine desensitization].
Schydlowsky, P, 1993
)
0.29
" The latter were successfully treated with oral vancomycine, but in the last relapse an increased dosage of prednisone was required, too."( [Clostridium difficile in early childhood ulcerative pancolitis].
Hoppen, T; Keller, KM; Rister, M; Stolte, M, 1993
)
0.29
" Available evidence indicates that 5-aminosalicylic acid is beneficial in this role, although high dosage is needed."( Maintenance strategies in Crohn's disease.
Sachar, DB, 1996
)
0.29
" Four chemicals, using three different routes of exposure (in utero [accomplished by feeding the dam dosed feed], dosed feed, and gavage) were used to 1) evaluate the effect of diet restriction on the sensitivity of the bioassay toward chemically-induced chronic toxicity and carcinogenicity; and 2) evaluate the effect of weight-matched control groups on the sensitivity of the bioassays."( The sensitivity of the NTP bioassay for carcinogen hazard evaluation can be modulated by dietary restriction.
Abdo, KM; Kari, FW, 1996
)
0.29
"To determine whether sulfasalazine (SSZ) at a dosage of 2,000 mg/day is effective for the treatment of active ankylosing spondylitis (AS) that is not controlled with nonsteroidal antiinflammatory drug therapy."( Comparison of sulfasalazine and placebo in the treatment of ankylosing spondylitis. A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Blackburn, WD; Budiman-Mak, E; Buxbaum, J; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Luggen, ME; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Reda, DJ; Schumacher, HR; Silverman, SL; Taylor, T; Vasey, FB; Ward, JR; Ward, RH; Weisman, MH, 1996
)
0.97
"SSZ at a dosage of 2,000 mg/day does not seem to be more effective than placebo in the treatment of AS patients with chronic, longstanding disease."( Comparison of sulfasalazine and placebo in the treatment of ankylosing spondylitis. A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Blackburn, WD; Budiman-Mak, E; Buxbaum, J; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Luggen, ME; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Reda, DJ; Schumacher, HR; Silverman, SL; Taylor, T; Vasey, FB; Ward, JR; Ward, RH; Weisman, MH, 1996
)
0.65
"To determine whether sulfasalazine (SSZ) at a dosage of 2,000 mg/day is effective for the treatment of active psoriatic arthritis (PsA) resistant to nonsteroidal antiinflammatory drug therapy."( Comparison of sulfasalazine and placebo in the treatment of psoriatic arthritis. A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Blackburn, WD; Budiman-Mak, E; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Luggen, ME; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Reda, DJ; Schumacher, HR; Silverman, SL; Taylor, T; Vasey, FB; Ward, JR; Ward, RH; Weisman, MH, 1996
)
0.97
"SSZ at a dosage of 2,000 mg/day is well tolerated and may be more effective than placebo in the treatment of patients with PsA."( Comparison of sulfasalazine and placebo in the treatment of psoriatic arthritis. A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Blackburn, WD; Budiman-Mak, E; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Luggen, ME; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Reda, DJ; Schumacher, HR; Silverman, SL; Taylor, T; Vasey, FB; Ward, JR; Ward, RH; Weisman, MH, 1996
)
0.65
"To determine whether sulfasalazine (SSZ) at a dosage of 2,000 mg/day is effective in the treatment of reactive arthritis (ReA) that has been unresponsive to nonsteroidal antiinflammatory drug (NSAID) therapy."( Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome). A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Balestra, DJ; Blackburn, WD; Budiman-Mak, E; Buxbaum, J; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Higashida, J; Inman, RD; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Parhami, N; Reda, DJ; Schumacher, HR; Silverman, SL; Vasey, FB; Ward, RH; Weisman, MH, 1996
)
0.97
"SSZ at a dosage of 2,000 mg/day is well tolerated and effective in patients with chronically active ReA."( Comparison of sulfasalazine and placebo in the treatment of reactive arthritis (Reiter's syndrome). A Department of Veterans Affairs Cooperative Study.
Alepa, FP; Anderson, RJ; Balestra, DJ; Blackburn, WD; Budiman-Mak, E; Buxbaum, J; Cannon, GW; Clegg, DO; Cohen, MR; Cush, JJ; Haakenson, CM; Henderson, WG; Higashida, J; Inman, RD; Mahowald, ML; Makkena, R; Manaster, BJ; Mejias, E; Parhami, N; Reda, DJ; Schumacher, HR; Silverman, SL; Vasey, FB; Ward, RH; Weisman, MH, 1996
)
0.65
" There is no evidence that the dosage of drugs metabolized by the CYP3A4 isoenzyme needs to be adjusted for disease activity in RA."( Urinary 6 beta-hydroxycortisol excretion in rheumatoid arthritis.
Beyeler, C; Bird, HA; Frey, BM, 1997
)
0.3
" The optimal dosage of oral 5-ASA in the maintenance therapy of ulcerative colitis in remission is not clear."( Guidelines for the treatment of ulcerative colitis in remission.
Ardizzone, S; Bianchi Porro, G; Bollani, S; Molteni, P, 1997
)
0.3
" Although there is controversy concerning dosage or duration of therapy, oral and topical mesalazine is effective in the treatment of mild to moderately active distal ulcerative colitis."( A practical guide to the management of distal ulcerative colitis.
Ardizzone, S; Bianchi Porro, G, 1998
)
0.3
" Patients were treated with a dosage of 50 mg/kg/day of SSZ (maximum 2,000 mg/day) or placebo."( Sulfasalazine in the treatment of juvenile chronic arthritis: a randomized, double-blind, placebo-controlled, multicenter study. Dutch Juvenile Chronic Arthritis Study Group.
Dijkmans, BA; Dijkstra, PF; Fiselier, TJ; Franssen, MJ; Kuis, W; Oostveen, JC; ten Cate, R; van Ede, CF; van Luijk, WH; van Rossum, MA; van Soesbergen, RM; van Suijlekom-Smit, LW; Wulffraat, NM; Zwinderman, AH, 1998
)
1.74
" The dose-response patterns suggested that the active therapeutic moiety for the two drugs appears to be mainly the liberated 5-ASA molecule."( Experimental colitis induced by dextran sulphate sodium in mice: beneficial effects of sulphasalazine and olsalazine.
Axelsson, LG; Bylund-Fellenius, AC; Landström, E, 1998
)
0.3
"The 'aggressive' drug treatment consisted of institution of relatively fast-acting disease-modifying anti-rheumatic drugs (DMARDs) (sulphasalazine, methotrexate) immediately after diagnosis, and rapid adjustment of dosage and/or drug in the case of insufficient response as measured by a change in C-reactive protein (CRP) level."( Early effective suppression of inflammation in rheumatoid arthritis reduces radiographic progression.
Barendsen, BC; Bruyn, GA; Houtman, PM; Speerstra, F; Stenger, AA; Van Leeuwen, MA; van Rijswijk, MH; Velthuysen, E, 1998
)
0.3
" To directly evaluate the ability of 5-ASA to suppress intestinal tumors, we studied several formulations of 5-ASA (free acid, sulfasalazine, and Pentasa) at multiple oral dosage levels [500, 2400, 4800, and 9600 parts/million (ppm)] in the adenomatous polyposis coli (Apc) mouse model of multiple intestinal neoplasia (Min)."( Evaluation of 5-aminosalicylic acid (5-ASA) for cancer chemoprevention: lack of efficacy against nascent adenomatous polyps in the Apc(Min) mouse.
Gendler, SJ; Hirsch, RE; Leighton, JA; Morrow, JD; Ritland, SR; Weaver, AL, 1999
)
0.51
"Cells were dosed with each compound for 24 h in the presence or absence of PMA inducer and messenger RNA (mRNA) extracted and subjected to Northern blot analysis."( Effects of sulfasalazine and its metabolites on steady state messenger RNA concentrations for inflammatory cytokines, matrix metalloproteinases, and tissue inhibitors of metalloproteinase in rheumatoid synovial fibroblasts.
Blackburn, WD; Minghetti, PP, 2000
)
0.7
" Efficacy was evaluated on the basis of clinical and laboratory variables, radiographic signs of disease progression and daily dosage of indomethacin."( Efficacy of methotrexate in the treatment of ankylosing spondylitis: a three-year open study.
Bambara, LM; Biasi, D; Caramaschi, P; Carletto, A; Maleknia, T; Pacor, ML, 2000
)
0.31
" A dose-response trend for 5-ASA was also observed."( Oral 5-aminosalicylic acid for inducing remission in ulcerative colitis.
Beck, P; Makiyama, K; May, G; Roth, D; Sutherland, L, 2000
)
0.31
" Metronidazole and 6-mercaptopurine or azathioprine also seem to be of benefit in postoperative prophylaxis of disease recurrence, but additional controlled studies are required to define better the efficacy and dose-response of these agents."( Medical therapy to reduce postoperative Crohn's disease recurrence.
Achkar, JP; Hanauer, SB, 2000
)
0.31
" The new warfarin dosage was 75 mg per week, a 250% dosage increase."( Warfarin resistance due to sulfasalazine.
Kovacs, MJ; Martin, JE; Teefy, AM, 2000
)
0.6
"A multiple unit dosage form for oral delivery based on the microencapsulation of anti-inflammatory drugs using different biodegradable polymers, poly(epsilon-caprolactone), polylactic acid and poly(lactic-co-glycolic acid), prepared either by the water-in-oil-in-water (w/o/w) or the solid-in-oil-in-water (s/o/w) solvent evaporation method was developed."( Biodegradable microparticles as a two-drug controlled release formulation: a potential treatment of inflammatory bowel disease.
Lamprecht, A; Lehr, CM; Rodero Torres, H; Schäfer, U, 2000
)
0.31
" Median oral sulfasalazine dosage was 3 g (range, 1-4 g)."( Treatment of ocular cicatricial pemphigoid with sulfasalazine.
Doan, S; Hoang-Xuan, T; Lerouic, JF; Prost, C; Robin, H; Savoldelli, M, 2001
)
0.94
" In this study, the correlation between the NAT2 genotype and the pharmacokinetics of SP after multiple oral dosing of sulfasalazine (SASP) was examined to elucidate the effect of multiple dosing on the predictability of the phenotype by NAT2 genotyping."( N-Acetyltransferase 2 genotype correlates with sulfasalazine pharmacokinetics after multiple dosing in healthy Japanese subjects.
Adachi, S; Aoyama, N; Hatanaka, H; Kasuga, M; Kita, T; Okumura, K; Sakaeda, T; Sakai, T, 2001
)
0.78
" The average dosage of MTX used was calculated to be 590 mg."( [The effect of low dose methotrexate treatment on bone mineral density in patients with rheumatoid arthritis].
Kita, K; Sierakowski, S, 2002
)
0.31
" All achieved remission again after restarting the regimen and increasing the SSZ dosage by one-third."( Sulfasalazine therapy for juvenile rheumatoid arthritis.
Chen, CC; Chiang, BL; Lin, YT; Yang, YH, 2002
)
1.76
"These results show that an accelerated dosing schedule of sulphasalazine has identical effects to diclofenac in reducing symptoms, indicating it is a rapidly effective DMARD."( Treating rheumatoid arthritis early with disease modifying drugs reduces joint damage: a randomised double blind trial of sulphasalazine vs diclofenac sodium.
Choy, EH; Erhardt, C; Henderson, E; Kingsley, GH; Macfarlane, D; Panayi, GS; Papasavvas, G; Plant, MJ; Scott, DL; Williams, P; Wojtulewski, J; Young, A,
)
0.13
" HCQ was given at a dosage of 200 mg twice a day."( Treatment of rheumatoid arthritis with methotrexate and hydroxychloroquine, methotrexate and sulfasalazine, or a combination of the three medications: results of a two-year, randomized, double-blind, placebo-controlled trial.
Blakely, K; Churchill, M; Eckhoff, PJ; Felt, J; Fernandez, A; Hadley, S; Haire, C; Klassen, L; Leff, R; Mallek, J; Moore, G; O'Dell, JR; Palmer, W; Paulsen, G; Stoner, J; Waytz, P; Wees, S, 2002
)
0.53
" Synovial tissue explants from RA patients secreted a decreased amount of the chemokines IL-8 and growth-related gene product alpha (GROalpha) when treated with SASP over a broad range of concentrations based on the typical clinical dosage of 2 g/day."( The effect of sulfasalazine on rheumatoid arthritic synovial tissue chemokine production.
Campbell, PL; Connors, MA; Koch, AE; Volin, MV; Woodruff, DC, 2002
)
0.68
" Mesalazine has been shown equivalent or superior to sulfasalazine, and superior to placebo, with a dose-response benefit, in inducing remission of acute disease."( Role of mesalazine in acute and long-term treatment of ulcerative colitis and its complications.
Schroeder, KW, 2002
)
0.56
" All patients received oral corticosteroids in a tapering dosage schedule initially."( Azathioprine versus sulfasalazine in maintenance of remission in severe ulcerative colitis.
Avasthi, G; Midha, V; Sood, A; Sood, N,
)
0.45
" A dose-response trend for 5-ASA was also observed."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
MacDonald, JK; Sutherland, L, 2003
)
0.32
"Current dosing strategies should be re-evaluated, and coping strategies for common AEs should be investigated."( Survival and effectiveness of leflunomide compared with methotrexate and sulfasalazine in rheumatoid arthritis: a matched observational study.
Aletaha, D; Eberl, G; Grisar, J; Kapral, T; Machold, KP; Smolen, JS; Stamm, T, 2003
)
0.55
" Continuation of small dosage for long intervals seemed advantageous in the small number of patients treated in this study."( Salicylazosulfapyridine (salazopyrin or azopyrin) in rheumatoid arthritis and experimental polyarthritis.
GARDNER, GM; KUZELL, WC, 1950
)
0.23
" Four patients received infliximab, an anti-TNFalpha monoclonal antibody, at a dosage of 5 mg/kg body weight and one patient was treated with etanercept, a TNFalpha receptor p75-Fc fusion protein, at a dosage of 25 mg twice weekly."( [The treatment of recurrent uveitis with TNF-alpha inhibitors].
Covelli, M; Falappone, PC; Grattagliano, V; Iannone, F; Lapadula, G; Scioscia, C,
)
0.13
" The above changes of gene expression were detectable within a short period after the dosing prior to the appearance of obvious pathological changes."( Effects of male reproductive toxicants on gene expression in rat testes.
Fukushima, T; Hamada, Y; Horii, I; Kikkawa, R; Komiyama, M; Mori, C; Yamamoto, T, 2005
)
0.33
" A total of twenty patients with progressive malignant glioma despite surgery, radiation therapy and a first line of chemotherapy will be recruited and assigned to four dosage regimen of Sulfasalazine."( A phase 1-2, prospective, double blind, randomized study of the safety and efficacy of Sulfasalazine for the treatment of progressing malignant gliomas: study protocol of [ISRCTN45828668].
Albert, A; Bours, V; Chariot, A; Deprez, M; Martin, D; Robe, PA, 2006
)
0.75
" Medical treatment, including increased dosage of steroids, failed to control UC and acute thrombocytopenia in this patient."( Acute thrombocytopenia associated with preexisting ulcerative colitis successfully treated with colectomy.
Hisada, T; Iida, T; Ishizuka, T; Kusano, M; Masuo, T; Miyamae, Y; Mizuide, M; Mori, M; Okada, S; Sagawa, T; Shibusawa, N, 2006
)
0.33
" A dose-response trend for 5-ASA was also observed."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Macdonald, JK; Sutherland, L, 2006
)
0.33
" Therapeutic success of mesalazine may be optimized by a combination of high dose and low frequency of dosage to improve compliance."( Indications for 5-aminosalicylate in inflammatory bowel disease: is the body of evidence complete?
Mulder, CJ; van Bodegraven, AA, 2006
)
0.33
" Dosage adjustments and additions of further DMARDs were contingent on response to therapy and tolerance."( Response-driven combination therapy with conventional disease-modifying antirheumatic drugs can achieve high response rates in early rheumatoid arthritis with minimal glucocorticoid and nonsteroidal anti-inflammatory drug use.
Ayres, OC; Caughey, GE; Cleland, LG; Goldblatt, F; Hill, CL; James, MJ; Keen, HI; Lee, AT; Proudman, SM; Rischmueller, M; Stamp, LK, 2007
)
0.34
"This implementation study demonstrates the feasibility, safety, and efficacy of combination therapy with inexpensive DMARDs, fish oil, and minimal glucocorticoid use, in routine clinical practice using predefined rules for dosage adjustment."( Response-driven combination therapy with conventional disease-modifying antirheumatic drugs can achieve high response rates in early rheumatoid arthritis with minimal glucocorticoid and nonsteroidal anti-inflammatory drug use.
Ayres, OC; Caughey, GE; Cleland, LG; Goldblatt, F; Hill, CL; James, MJ; Keen, HI; Lee, AT; Proudman, SM; Rischmueller, M; Stamp, LK, 2007
)
0.34
"8 g per day of the active 5-aminosalicylate moiety, rather than starting at a lower dosage and increasing if treatment fails."( Ulcerative colitis: responding to the challenges.
Achkar, JP, 2007
)
0.34
" More patients completed the first year without unplanned DMARD changes and without dosage adjustment and fewer had DMARD changes due to side effects or inefficacy in the step-down group compared with step-up, whereas the number of adverse events was comparable."( Daily practice effectiveness of a step-down treatment in comparison with a tight step-up for early rheumatoid arthritis.
Esselens, G; Verschueren, P; Westhovens, R, 2008
)
0.35
" Following our positive results with nIFN-beta in a previously published open-labeled study, the present study was designed as an extension with the hypothesis that administration of higher dosage of nIFN-beta (1."( Successful treatment of steroid refractory active ulcerative colitis with natural interferon-beta--an open long-term trial.
Andus, T; Chrissafidou, A; Malek, M; Musch, E; Schulz, M, 2007
)
0.34
"5 months) were randomized to receive step-up therapy (sulfasalazine [SSZ] monotherapy, then after 3 months, methotrexate [MTX] was added, and when the maximum tolerated dosage of MTX was reached, hydroxychloroquine [HCQ] was added) or parallel triple therapy (SSZ/MTX/HCQ)."( Triple therapy in early active rheumatoid arthritis: a randomized, single-blind, controlled trial comparing step-up and parallel treatment strategies.
Capell, HA; Kincaid, W; McMahon, AD; Porter, DR; Saunders, SA; Stirling, A; Vallance, R, 2008
)
0.59
" Accordingly, noninvasive, serial quantification of colonic inflammation could advantageously guide dosing regimens and assess drug efficacy, thus enhancing the value of colitis models in research."( Progression and variability of TNBS colitis-associated inflammation in rats assessed by contrast-enhanced and T2-weighted MRI.
Hobson, AR; James, MF; Kruidenier, L; Lewis, HD; McCleary, S; Pohlmann, A; Robinson, A; Tilling, LC; Warnock, LC; Woolmer, O, 2009
)
0.35
" This methodology provides unique and objective in vivo measures of inflammation that can guide dosing strategies, enhancing colitis research effectiveness and the assessment of potential IBD therapeutics."( Progression and variability of TNBS colitis-associated inflammation in rats assessed by contrast-enhanced and T2-weighted MRI.
Hobson, AR; James, MF; Kruidenier, L; Lewis, HD; McCleary, S; Pohlmann, A; Robinson, A; Tilling, LC; Warnock, LC; Woolmer, O, 2009
)
0.35
" Recent experience indicates that the most effective dosage of nystatin for dogs and cats is 50."( [A cat with diarrhoea associated with the massive presence of Cyniclomyces guttulatus in the faeces].
Houwers, DJ; Peters, S, 2009
)
0.35
" The effects of P-glycoprotein (P-gp), multidrug resistance-associated protein 2 (MRP2), and breast cancer resistance protein (BCRP) inhibitors on sulfasalazine bidirectional permeability were studied across Caco-2 cell monolayers, including dose-response analysis."( Small intestinal efflux mediated by MRP2 and BCRP shifts sulfasalazine intestinal permeability from high to low, enabling its colonic targeting.
Amidon, GL; Dahan, A, 2009
)
0.8
" After two years, the choice and dosing of DMARDs and prednisolone were not restricted, but the treatment was still targeted to achieve or maintain remission."( Renal safety of initial combination versus single DMARD therapy in patients with early rheumatoid arthritis: an 11-year experience from the FIN-RACo Trial.
Hannonen, PJ; Kaipiainen-Seppänen, OA; Karjalainen, AH; Karstila, KL; Korpela, MM; Leirisalo-Repo, M; Möttönen, TT; Mustonen, JT; Rantalaiho, VM,
)
0.13
"Sulphasalazine, THC and CBD proved beneficial in this model of colitis with the dose-response relationship for the phytocannabinoids showing a bell-shaped pattern on the majority of parameters (optimal THC and CBD dose, 10 mg."( The effects of Delta-tetrahydrocannabinol and cannabidiol alone and in combination on damage, inflammation and in vitro motility disturbances in rat colitis.
Jamontt, JM; Molleman, A; Parsons, ME; Pertwee, RG, 2010
)
0.36
"An HPLC method for the quantitative analysis of mebeverine HCl, 5-aminosalicylic acid (5-ASA), sulphasalazine and dispersible aspirin has been developed and then applied to these specific medicines when stored, with other medications, in Venalink blister packs (monitored dosage system) for periods of up to 35 days."( Quantitative HPLC analysis of mebeverine, mesalazine, sulphasalazine and dispersible aspirin stored in a Venalink monitored dosage system with co-prescribed medicines.
Blagbrough, IS; Elmasry, MS; Kheir, AA; Rogers, PJ; Rowan, MG; Saleh, HM, 2011
)
0.37
" However, several randomized controlled trials (RCTs) have been published recently, and no previous meta-analysis has studied the effect of 5-ASA dosage used."( Efficacy of 5-aminosalicylates in ulcerative colitis: systematic review and meta-analysis.
Achkar, JP; Ford, AC; Kane, SV; Khan, KJ; Marshall, JK; Moayyedi, P; Talley, NJ, 2011
)
0.37
" The effects of reaction parameters such as Fe(3+) concentration, initial H(2)O(2) dosage and the reaction temperature are evaluated."( Removal and degradation pathway study of sulfasalazine with Fenton-like reaction.
Chen, F; Fan, X; Hao, H; Shen, X; Zhang, J, 2011
)
0.64
" Recent change in permitted maximum dosage of MTX from 8 to 16 mg/week may improve its efficacy and continuation rate in treating Japanese RA patients."( Recent trends in use of nonbiologic DMARDs and evaluation of their continuation rates in single and dual combination therapies in rheumatoid arthritis patients in Japan.
Kageyama, M; Kempe, K; Kon, T; Kusaoi, M; Matsudaira, R; Matsushita, M; Ogasawara, M; Onuma, S; Sekiya, F; Sugimoto, K; Tada, K; Takasaki, Y; Tamura, N; Yamaji, K, 2012
)
0.38
" Using data from the randomized double-blind Ankylosing Spondylitis Study Comparing Enbrel with Sulfasalazine Dosed Weekly (ASCEND) trial, we tested ASDAS validity and assessed its capacity to discriminate between treatment effects and change-from-baseline improvements."( Sensitivity and discriminatory ability of the Ankylosing Spondylitis Disease Activity Score in patients treated with etanercept or sulphasalazine in the ASCEND trial.
Braun, J; Dougados, M; Koenig, AS; Pedersen, R; Sieper, J; Szumski, A; van der Heijde, D, 2012
)
0.6
" A secondary objective of this systematic review was to compare the efficacy and safety of once daily dosing of oral 5-ASA with conventional (two or three times daily) dosing regimens."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" Studies that compared once daily 5-ASA treatment with conventional dosing of 5-ASA (two or three times daily) and 5-ASA dose ranging studies were also considered for inclusion."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" Trials were separated into five comparison groups: 5-ASA versus placebo, 5-ASA versus sulfasalazine, once daily dosing versus conventional dosing, 5-ASA versus comparator 5-ASA, and 5-ASA dose-ranging."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.6
" A dose-response trend for 5-ASA was also observed."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" 5-ASA dosed once daily appears to be as efficacious and safe as conventionally dosed 5-ASA."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" A secondary objective was to compare the efficacy and safety of once daily dosing of oral 5-ASA with conventional (two or three times daily) dosing regimens."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" Studies that compared once daily 5-ASA treatment with conventional dosing of 5-ASA and 5-ASA dose ranging studies were also considered for inclusion."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" Trials were separated into five comparison groups: 5-ASA versus placebo, 5-ASA versus sulfasalazine, once daily dosing versus conventional dosing, 5-ASA versus comparator 5-ASA formulation, and 5-ASA dose-ranging."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.6
" No statistically significant differences in efficacy or adherence were found between once daily and conventionally dosed 5-ASA."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
" Oral 5-ASA administered once daily is as effective and safe as conventional dosing for maintenance of remission in quiescent ulcerative colitis."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; Macdonald, JK, 2012
)
0.38
"A post hoc analysis of data from the Ankylosing Spondylitis Study Comparing ENbrel and Sulfasalazine Dosed Weekly (ASCEND) study was performed using the Natural History Staggered Start (NHSS) method."( Disease-modifying effect of etanercept versus sulphasalazine on spinal mobility in patients with ankylosing spondylitis.
Hendrix, S; Koenig, A; Li, W; Singh, A, 2013
)
0.61
"If SASP is initiated at a low dosage (≤ 500 mg) and increased up to 1000 mg under careful monitoring, it is safe for HD patients."( Retrospective study of salazosulfapyridine in eight patients with rheumatoid arthritis on hemodialysis.
Akiyama, Y; Furuta, E; Kato, Y; Mimura, T; Sakurai, Y, 2014
)
0.4
" Therefore, we decided to decrease the TCZ dosage by 10-20% approximately."( Tocilizumab-induced neutropenia in rheumatoid arthritis patients with previous history of neutropenia: case series and review of literature.
Langevitz, P; Shoenfeld, Y; Shovman, O, 2015
)
0.42
"The most extensively used test for predicting in-vivo release kinetics of a drug from its orally administered dosage forms is dissolution testing."( A novel dissolution method for evaluation of polysaccharide based colon specific delivery systems: A suitable alternative to animal sacrifice.
Gulati, M; Kaur, P; Prudhviraj, G; Singh, SK; Vaidya, Y; Yadav, AK, 2015
)
0.42
" Immediate release products of two highly dosed active pharmaceutical ingredients (APIs), sulfasalazine and L-870,810, and one mesalamine colon targeting product were used for evaluating their usefulness."( Two-Stage Single-Compartment Models to Evaluate Dissolution in the Lower Intestine.
Kesisoglou, F; Markopoulos, C; Reppas, C; Symillides, M; Vertzoni, M, 2015
)
0.64
"Significant clinical success of colon targeted dosage forms has been limited by their inappropriate release profile at the target site."( Effect of co-administration of probiotics with polysaccharide based colon targeted delivery systems to optimize site specific drug release.
Gowthamarajan, K; Gulati, M; Kaur, P; Prudhviraj, G; Singh, SK; Vaidya, Y; Yadav, AK, 2015
)
0.42
"Eleven patients were enrolled and received a dosage from 8 to 12 g/day."( Dose-escalation study for the targeting of CD44v
Doi, T; Einaga, Y; Fukutani, M; Hasegawa, H; Hironaka, S; Imamura, CK; Ishii, Y; Kuwata, T; Nagano, O; Nakajima, TE; Nomura, S; Ohtsu, A; Ozeki, T; Sato, A; Saya, H; Shitara, K; Takahashi, S; Tsuchihashi, K, 2017
)
0.46
" A secondary objective of this systematic review was to compare the efficacy and safety of once daily dosing of oral 5-ASA with conventional (two or three times daily) dosing regimens."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Bhanji, T; Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" Studies that compared once daily 5-ASA treatment with conventional dosing of 5-ASA (two or three times daily) and 5-ASA dose ranging studies were also considered for inclusion."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Bhanji, T; Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" Trials were separated into five comparison groups: 5-ASA versus placebo, 5-ASA versus sulfasalazine, once daily dosing versus conventional dosing, 5-ASA versus comparator 5-ASA, and 5-ASA dose-ranging."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Bhanji, T; Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.66
" A dose-response trend for 5-ASA was also observed."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Bhanji, T; Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" 5-ASA dosed once daily appears to be as efficacious and safe as conventionally dosed 5-ASA."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Bhanji, T; Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" A secondary objective was to compare the efficacy and safety of once daily dosing of oral 5-ASA with conventional (two or three times daily) dosing regimens."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" Studies that compared once daily 5-ASA treatment with conventional dosing of 5-ASA and 5-ASA dose ranging studies were also considered for inclusion."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" Trials were separated into five comparison groups: 5-ASA versus placebo, 5-ASA versus sulfasalazine, once daily dosing versus conventional dosing, 5-ASA versus comparator 5-ASA formulation, and 5-ASA dose-ranging."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.66
" No statistically significant differences in efficacy or adherence were found between once daily and conventionally dosed 5-ASA."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" Oral 5-ASA administered once daily is as effective and safe as conventional dosing for maintenance of remission in quiescent ulcerative colitis."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Parker, CE; Wang, Y, 2016
)
0.43
" We used the WHO defined daily dose (DDD) as a tool to assess the dosage of sulfasalazine and celecoxib exposure."( Celecoxib and sulfasalazine had negative association with coronary artery diseases in patients with ankylosing spondylitis: A nation-wide, population-based case-control study.
Chiou, JY; Leong, PY; Li, TY; Wang, YH; Wei, JC; Wu, LC; Yeo, KJ, 2016
)
1.02
"Efficacy of maintenance therapy in ulcerative colitis (UC) in the remission stage has been reported to depend on release profile or dosing regimen of oral 5-aminosalicylic acid (5-ASA) products used."( Real life results in using 5-ASA for maintaining mild to moderate UC patients in Japan, a multi-center study, OPTIMUM Study.
Hanai, H; Hibi, T; Kochi, S; Nagahori, M; Nakamura, S; Omuro, S; Watanabe, M; Yamamoto, T, 2017
)
0.46
" The remission maintenance rate at week 52 by dosage and frequency did not significantly differ between Pentasa® Tablets at 4000 mg/day in 2 divided doses (76."( Real life results in using 5-ASA for maintaining mild to moderate UC patients in Japan, a multi-center study, OPTIMUM Study.
Hanai, H; Hibi, T; Kochi, S; Nagahori, M; Nakamura, S; Omuro, S; Watanabe, M; Yamamoto, T, 2017
)
0.46
" Short course IFX dosing followed by continuation of MTX and SSZ combination can prolong time to disease flare and decrease requirement for additional IFX dose in SpA."( TNFα blockers followed by continuation of sulfasalazine and methotrexate combination: a retrospective study on cost saving options of treatment in Spondyloarthritis.
Danda, D; Nair, AM; Sandhya, P; Yadav, B, 2017
)
0.72
" The highest risk of infection is associated with corticosteroids depending on the dose, so that a dosage as low as possible but stable in the perioperative period is recommended."( [Perioperative management of immunosuppressive treatment in patients undergoing joint surgery].
Krüger, K, 2017
)
0.46
" With several medications (eg, sulfasalazine, diazo-bonded 5-aminosalicylates [ASA], mesalamines, and corticosteroids, including budesonide) and complex dosing formulations, regimens, and routes, to treat a disease with variable anatomic extent, there is considerable practice variability in the management of patients with mild-moderate UC."( AGA Technical Review on the Management of Mild-to-Moderate Ulcerative Colitis.
Binion, DG; Feuerstein, JD; Singh, S; Tremaine, WJ, 2019
)
0.8
" A secondary objective was to compare the efficacy and safety of once-daily dosing of oral 5-ASA versus conventional dosing regimens (two or three times daily)."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" We also included studies that compared once-daily to conventional dosing as well as dose-ranging studies."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" We analyzed five comparisons: 5-ASA versus placebo, 5-ASA versus sulfasalazine, once-daily dosing versus conventional dosing, 5-ASA (e."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.8
" We also observed a dose-response trend for 5-ASA."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" High-certainty evidence suggests 5-ASA dosed once daily appears to be as efficacious as conventionally-dosed 5-ASA."( Oral 5-aminosalicylic acid for induction of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
"To assess the efficacy, dose-responsiveness, and safety of oral 5-ASA compared to placebo, SASP, or 5-ASA comparators for maintenance of remission in quiescent UC and to compare the efficacy and safety of once-daily dosing of oral 5-ASA with conventional (two or three times daily) dosing regimens."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" We also included studies that compared once-daily 5-ASA treatment with conventional dosing of 5-ASA and 5-ASA dose-ranging studies."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" Trials were separated into five comparison groups: 5-ASA versus placebo, 5-ASA versus SASP, once-daily dosing versus conventional dosing, 5-ASA (balsalazide, Pentasa, and olsalazine) versus comparator 5-ASA formulation (Asacol and Salofalk), and 5-ASA dose-ranging."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" There is little or no difference in clinical or endoscopic remission rates between once-daily and conventionally dosed 5-ASA."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" Oral 5-ASA administered once daily has a similar benefit and harm profile as conventional dosing for maintenance of remission in quiescent UC."( Oral 5-aminosalicylic acid for maintenance of remission in ulcerative colitis.
Feagan, BG; MacDonald, JK; Murray, A; Nguyen, TM; Parker, CE, 2020
)
0.56
" Therapeutic plan adjustment included the addition or increased dosage of anti-inflammatory drugs, steroids, immunomodulators, and biologics."( Endoscopy within 7 days after detecting high calprotectin levels can be useful for therapeutic decision-making in ulcerative colitis.
Goong, HJ; Jeon, SR; Kim, HG; Kim, JO; Ko, BM; Lee, JS; Lee, TH; Park, H; Park, J; Park, S; Park, SJ; Yong, HM, 2021
)
0.62
"There is paucity of data on extended dosing interval between two doses of AZD1222 (AstraZeneca) in patients with Autoimmune Rheumatic Diseases (AIRD)."( Effectiveness of delayed second dose of AZD1222 vaccine in patients with autoimmune rheumatic disease.
Ahmed, S; Benny, J; Cherian, S; Mehta, P; Panthak, A; Paul, A; Shenoy, P, 2022
)
0.72
"We observed previously established medical associations for MND and an inverse dose-response association between lovastatin and MND, with 28% reduced risk at 40 mg/day."( Protective Effects of Lovastatin in a Population-Based ALS Study and Mouse Model.
Kreple, CJ; Miller, TM; Racette, BA; Schoch, KM; Searles Nielsen, S; Shabsovich, M; Shen, T; Song, Y, 2023
)
0.91
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Pathways (2)

PathwayProteinsCompounds
Amino acid metabolism in triple-negative breast cancer cells016
Ferroptosis133

Protein Targets (57)

Potency Measurements

ProteinTaxonomyMeasurementAverage (µ)Min (ref.)Avg (ref.)Max (ref.)Bioassay(s)
LuciferasePhotinus pyralis (common eastern firefly)Potency63.82540.007215.758889.3584AID1224835
acetylcholinesteraseHomo sapiens (human)Potency49.30800.002541.796015,848.9004AID1347397; AID1347398; AID1347399
RAR-related orphan receptor gammaMus musculus (house mouse)Potency13.33320.006038.004119,952.5996AID1159521
ATAD5 protein, partialHomo sapiens (human)Potency2.22970.004110.890331.5287AID624249
USP1 protein, partialHomo sapiens (human)Potency50.11870.031637.5844354.8130AID504865
Microtubule-associated protein tauHomo sapiens (human)Potency12.58930.180013.557439.8107AID1460
AR proteinHomo sapiens (human)Potency21.95540.000221.22318,912.5098AID743063
aldehyde dehydrogenase 1 family, member A1Homo sapiens (human)Potency39.81070.011212.4002100.0000AID1030
hypoxia-inducible factor 1, alpha subunit (basic helix-loop-helix transcription factor)Homo sapiens (human)Potency0.22390.00137.762544.6684AID2120
thyroid stimulating hormone receptorHomo sapiens (human)Potency1.58490.001318.074339.8107AID926; AID938
nuclear receptor subfamily 1, group I, member 3Homo sapiens (human)Potency61.31710.001022.650876.6163AID1224838; AID1224893
retinoic acid nuclear receptor alpha variant 1Homo sapiens (human)Potency47.89910.003041.611522,387.1992AID1159552; AID1159555
retinoid X nuclear receptor alphaHomo sapiens (human)Potency28.42040.000817.505159.3239AID1159527; AID1159531
estrogen-related nuclear receptor alphaHomo sapiens (human)Potency6.87990.001530.607315,848.9004AID1224841; AID1259401
farnesoid X nuclear receptorHomo sapiens (human)Potency13.33220.375827.485161.6524AID743220
estrogen nuclear receptor alphaHomo sapiens (human)Potency46.36370.000229.305416,493.5996AID743069; AID743080
GVesicular stomatitis virusPotency12.30180.01238.964839.8107AID1645842
peroxisome proliferator activated receptor gammaHomo sapiens (human)Potency50.11870.001019.414170.9645AID588537
thyroid stimulating hormone receptorHomo sapiens (human)Potency68.58960.001628.015177.1139AID1259385
Histone H2A.xCricetulus griseus (Chinese hamster)Potency41.93150.039147.5451146.8240AID1224845
cytochrome P450 2C9 precursorHomo sapiens (human)Potency7.94330.00636.904339.8107AID883
15-hydroxyprostaglandin dehydrogenase [NAD(+)] isoform 1Homo sapiens (human)Potency14.18790.001815.663839.8107AID894
histone deacetylase 9 isoform 3Homo sapiens (human)Potency29.26630.037617.082361.1927AID1259364; AID1259388
ubiquitin carboxyl-terminal hydrolase 2 isoform aHomo sapiens (human)Potency6.30960.65619.452025.1189AID927
nuclear factor erythroid 2-related factor 2 isoform 1Homo sapiens (human)Potency40.23640.000627.21521,122.0200AID651741; AID743202
lamin isoform A-delta10Homo sapiens (human)Potency0.03160.891312.067628.1838AID1487
Interferon betaHomo sapiens (human)Potency12.30180.00339.158239.8107AID1645842
HLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)Potency12.30180.01238.964839.8107AID1645842
Histamine H2 receptorCavia porcellus (domestic guinea pig)Potency7.94330.00638.235039.8107AID883
Disintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)Potency6.30961.584913.004325.1189AID927
Inositol hexakisphosphate kinase 1Homo sapiens (human)Potency12.30180.01238.964839.8107AID1645842
cytochrome P450 2C9, partialHomo sapiens (human)Potency12.30180.01238.964839.8107AID1645842
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Inhibition Measurements

ProteinTaxonomyMeasurementAverageMin (ref.)Avg (ref.)Max (ref.)Bioassay(s)
Chain A, Glutathione S-transferaseHomo sapiens (human)Ki24.000024.000024.000024.0000AID977610
ATP-binding cassette sub-family C member 3Homo sapiens (human)IC50 (µMol)14.60000.63154.45319.3000AID1473740
Multidrug resistance-associated protein 4Homo sapiens (human)IC50 (µMol)1.50000.20005.677410.0000AID1473741
Solute carrier organic anion transporter family member 2B1 Homo sapiens (human)IC50 (µMol)3.00000.55003.70836.1000AID699544
Solute carrier organic anion transporter family member 2B1 Homo sapiens (human)Ki3.00000.53004.11578.4800AID699544
Bile salt export pumpHomo sapiens (human)IC50 (µMol)134.00000.11007.190310.0000AID1443980; AID1473738
Carbonic anhydrase 1Homo sapiens (human)IC50 (µMol)3.04000.00582.14107.9000AID349140
Carbonic anhydrase 1Homo sapiens (human)Ki6.87000.00001.372610.0000AID349142
Carbonic anhydrase 2Homo sapiens (human)IC50 (µMol)4.49000.00021.10608.3000AID349141
Carbonic anhydrase 2Homo sapiens (human)Ki8.72000.00000.72369.9200AID349145
Interstitial collagenaseHomo sapiens (human)IC50 (µMol)23.54900.00020.850210.0000AID625177
Cytochrome P450 2C9 Homo sapiens (human)IC50 (µMol)50.00000.00002.800510.0000AID1210069
Androgen receptorRattus norvegicus (Norway rat)IC50 (µMol)43.95100.00101.979414.1600AID625228
Androgen receptorRattus norvegicus (Norway rat)Ki29.30100.00031.21858.9270AID625228
Thromboxane-A synthase Homo sapiens (human)IC50 (µMol)19.63900.00091.230410.0000AID625229
Mitogen-activated protein kinase 1Homo sapiens (human)IC50 (µMol)6.33200.00031.68789.2000AID625181
Caspase-1Homo sapiens (human)IC50 (µMol)28.81200.00201.70138.8000AID625174
Bifunctional purine biosynthesis protein ATICHomo sapiens (human)Ki22.00000.40000.64000.8800AID1660992
Cytochrome P450 2J2Homo sapiens (human)IC50 (µMol)50.00000.01202.53129.4700AID1210069
Sodium/bile acid cotransporterHomo sapiens (human)IC50 (µMol)6.73331.00005.92679.6000AID1600822; AID1896148; AID1896149
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)IC50 (µMol)12.00000.10472.71957.0795AID699543
Solute carrier organic anion transporter family member 1B3Homo sapiens (human)Ki11.00000.08002.46889.8000AID699543
Broad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)IC50 (µMol)0.46000.00401.966610.0000AID1873197
Cystine/glutamate transporterHomo sapiens (human)IC50 (µMol)235.04000.14001.14005.0000AID1534336; AID1534337; AID1534338; AID622159
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)IC50 (µMol)0.56000.05002.37979.7000AID699542
Solute carrier organic anion transporter family member 1B1Homo sapiens (human)Ki0.53000.04401.36305.0000AID699542
[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)
Replicase polyprotein 1abBetacoronavirus England 1Kd7.60007.60007.60007.6000AID1594519
Tumor necrosis factorHomo sapiens (human)Kd9.00000.00274.29269.7700AID1802828
Fibroblast growth factor 1Homo sapiens (human)Kd609.00000.00800.12400.2400AID73456
ATP-dependent translocase ABCB1Homo sapiens (human)EC50 (µMol)0.91600.01600.67863.1000AID1690379
Flavin reductase (NADPH)Homo sapiens (human)Kd0.43830.07000.79681.7100AID1815675
[prepared from compound, protein, and bioassay information from National Library of Medicine (NLM), extracted Dec-2023]

Biological Processes (488)

Processvia Protein(s)Taxonomy
xenobiotic metabolic processATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
bile acid and bile salt transportATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transportATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
leukotriene transportATP-binding cassette sub-family C member 3Homo sapiens (human)
monoatomic anion transmembrane transportATP-binding cassette sub-family C member 3Homo sapiens (human)
transport across blood-brain barrierATP-binding cassette sub-family C member 3Homo sapiens (human)
prostaglandin secretionMultidrug resistance-associated protein 4Homo sapiens (human)
cilium assemblyMultidrug resistance-associated protein 4Homo sapiens (human)
platelet degranulationMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
bile acid and bile salt transportMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transportMultidrug resistance-associated protein 4Homo sapiens (human)
urate transportMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
cAMP transportMultidrug resistance-associated protein 4Homo sapiens (human)
leukotriene transportMultidrug resistance-associated protein 4Homo sapiens (human)
monoatomic anion transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
export across plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
transport across blood-brain barrierMultidrug resistance-associated protein 4Homo sapiens (human)
guanine nucleotide transmembrane transportMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
prostaglandin transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transport across blood-brain barrierSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
fatty acid metabolic processBile salt export pumpHomo sapiens (human)
bile acid biosynthetic processBile salt export pumpHomo sapiens (human)
xenobiotic metabolic processBile salt export pumpHomo sapiens (human)
xenobiotic transmembrane transportBile salt export pumpHomo sapiens (human)
response to oxidative stressBile salt export pumpHomo sapiens (human)
bile acid metabolic processBile salt export pumpHomo sapiens (human)
response to organic cyclic compoundBile salt export pumpHomo sapiens (human)
bile acid and bile salt transportBile salt export pumpHomo sapiens (human)
canalicular bile acid transportBile salt export pumpHomo sapiens (human)
protein ubiquitinationBile salt export pumpHomo sapiens (human)
regulation of fatty acid beta-oxidationBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transportBile salt export pumpHomo sapiens (human)
bile acid signaling pathwayBile salt export pumpHomo sapiens (human)
cholesterol homeostasisBile salt export pumpHomo sapiens (human)
response to estrogenBile salt export pumpHomo sapiens (human)
response to ethanolBile salt export pumpHomo sapiens (human)
xenobiotic export from cellBile salt export pumpHomo sapiens (human)
lipid homeostasisBile salt export pumpHomo sapiens (human)
phospholipid homeostasisBile salt export pumpHomo sapiens (human)
positive regulation of bile acid secretionBile salt export pumpHomo sapiens (human)
regulation of bile acid metabolic processBile salt export pumpHomo sapiens (human)
transmembrane transportBile salt export pumpHomo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 1Homo sapiens (human)
morphogenesis of an epitheliumCarbonic anhydrase 2Homo sapiens (human)
positive regulation of synaptic transmission, GABAergicCarbonic anhydrase 2Homo sapiens (human)
positive regulation of cellular pH reductionCarbonic anhydrase 2Homo sapiens (human)
angiotensin-activated signaling pathwayCarbonic anhydrase 2Homo sapiens (human)
regulation of monoatomic anion transportCarbonic anhydrase 2Homo sapiens (human)
secretionCarbonic anhydrase 2Homo sapiens (human)
regulation of intracellular pHCarbonic anhydrase 2Homo sapiens (human)
neuron cellular homeostasisCarbonic anhydrase 2Homo sapiens (human)
positive regulation of dipeptide transmembrane transportCarbonic anhydrase 2Homo sapiens (human)
regulation of chloride transportCarbonic anhydrase 2Homo sapiens (human)
carbon dioxide transportCarbonic anhydrase 2Homo sapiens (human)
one-carbon metabolic processCarbonic anhydrase 2Homo sapiens (human)
positive regulation of gene expressionTumor necrosis factorHomo sapiens (human)
negative regulation of gene expressionTumor necrosis factorHomo sapiens (human)
positive regulation of MAP kinase activityTumor necrosis factorHomo sapiens (human)
positive regulation of MAPK cascadeTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-33 productionTumor necrosis factorHomo sapiens (human)
positive regulation of cytokine production involved in inflammatory responseTumor necrosis factorHomo sapiens (human)
negative regulation of miRNA transcriptionTumor necrosis factorHomo sapiens (human)
positive regulation of miRNA transcriptionTumor necrosis factorHomo sapiens (human)
negative regulation of signaling receptor activityTumor necrosis factorHomo sapiens (human)
negative regulation of transcription by RNA polymerase IITumor necrosis factorHomo sapiens (human)
positive regulation of gene expressionTumor necrosis factorHomo sapiens (human)
negative regulation of gene expressionTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-8 productionTumor necrosis factorHomo sapiens (human)
negative regulation of cysteine-type endopeptidase activity involved in apoptotic processTumor necrosis factorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IITumor necrosis factorHomo sapiens (human)
positive regulation of NF-kappaB transcription factor activityTumor necrosis factorHomo sapiens (human)
positive regulation of calcineurin-NFAT signaling cascadeTumor necrosis factorHomo sapiens (human)
positive regulation of cytokine production involved in inflammatory responseTumor necrosis factorHomo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionTumor necrosis factorHomo sapiens (human)
positive regulation of synoviocyte proliferationTumor necrosis factorHomo sapiens (human)
positive regulation of I-kappaB phosphorylationTumor necrosis factorHomo sapiens (human)
negative regulation of apoptotic signaling pathwayTumor necrosis factorHomo sapiens (human)
negative regulation of transcription by RNA polymerase IITumor necrosis factorHomo sapiens (human)
response to hypoxiaTumor necrosis factorHomo sapiens (human)
microglial cell activationTumor necrosis factorHomo sapiens (human)
positive regulation of cytokine productionTumor necrosis factorHomo sapiens (human)
positive regulation of protein phosphorylationTumor necrosis factorHomo sapiens (human)
negative regulation of endothelial cell proliferationTumor necrosis factorHomo sapiens (human)
negative regulation of L-glutamate import across plasma membraneTumor necrosis factorHomo sapiens (human)
macrophage activation involved in immune responseTumor necrosis factorHomo sapiens (human)
chronic inflammatory response to antigenic stimulusTumor necrosis factorHomo sapiens (human)
leukocyte migration involved in inflammatory responseTumor necrosis factorHomo sapiens (human)
regulation of immunoglobulin productionTumor necrosis factorHomo sapiens (human)
negative regulation of cytokine production involved in immune responseTumor necrosis factorHomo sapiens (human)
positive regulation of chronic inflammatory response to antigenic stimulusTumor necrosis factorHomo sapiens (human)
positive regulation of humoral immune response mediated by circulating immunoglobulinTumor necrosis factorHomo sapiens (human)
skeletal muscle contractionTumor necrosis factorHomo sapiens (human)
negative regulation of systemic arterial blood pressureTumor necrosis factorHomo sapiens (human)
glucose metabolic processTumor necrosis factorHomo sapiens (human)
activation of cysteine-type endopeptidase activity involved in apoptotic processTumor necrosis factorHomo sapiens (human)
inflammatory responseTumor necrosis factorHomo sapiens (human)
humoral immune responseTumor necrosis factorHomo sapiens (human)
JNK cascadeTumor necrosis factorHomo sapiens (human)
circadian rhythmTumor necrosis factorHomo sapiens (human)
extrinsic apoptotic signaling pathway via death domain receptorsTumor necrosis factorHomo sapiens (human)
intrinsic apoptotic signaling pathway in response to DNA damageTumor necrosis factorHomo sapiens (human)
response to xenobiotic stimulusTumor necrosis factorHomo sapiens (human)
response to virusTumor necrosis factorHomo sapiens (human)
response to salt stressTumor necrosis factorHomo sapiens (human)
response to fructoseTumor necrosis factorHomo sapiens (human)
negative regulation of heart rateTumor necrosis factorHomo sapiens (human)
vascular endothelial growth factor productionTumor necrosis factorHomo sapiens (human)
positive regulation of gene expressionTumor necrosis factorHomo sapiens (human)
negative regulation of gene expressionTumor necrosis factorHomo sapiens (human)
negative regulation of lipid storageTumor necrosis factorHomo sapiens (human)
response to activityTumor necrosis factorHomo sapiens (human)
regulation of metabolic processTumor necrosis factorHomo sapiens (human)
calcium-mediated signalingTumor necrosis factorHomo sapiens (human)
extracellular matrix organizationTumor necrosis factorHomo sapiens (human)
osteoclast differentiationTumor necrosis factorHomo sapiens (human)
sequestering of triglycerideTumor necrosis factorHomo sapiens (human)
cortical actin cytoskeleton organizationTumor necrosis factorHomo sapiens (human)
positive regulation of protein-containing complex assemblyTumor necrosis factorHomo sapiens (human)
positive regulation of fever generationTumor necrosis factorHomo sapiens (human)
negative regulation of myelinationTumor necrosis factorHomo sapiens (human)
response to nutrient levelsTumor necrosis factorHomo sapiens (human)
negative regulation of interleukin-6 productionTumor necrosis factorHomo sapiens (human)
positive regulation of chemokine productionTumor necrosis factorHomo sapiens (human)
positive regulation of fractalkine productionTumor necrosis factorHomo sapiens (human)
positive regulation of type II interferon productionTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-1 beta productionTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-18 productionTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-6 productionTumor necrosis factorHomo sapiens (human)
positive regulation of interleukin-8 productionTumor necrosis factorHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylationTumor necrosis factorHomo sapiens (human)
tumor necrosis factor-mediated signaling pathwayTumor necrosis factorHomo sapiens (human)
positive regulation of heterotypic cell-cell adhesionTumor necrosis factorHomo sapiens (human)
toll-like receptor 3 signaling pathwayTumor necrosis factorHomo sapiens (human)
negative regulation of myosin-light-chain-phosphatase activityTumor necrosis factorHomo sapiens (human)
response to isolation stressTumor necrosis factorHomo sapiens (human)
response to macrophage colony-stimulating factorTumor necrosis factorHomo sapiens (human)
vasodilationTumor necrosis factorHomo sapiens (human)
positive regulation of tyrosine phosphorylation of STAT proteinTumor necrosis factorHomo sapiens (human)
positive regulation of apoptotic processTumor necrosis factorHomo sapiens (human)
positive regulation of programmed cell deathTumor necrosis factorHomo sapiens (human)
regulation of canonical NF-kappaB signal transductionTumor necrosis factorHomo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionTumor necrosis factorHomo sapiens (human)
negative regulation of protein-containing complex disassemblyTumor necrosis factorHomo sapiens (human)
positive regulation of protein-containing complex disassemblyTumor necrosis factorHomo sapiens (human)
positive regulation of cysteine-type endopeptidase activity involved in apoptotic processTumor necrosis factorHomo sapiens (human)
positive regulation of MAP kinase activityTumor necrosis factorHomo sapiens (human)
positive regulation of MAPK cascadeTumor necrosis factorHomo sapiens (human)
phosphatidylinositol 3-kinase/protein kinase B signal transductionTumor necrosis factorHomo sapiens (human)
positive regulation of JUN kinase activityTumor necrosis factorHomo sapiens (human)
positive regulation of neuron apoptotic processTumor necrosis factorHomo sapiens (human)
negative regulation of blood vessel endothelial cell migrationTumor necrosis factorHomo sapiens (human)
negative regulation of viral genome replicationTumor necrosis factorHomo sapiens (human)
positive regulation of nitric oxide biosynthetic processTumor necrosis factorHomo sapiens (human)
response to ethanolTumor necrosis factorHomo sapiens (human)
regulation of fat cell differentiationTumor necrosis factorHomo sapiens (human)
negative regulation of fat cell differentiationTumor necrosis factorHomo sapiens (human)
negative regulation of myoblast differentiationTumor necrosis factorHomo sapiens (human)
negative regulation of osteoblast differentiationTumor necrosis factorHomo sapiens (human)
positive regulation of osteoclast differentiationTumor necrosis factorHomo sapiens (human)
positive regulation of protein catabolic processTumor necrosis factorHomo sapiens (human)
positive regulation of action potentialTumor necrosis factorHomo sapiens (human)
positive regulation of cell adhesionTumor necrosis factorHomo sapiens (human)
positive regulation of mitotic nuclear divisionTumor necrosis factorHomo sapiens (human)
negative regulation of DNA-templated transcriptionTumor necrosis factorHomo sapiens (human)
positive regulation of DNA-templated transcriptionTumor necrosis factorHomo sapiens (human)
negative regulation of mitotic cell cycleTumor necrosis factorHomo sapiens (human)
positive regulation of transcription by RNA polymerase IITumor necrosis factorHomo sapiens (human)
positive regulation of translational initiation by ironTumor necrosis factorHomo sapiens (human)
negative regulation of glucose importTumor necrosis factorHomo sapiens (human)
positive regulation of JNK cascadeTumor necrosis factorHomo sapiens (human)
positive regulation of receptor signaling pathway via JAK-STATTumor necrosis factorHomo sapiens (human)
astrocyte activationTumor necrosis factorHomo sapiens (human)
embryonic digestive tract developmentTumor necrosis factorHomo sapiens (human)
positive regulation of smooth muscle cell proliferationTumor necrosis factorHomo sapiens (human)
positive regulation of inflammatory responseTumor necrosis factorHomo sapiens (human)
negative regulation of neurogenesisTumor necrosis factorHomo sapiens (human)
regulation of insulin secretionTumor necrosis factorHomo sapiens (human)
positive regulation of synaptic transmissionTumor necrosis factorHomo sapiens (human)
regulation of synapse organizationTumor necrosis factorHomo sapiens (human)
defense response to Gram-positive bacteriumTumor necrosis factorHomo sapiens (human)
cognitionTumor necrosis factorHomo sapiens (human)
leukocyte tethering or rollingTumor necrosis factorHomo sapiens (human)
detection of mechanical stimulus involved in sensory perception of painTumor necrosis factorHomo sapiens (human)
negative regulation of lipid catabolic processTumor necrosis factorHomo sapiens (human)
positive regulation of membrane protein ectodomain proteolysisTumor necrosis factorHomo sapiens (human)
positive regulation of DNA-binding transcription factor activityTumor necrosis factorHomo sapiens (human)
positive regulation of NF-kappaB transcription factor activityTumor necrosis factorHomo sapiens (human)
positive regulation of protein transportTumor necrosis factorHomo sapiens (human)
response to glucocorticoidTumor necrosis factorHomo sapiens (human)
positive regulation of hair follicle developmentTumor necrosis factorHomo sapiens (human)
positive regulation of phosphatidylinositol 3-kinase/protein kinase B signal transductionTumor necrosis factorHomo sapiens (human)
regulation of synaptic transmission, glutamatergicTumor necrosis factorHomo sapiens (human)
positive regulation of glial cell proliferationTumor necrosis factorHomo sapiens (human)
positive regulation of vitamin D biosynthetic processTumor necrosis factorHomo sapiens (human)
positive regulation of calcidiol 1-monooxygenase activityTumor necrosis factorHomo sapiens (human)
epithelial cell proliferation involved in salivary gland morphogenesisTumor necrosis factorHomo sapiens (human)
regulation of branching involved in salivary gland morphogenesisTumor necrosis factorHomo sapiens (human)
negative regulation of vascular wound healingTumor necrosis factorHomo sapiens (human)
negative regulation of branching involved in lung morphogenesisTumor necrosis factorHomo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeTumor necrosis factorHomo sapiens (human)
cellular response to lipopolysaccharideTumor necrosis factorHomo sapiens (human)
cellular response to amino acid stimulusTumor necrosis factorHomo sapiens (human)
cellular response to retinoic acidTumor necrosis factorHomo sapiens (human)
cellular response to nicotineTumor necrosis factorHomo sapiens (human)
cellular response to type II interferonTumor necrosis factorHomo sapiens (human)
cellular response to ionizing radiationTumor necrosis factorHomo sapiens (human)
positive regulation of mononuclear cell migrationTumor necrosis factorHomo sapiens (human)
positive regulation of podosome assemblyTumor necrosis factorHomo sapiens (human)
endothelial cell apoptotic processTumor necrosis factorHomo sapiens (human)
protein localization to plasma membraneTumor necrosis factorHomo sapiens (human)
negative regulation of oxidative phosphorylationTumor necrosis factorHomo sapiens (human)
inflammatory response to woundingTumor necrosis factorHomo sapiens (human)
extrinsic apoptotic signaling pathwayTumor necrosis factorHomo sapiens (human)
cellular response to toxic substanceTumor necrosis factorHomo sapiens (human)
liver regenerationTumor necrosis factorHomo sapiens (human)
necroptotic signaling pathwayTumor necrosis factorHomo sapiens (human)
negative regulation of bile acid secretionTumor necrosis factorHomo sapiens (human)
antiviral innate immune responseTumor necrosis factorHomo sapiens (human)
response to Gram-negative bacteriumTumor necrosis factorHomo sapiens (human)
positive regulation of neuroinflammatory responseTumor necrosis factorHomo sapiens (human)
negative regulation of amyloid-beta clearanceTumor necrosis factorHomo sapiens (human)
positive regulation of non-canonical NF-kappaB signal transductionTumor necrosis factorHomo sapiens (human)
positive regulation of amyloid-beta formationTumor necrosis factorHomo sapiens (human)
response to L-glutamateTumor necrosis factorHomo sapiens (human)
positive regulation of neutrophil activationTumor necrosis factorHomo sapiens (human)
positive regulation of protein localization to plasma membraneTumor necrosis factorHomo sapiens (human)
regulation of establishment of endothelial barrierTumor necrosis factorHomo sapiens (human)
negative regulation of bicellular tight junction assemblyTumor necrosis factorHomo sapiens (human)
cellular response to amyloid-betaTumor necrosis factorHomo sapiens (human)
positive regulation of vascular associated smooth muscle cell proliferationTumor necrosis factorHomo sapiens (human)
positive regulation of leukocyte adhesion to vascular endothelial cellTumor necrosis factorHomo sapiens (human)
positive regulation of leukocyte adhesion to arterial endothelial cellTumor necrosis factorHomo sapiens (human)
regulation of membrane lipid metabolic processTumor necrosis factorHomo sapiens (human)
response to 3,3',5-triiodo-L-thyronineTumor necrosis factorHomo sapiens (human)
response to gold nanoparticleTumor necrosis factorHomo sapiens (human)
positive regulation of protein localization to cell surfaceTumor necrosis factorHomo sapiens (human)
positive regulation of blood microparticle formationTumor necrosis factorHomo sapiens (human)
positive regulation of chemokine (C-X-C motif) ligand 2 productionTumor necrosis factorHomo sapiens (human)
positive regulation of hepatocyte proliferationTumor necrosis factorHomo sapiens (human)
regulation of endothelial cell apoptotic processTumor necrosis factorHomo sapiens (human)
regulation of reactive oxygen species metabolic processTumor necrosis factorHomo sapiens (human)
positive regulation of DNA biosynthetic processTumor necrosis factorHomo sapiens (human)
negative regulation of extrinsic apoptotic signaling pathway in absence of ligandTumor necrosis factorHomo sapiens (human)
positive regulation of extrinsic apoptotic signaling pathwayTumor necrosis factorHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell activation involved in immune responseInterferon betaHomo sapiens (human)
cell surface receptor signaling pathwayInterferon betaHomo sapiens (human)
cell surface receptor signaling pathway via JAK-STATInterferon betaHomo sapiens (human)
response to virusInterferon betaHomo sapiens (human)
positive regulation of autophagyInterferon betaHomo sapiens (human)
cytokine-mediated signaling pathwayInterferon betaHomo sapiens (human)
natural killer cell activationInterferon betaHomo sapiens (human)
positive regulation of peptidyl-serine phosphorylation of STAT proteinInterferon betaHomo sapiens (human)
cellular response to interferon-betaInterferon betaHomo sapiens (human)
B cell proliferationInterferon betaHomo sapiens (human)
negative regulation of viral genome replicationInterferon betaHomo sapiens (human)
innate immune responseInterferon betaHomo sapiens (human)
positive regulation of innate immune responseInterferon betaHomo sapiens (human)
regulation of MHC class I biosynthetic processInterferon betaHomo sapiens (human)
negative regulation of T cell differentiationInterferon betaHomo sapiens (human)
positive regulation of transcription by RNA polymerase IIInterferon betaHomo sapiens (human)
defense response to virusInterferon betaHomo sapiens (human)
type I interferon-mediated signaling pathwayInterferon betaHomo sapiens (human)
neuron cellular homeostasisInterferon betaHomo sapiens (human)
cellular response to exogenous dsRNAInterferon betaHomo sapiens (human)
cellular response to virusInterferon betaHomo sapiens (human)
negative regulation of Lewy body formationInterferon betaHomo sapiens (human)
negative regulation of T-helper 2 cell cytokine productionInterferon betaHomo sapiens (human)
positive regulation of apoptotic signaling pathwayInterferon betaHomo sapiens (human)
response to exogenous dsRNAInterferon betaHomo sapiens (human)
B cell differentiationInterferon betaHomo sapiens (human)
natural killer cell activation involved in immune responseInterferon betaHomo sapiens (human)
adaptive immune responseInterferon betaHomo sapiens (human)
T cell activation involved in immune responseInterferon betaHomo sapiens (human)
humoral immune responseInterferon betaHomo sapiens (human)
positive regulation of T cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
adaptive immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class I via ER pathway, TAP-independentHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of T cell anergyHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
defense responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
detection of bacteriumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-12 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of interleukin-6 productionHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protection from natural killer cell mediated cytotoxicityHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
innate immune responseHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
regulation of dendritic cell differentiationHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
antigen processing and presentation of endogenous peptide antigen via MHC class IbHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
proteolysisInterstitial collagenaseHomo sapiens (human)
protein metabolic processInterstitial collagenaseHomo sapiens (human)
extracellular matrix disassemblyInterstitial collagenaseHomo sapiens (human)
collagen catabolic processInterstitial collagenaseHomo sapiens (human)
positive regulation of protein-containing complex assemblyInterstitial collagenaseHomo sapiens (human)
cellular response to UV-AInterstitial collagenaseHomo sapiens (human)
extracellular matrix organizationInterstitial collagenaseHomo sapiens (human)
positive regulation of cell population proliferationFibroblast growth factor 1Homo sapiens (human)
fibroblast growth factor receptor signaling pathwayFibroblast growth factor 1Homo sapiens (human)
angiogenesisFibroblast growth factor 1Homo sapiens (human)
organ inductionFibroblast growth factor 1Homo sapiens (human)
signal transductionFibroblast growth factor 1Homo sapiens (human)
positive regulation of cell population proliferationFibroblast growth factor 1Homo sapiens (human)
fibroblast growth factor receptor signaling pathwayFibroblast growth factor 1Homo sapiens (human)
anatomical structure morphogenesisFibroblast growth factor 1Homo sapiens (human)
positive regulation of endothelial cell migrationFibroblast growth factor 1Homo sapiens (human)
lung developmentFibroblast growth factor 1Homo sapiens (human)
positive regulation of cell migrationFibroblast growth factor 1Homo sapiens (human)
activation of protein kinase B activityFibroblast growth factor 1Homo sapiens (human)
cellular response to heatFibroblast growth factor 1Homo sapiens (human)
wound healingFibroblast growth factor 1Homo sapiens (human)
positive regulation of MAP kinase activityFibroblast growth factor 1Homo sapiens (human)
positive regulation of cholesterol biosynthetic processFibroblast growth factor 1Homo sapiens (human)
positive regulation of angiogenesisFibroblast growth factor 1Homo sapiens (human)
positive regulation of transcription by RNA polymerase IIFibroblast growth factor 1Homo sapiens (human)
epithelial cell proliferationFibroblast growth factor 1Homo sapiens (human)
positive regulation of cell divisionFibroblast growth factor 1Homo sapiens (human)
branch elongation involved in ureteric bud branchingFibroblast growth factor 1Homo sapiens (human)
positive regulation of ERK1 and ERK2 cascadeFibroblast growth factor 1Homo sapiens (human)
mesonephric epithelium developmentFibroblast growth factor 1Homo sapiens (human)
regulation of endothelial tube morphogenesisFibroblast growth factor 1Homo sapiens (human)
positive regulation of intracellular signal transductionFibroblast growth factor 1Homo sapiens (human)
positive regulation of sprouting angiogenesisFibroblast growth factor 1Homo sapiens (human)
positive regulation of hepatocyte proliferationFibroblast growth factor 1Homo sapiens (human)
regulation of endothelial cell chemotaxis to fibroblast growth factorFibroblast growth factor 1Homo sapiens (human)
cell differentiationFibroblast growth factor 1Homo sapiens (human)
positive regulation of gene expressionFibroblast growth factor 1Homo sapiens (human)
animal organ morphogenesisFibroblast growth factor 1Homo sapiens (human)
regulation of cell migrationFibroblast growth factor 1Homo sapiens (human)
G2/M transition of mitotic cell cycleATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic metabolic processATP-dependent translocase ABCB1Homo sapiens (human)
response to xenobiotic stimulusATP-dependent translocase ABCB1Homo sapiens (human)
phospholipid translocationATP-dependent translocase ABCB1Homo sapiens (human)
terpenoid transportATP-dependent translocase ABCB1Homo sapiens (human)
regulation of response to osmotic stressATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
transepithelial transportATP-dependent translocase ABCB1Homo sapiens (human)
stem cell proliferationATP-dependent translocase ABCB1Homo sapiens (human)
ceramide translocationATP-dependent translocase ABCB1Homo sapiens (human)
export across plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
positive regulation of anion channel activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transportATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic detoxification by transmembrane export across the plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transport across blood-brain barrierATP-dependent translocase ABCB1Homo sapiens (human)
regulation of chloride transportATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 2C9 Homo sapiens (human)
steroid metabolic processCytochrome P450 2C9 Homo sapiens (human)
cholesterol metabolic processCytochrome P450 2C9 Homo sapiens (human)
estrogen metabolic processCytochrome P450 2C9 Homo sapiens (human)
monoterpenoid metabolic processCytochrome P450 2C9 Homo sapiens (human)
epoxygenase P450 pathwayCytochrome P450 2C9 Homo sapiens (human)
urea metabolic processCytochrome P450 2C9 Homo sapiens (human)
monocarboxylic acid metabolic processCytochrome P450 2C9 Homo sapiens (human)
xenobiotic catabolic processCytochrome P450 2C9 Homo sapiens (human)
long-chain fatty acid biosynthetic processCytochrome P450 2C9 Homo sapiens (human)
amide metabolic processCytochrome P450 2C9 Homo sapiens (human)
icosanoid biosynthetic processCytochrome P450 2C9 Homo sapiens (human)
oxidative demethylationCytochrome P450 2C9 Homo sapiens (human)
omega-hydroxylase P450 pathwayCytochrome P450 2C9 Homo sapiens (human)
prostaglandin biosynthetic processThromboxane-A synthase Homo sapiens (human)
icosanoid metabolic processThromboxane-A synthase Homo sapiens (human)
cyclooxygenase pathwayThromboxane-A synthase Homo sapiens (human)
intracellular chloride ion homeostasisThromboxane-A synthase Homo sapiens (human)
response to ethanolThromboxane-A synthase Homo sapiens (human)
positive regulation of vasoconstrictionThromboxane-A synthase Homo sapiens (human)
response to fatty acidThromboxane-A synthase Homo sapiens (human)
positive regulation of macrophage chemotaxisMitogen-activated protein kinase 1Homo sapiens (human)
positive regulation of macrophage proliferationMitogen-activated protein kinase 1Homo sapiens (human)
regulation of transcription by RNA polymerase IIMitogen-activated protein kinase 1Homo sapiens (human)
protein phosphorylationMitogen-activated protein kinase 1Homo sapiens (human)
apoptotic processMitogen-activated protein kinase 1Homo sapiens (human)
chemotaxisMitogen-activated protein kinase 1Homo sapiens (human)
DNA damage responseMitogen-activated protein kinase 1Homo sapiens (human)
signal transductionMitogen-activated protein kinase 1Homo sapiens (human)
chemical synaptic transmissionMitogen-activated protein kinase 1Homo sapiens (human)
learning or memoryMitogen-activated protein kinase 1Homo sapiens (human)
insulin receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
positive regulation of peptidyl-threonine phosphorylationMitogen-activated protein kinase 1Homo sapiens (human)
Schwann cell developmentMitogen-activated protein kinase 1Homo sapiens (human)
peptidyl-serine phosphorylationMitogen-activated protein kinase 1Homo sapiens (human)
peptidyl-threonine phosphorylationMitogen-activated protein kinase 1Homo sapiens (human)
cytosine metabolic processMitogen-activated protein kinase 1Homo sapiens (human)
regulation of ossificationMitogen-activated protein kinase 1Homo sapiens (human)
androgen receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
regulation of cellular pHMitogen-activated protein kinase 1Homo sapiens (human)
thyroid gland developmentMitogen-activated protein kinase 1Homo sapiens (human)
regulation of protein stabilityMitogen-activated protein kinase 1Homo sapiens (human)
lipopolysaccharide-mediated signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
positive regulation of telomere maintenance via telomeraseMitogen-activated protein kinase 1Homo sapiens (human)
regulation of stress-activated MAPK cascadeMitogen-activated protein kinase 1Homo sapiens (human)
mammary gland epithelial cell proliferationMitogen-activated protein kinase 1Homo sapiens (human)
cellular response to amino acid starvationMitogen-activated protein kinase 1Homo sapiens (human)
cellular response to reactive oxygen speciesMitogen-activated protein kinase 1Homo sapiens (human)
response to nicotineMitogen-activated protein kinase 1Homo sapiens (human)
ERBB signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
ERBB2-ERBB3 signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
outer ear morphogenesisMitogen-activated protein kinase 1Homo sapiens (human)
myelinationMitogen-activated protein kinase 1Homo sapiens (human)
response to exogenous dsRNAMitogen-activated protein kinase 1Homo sapiens (human)
steroid hormone mediated signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
negative regulation of cell differentiationMitogen-activated protein kinase 1Homo sapiens (human)
insulin-like growth factor receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
thymus developmentMitogen-activated protein kinase 1Homo sapiens (human)
progesterone receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
T cell receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
B cell receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
stress-activated MAPK cascadeMitogen-activated protein kinase 1Homo sapiens (human)
regulation of cytoskeleton organizationMitogen-activated protein kinase 1Homo sapiens (human)
positive regulation of telomerase activityMitogen-activated protein kinase 1Homo sapiens (human)
Bergmann glial cell differentiationMitogen-activated protein kinase 1Homo sapiens (human)
long-term synaptic potentiationMitogen-activated protein kinase 1Homo sapiens (human)
face developmentMitogen-activated protein kinase 1Homo sapiens (human)
lung morphogenesisMitogen-activated protein kinase 1Homo sapiens (human)
trachea formationMitogen-activated protein kinase 1Homo sapiens (human)
labyrinthine layer blood vessel developmentMitogen-activated protein kinase 1Homo sapiens (human)
cardiac neural crest cell development involved in heart developmentMitogen-activated protein kinase 1Homo sapiens (human)
ERK1 and ERK2 cascadeMitogen-activated protein kinase 1Homo sapiens (human)
response to epidermal growth factorMitogen-activated protein kinase 1Homo sapiens (human)
cellular response to cadmium ionMitogen-activated protein kinase 1Homo sapiens (human)
cellular response to tumor necrosis factorMitogen-activated protein kinase 1Homo sapiens (human)
caveolin-mediated endocytosisMitogen-activated protein kinase 1Homo sapiens (human)
regulation of Golgi inheritanceMitogen-activated protein kinase 1Homo sapiens (human)
positive regulation of telomere cappingMitogen-activated protein kinase 1Homo sapiens (human)
regulation of early endosome to late endosome transportMitogen-activated protein kinase 1Homo sapiens (human)
cell surface receptor signaling pathwayMitogen-activated protein kinase 1Homo sapiens (human)
intracellular signal transductionMitogen-activated protein kinase 1Homo sapiens (human)
cellular response to organic substanceCaspase-1Homo sapiens (human)
pattern recognition receptor signaling pathwayCaspase-1Homo sapiens (human)
proteolysisCaspase-1Homo sapiens (human)
apoptotic processCaspase-1Homo sapiens (human)
signal transductionCaspase-1Homo sapiens (human)
osmosensory signaling pathwayCaspase-1Homo sapiens (human)
protein autoprocessingCaspase-1Homo sapiens (human)
positive regulation of interleukin-1 beta productionCaspase-1Homo sapiens (human)
positive regulation of interleukin-18 productionCaspase-1Homo sapiens (human)
defense response to bacteriumCaspase-1Homo sapiens (human)
regulation of apoptotic processCaspase-1Homo sapiens (human)
positive regulation of canonical NF-kappaB signal transductionCaspase-1Homo sapiens (human)
positive regulation of cysteine-type endopeptidase activity involved in apoptotic processCaspase-1Homo sapiens (human)
icosanoid biosynthetic processCaspase-1Homo sapiens (human)
regulation of inflammatory responseCaspase-1Homo sapiens (human)
positive regulation of inflammatory responseCaspase-1Homo sapiens (human)
protein maturationCaspase-1Homo sapiens (human)
defense response to virusCaspase-1Homo sapiens (human)
pyroptosisCaspase-1Homo sapiens (human)
cellular response to lipopolysaccharideCaspase-1Homo sapiens (human)
cellular response to mechanical stimulusCaspase-1Homo sapiens (human)
cellular response to type II interferonCaspase-1Homo sapiens (human)
cytokine precursor processingCaspase-1Homo sapiens (human)
signaling receptor ligand precursor processingCaspase-1Homo sapiens (human)
AIM2 inflammasome complex assemblyCaspase-1Homo sapiens (human)
positive regulation of tumor necrosis factor-mediated signaling pathwayCaspase-1Homo sapiens (human)
megakaryocyte differentiationFlavin reductase (NADPH)Homo sapiens (human)
heme catabolic processFlavin reductase (NADPH)Homo sapiens (human)
negative regulation of insulin receptor signaling pathwayFlavin reductase (NADPH)Homo sapiens (human)
brainstem developmentBifunctional purine biosynthesis protein ATICHomo sapiens (human)
nucleobase-containing compound metabolic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
GMP biosynthetic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
'de novo' IMP biosynthetic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
response to inorganic substanceBifunctional purine biosynthesis protein ATICHomo sapiens (human)
cerebellum developmentBifunctional purine biosynthesis protein ATICHomo sapiens (human)
cerebral cortex developmentBifunctional purine biosynthesis protein ATICHomo sapiens (human)
animal organ regenerationBifunctional purine biosynthesis protein ATICHomo sapiens (human)
'de novo' AMP biosynthetic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
dihydrofolate metabolic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
tetrahydrofolate biosynthetic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
'de novo' XMP biosynthetic processBifunctional purine biosynthesis protein ATICHomo sapiens (human)
cellular response to interleukin-7Bifunctional purine biosynthesis protein ATICHomo sapiens (human)
fatty acid metabolic processCytochrome P450 2J2Homo sapiens (human)
icosanoid metabolic processCytochrome P450 2J2Homo sapiens (human)
xenobiotic metabolic processCytochrome P450 2J2Homo sapiens (human)
regulation of heart contractionCytochrome P450 2J2Homo sapiens (human)
epoxygenase P450 pathwayCytochrome P450 2J2Homo sapiens (human)
linoleic acid metabolic processCytochrome P450 2J2Homo sapiens (human)
organic acid metabolic processCytochrome P450 2J2Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to hypoxiaDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
neutrophil mediated immunityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
germinal center formationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of leukocyte chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane protein ectodomain proteolysisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch receptor processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell population proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to xenobiotic stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of T cell chemotaxisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein processingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
signal releaseDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
B cell differentiationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell growthDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of transforming growth factor beta receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
response to lipopolysaccharideDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of chemokine productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor productionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
regulation of mast cell apoptotic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
T cell differentiation in thymusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell adhesion mediated by integrinDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
wound healing, spreading of epidermal cellsDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of blood vessel endothelial cell migrationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of cyclin-dependent protein serine/threonine kinase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor-activated receptor activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of epidermal growth factor receptor signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
spleen developmentDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell motilityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
defense response to Gram-positive bacteriumDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cellular response to high density lipoprotein particle stimulusDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
commissural neuron axon guidanceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
negative regulation of cold-induced thermogenesisDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of G1/S transition of mitotic cell cycleDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of tumor necrosis factor-mediated signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
positive regulation of vascular endothelial cell proliferationDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch signaling pathwayDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
sodium ion transportSodium/bile acid cotransporterHomo sapiens (human)
response to organic cyclic compoundSodium/bile acid cotransporterHomo sapiens (human)
bile acid and bile salt transportSodium/bile acid cotransporterHomo sapiens (human)
response to nutrient levelsSodium/bile acid cotransporterHomo sapiens (human)
bile acid signaling pathwaySodium/bile acid cotransporterHomo sapiens (human)
response to estrogenSodium/bile acid cotransporterHomo sapiens (human)
response to ethanolSodium/bile acid cotransporterHomo sapiens (human)
symbiont entry into host cellSodium/bile acid cotransporterHomo sapiens (human)
transmembrane transportSodium/bile acid cotransporterHomo sapiens (human)
cellular response to xenobiotic stimulusSodium/bile acid cotransporterHomo sapiens (human)
regulation of bile acid secretionSodium/bile acid cotransporterHomo sapiens (human)
inositol phosphate metabolic processInositol hexakisphosphate kinase 1Homo sapiens (human)
phosphatidylinositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
negative regulation of cold-induced thermogenesisInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol phosphate biosynthetic processInositol hexakisphosphate kinase 1Homo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
lipid transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid biosynthetic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate metabolic processBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transmembrane transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transepithelial transportBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
renal urate salt excretionBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
export across plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
cellular detoxificationBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transport across blood-brain barrierBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
glutathione metabolic processCystine/glutamate transporterHomo sapiens (human)
visual learningCystine/glutamate transporterHomo sapiens (human)
response to toxic substanceCystine/glutamate transporterHomo sapiens (human)
response to organic cyclic compoundCystine/glutamate transporterHomo sapiens (human)
L-cystine transportCystine/glutamate transporterHomo sapiens (human)
L-glutamate transmembrane transportCystine/glutamate transporterHomo sapiens (human)
ventricular system developmentCystine/glutamate transporterHomo sapiens (human)
striatum developmentCystine/glutamate transporterHomo sapiens (human)
adult behaviorCystine/glutamate transporterHomo sapiens (human)
regulation of neutrophil apoptotic processCystine/glutamate transporterHomo sapiens (human)
cellular response to oxidative stressCystine/glutamate transporterHomo sapiens (human)
glutathione transmembrane transportCystine/glutamate transporterHomo sapiens (human)
response to nicotineCystine/glutamate transporterHomo sapiens (human)
regulation of cell population proliferationCystine/glutamate transporterHomo sapiens (human)
regulation of melanin biosynthetic processCystine/glutamate transporterHomo sapiens (human)
lung alveolus developmentCystine/glutamate transporterHomo sapiens (human)
modulation of chemical synaptic transmissionCystine/glutamate transporterHomo sapiens (human)
regulation of synapse organizationCystine/glutamate transporterHomo sapiens (human)
regulation of protein transportCystine/glutamate transporterHomo sapiens (human)
response to redox stateCystine/glutamate transporterHomo sapiens (human)
limb developmentCystine/glutamate transporterHomo sapiens (human)
lens fiber cell differentiationCystine/glutamate transporterHomo sapiens (human)
platelet aggregationCystine/glutamate transporterHomo sapiens (human)
intracellular glutamate homeostasisCystine/glutamate transporterHomo sapiens (human)
L-glutamate import across plasma membraneCystine/glutamate transporterHomo sapiens (human)
negative regulation of ferroptosisCystine/glutamate transporterHomo sapiens (human)
dipeptide import across plasma membraneCystine/glutamate transporterHomo sapiens (human)
L-kynurenine transmembrane transportCystine/glutamate transporterHomo sapiens (human)
regulation of cellular response to oxidative stressCystine/glutamate transporterHomo sapiens (human)
regulation of cysteine metabolic processCystine/glutamate transporterHomo sapiens (human)
regulation of glutathione biosynthetic processCystine/glutamate transporterHomo sapiens (human)
regulation of AMPA glutamate receptor clusteringCystine/glutamate transporterHomo sapiens (human)
regulation of glutamate metabolic processCystine/glutamate transporterHomo sapiens (human)
amino acid transmembrane transportCystine/glutamate transporterHomo sapiens (human)
xenobiotic metabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
monoatomic ion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid and bile salt transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
heme catabolic processSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
transmembrane transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transportSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Molecular Functions (132)

Processvia Protein(s)Taxonomy
ATP bindingATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
glucuronoside transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type bile acid transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATP hydrolysis activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
icosanoid transmembrane transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
ABC-type transporter activityATP-binding cassette sub-family C member 3Homo sapiens (human)
guanine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
protein bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ATP bindingMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type xenobiotic transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
prostaglandin transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
urate transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
purine nucleotide transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type glutathione S-conjugate transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type bile acid transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
efflux transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
15-hydroxyprostaglandin dehydrogenase (NAD+) activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATP hydrolysis activityMultidrug resistance-associated protein 4Homo sapiens (human)
glutathione transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
xenobiotic transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ATPase-coupled inorganic anion transmembrane transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
ABC-type transporter activityMultidrug resistance-associated protein 4Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
protein bindingBile salt export pumpHomo sapiens (human)
ATP bindingBile salt export pumpHomo sapiens (human)
ABC-type xenobiotic transporter activityBile salt export pumpHomo sapiens (human)
bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
canalicular bile acid transmembrane transporter activityBile salt export pumpHomo sapiens (human)
carbohydrate transmembrane transporter activityBile salt export pumpHomo sapiens (human)
ABC-type bile acid transporter activityBile salt export pumpHomo sapiens (human)
ATP hydrolysis activityBile salt export pumpHomo sapiens (human)
arylesterase activityCarbonic anhydrase 1Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 1Homo sapiens (human)
protein bindingCarbonic anhydrase 1Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 1Homo sapiens (human)
hydro-lyase activityCarbonic anhydrase 1Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 1Homo sapiens (human)
arylesterase activityCarbonic anhydrase 2Homo sapiens (human)
carbonate dehydratase activityCarbonic anhydrase 2Homo sapiens (human)
protein bindingCarbonic anhydrase 2Homo sapiens (human)
zinc ion bindingCarbonic anhydrase 2Homo sapiens (human)
cyanamide hydratase activityCarbonic anhydrase 2Homo sapiens (human)
transcription cis-regulatory region bindingTumor necrosis factorHomo sapiens (human)
protease bindingTumor necrosis factorHomo sapiens (human)
cytokine activityTumor necrosis factorHomo sapiens (human)
tumor necrosis factor receptor bindingTumor necrosis factorHomo sapiens (human)
protein bindingTumor necrosis factorHomo sapiens (human)
death receptor agonist activityTumor necrosis factorHomo sapiens (human)
identical protein bindingTumor necrosis factorHomo sapiens (human)
cytokine activityInterferon betaHomo sapiens (human)
cytokine receptor bindingInterferon betaHomo sapiens (human)
type I interferon receptor bindingInterferon betaHomo sapiens (human)
protein bindingInterferon betaHomo sapiens (human)
chloramphenicol O-acetyltransferase activityInterferon betaHomo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
signaling receptor bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
peptide antigen bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
TAP bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
protein-folding chaperone bindingHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endopeptidase activityInterstitial collagenaseHomo sapiens (human)
metalloendopeptidase activityInterstitial collagenaseHomo sapiens (human)
serine-type endopeptidase activityInterstitial collagenaseHomo sapiens (human)
peptidase activityInterstitial collagenaseHomo sapiens (human)
zinc ion bindingInterstitial collagenaseHomo sapiens (human)
fibroblast growth factor receptor bindingFibroblast growth factor 1Homo sapiens (human)
integrin bindingFibroblast growth factor 1Homo sapiens (human)
protein bindingFibroblast growth factor 1Homo sapiens (human)
growth factor activityFibroblast growth factor 1Homo sapiens (human)
heparin bindingFibroblast growth factor 1Homo sapiens (human)
Hsp70 protein bindingFibroblast growth factor 1Homo sapiens (human)
S100 protein bindingFibroblast growth factor 1Homo sapiens (human)
protein bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATP bindingATP-dependent translocase ABCB1Homo sapiens (human)
ABC-type xenobiotic transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
efflux transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ATP hydrolysis activityATP-dependent translocase ABCB1Homo sapiens (human)
transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
ubiquitin protein ligase bindingATP-dependent translocase ABCB1Homo sapiens (human)
ATPase-coupled transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
xenobiotic transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
carboxylic acid transmembrane transporter activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylcholine floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
phosphatidylethanolamine flippase activityATP-dependent translocase ABCB1Homo sapiens (human)
ceramide floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
floppase activityATP-dependent translocase ABCB1Homo sapiens (human)
monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
iron ion bindingCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
steroid hydroxylase activityCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid 14,15-epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
arachidonic acid 11,12-epoxygenase activityCytochrome P450 2C9 Homo sapiens (human)
oxidoreductase activityCytochrome P450 2C9 Homo sapiens (human)
(S)-limonene 6-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
(S)-limonene 7-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
caffeine oxidase activityCytochrome P450 2C9 Homo sapiens (human)
(R)-limonene 6-monooxygenase activityCytochrome P450 2C9 Homo sapiens (human)
aromatase activityCytochrome P450 2C9 Homo sapiens (human)
heme bindingCytochrome P450 2C9 Homo 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 2C9 Homo sapiens (human)
monooxygenase activityThromboxane-A synthase Homo sapiens (human)
thromboxane-A synthase activityThromboxane-A synthase Homo sapiens (human)
iron ion bindingThromboxane-A synthase Homo sapiens (human)
oxidoreductase activity, acting on paired donors, with incorporation or reduction of molecular oxygenThromboxane-A synthase Homo sapiens (human)
heme bindingThromboxane-A synthase Homo sapiens (human)
12-hydroxyheptadecatrienoic acid synthase activityThromboxane-A synthase Homo sapiens (human)
hydroperoxy icosatetraenoate dehydratase activityThromboxane-A synthase Homo sapiens (human)
phosphotyrosine residue bindingMitogen-activated protein kinase 1Homo sapiens (human)
DNA bindingMitogen-activated protein kinase 1Homo sapiens (human)
protein serine/threonine kinase activityMitogen-activated protein kinase 1Homo sapiens (human)
MAP kinase activityMitogen-activated protein kinase 1Homo sapiens (human)
protein bindingMitogen-activated protein kinase 1Homo sapiens (human)
ATP bindingMitogen-activated protein kinase 1Homo sapiens (human)
RNA polymerase II CTD heptapeptide repeat kinase activityMitogen-activated protein kinase 1Homo sapiens (human)
phosphatase bindingMitogen-activated protein kinase 1Homo sapiens (human)
identical protein bindingMitogen-activated protein kinase 1Homo sapiens (human)
protein serine kinase activityMitogen-activated protein kinase 1Homo sapiens (human)
endopeptidase activityCaspase-1Homo sapiens (human)
cysteine-type endopeptidase activityCaspase-1Homo sapiens (human)
protein bindingCaspase-1Homo sapiens (human)
cysteine-type endopeptidase activator activity involved in apoptotic processCaspase-1Homo sapiens (human)
kinase bindingCaspase-1Homo sapiens (human)
cytokine bindingCaspase-1Homo sapiens (human)
identical protein bindingCaspase-1Homo sapiens (human)
CARD domain bindingCaspase-1Homo sapiens (human)
caspase bindingCaspase-1Homo sapiens (human)
biliverdin reductase (NAD(P)H) activityFlavin reductase (NADPH)Homo sapiens (human)
protein bindingFlavin reductase (NADPH)Homo sapiens (human)
FMN reductase (NAD(P)H) activityFlavin reductase (NADPH)Homo sapiens (human)
peptidyl-cysteine S-nitrosylase activityFlavin reductase (NADPH)Homo sapiens (human)
riboflavin reductase (NADPH) activityFlavin reductase (NADPH)Homo sapiens (human)
FMN reductase (NADPH) activityFlavin reductase (NADPH)Homo sapiens (human)
FMN reductase (NADH) activityFlavin reductase (NADPH)Homo sapiens (human)
biliberdin reductase NAD+ activityFlavin reductase (NADPH)Homo sapiens (human)
biliverdin reductase (NADPH) activityFlavin reductase (NADPH)Homo sapiens (human)
IMP cyclohydrolase activityBifunctional purine biosynthesis protein ATICHomo sapiens (human)
protein homodimerization activityBifunctional purine biosynthesis protein ATICHomo sapiens (human)
cadherin bindingBifunctional purine biosynthesis protein ATICHomo sapiens (human)
phosphoribosylaminoimidazolecarboxamide formyltransferase activityBifunctional purine biosynthesis protein ATICHomo sapiens (human)
monooxygenase activityCytochrome P450 2J2Homo sapiens (human)
iron ion bindingCytochrome P450 2J2Homo sapiens (human)
arachidonic acid epoxygenase activityCytochrome P450 2J2Homo sapiens (human)
arachidonic acid 14,15-epoxygenase activityCytochrome P450 2J2Homo sapiens (human)
arachidonic acid 11,12-epoxygenase activityCytochrome P450 2J2Homo sapiens (human)
isomerase activityCytochrome P450 2J2Homo sapiens (human)
linoleic acid epoxygenase activityCytochrome P450 2J2Homo sapiens (human)
hydroperoxy icosatetraenoate isomerase activityCytochrome P450 2J2Homo sapiens (human)
arachidonic acid 5,6-epoxygenase activityCytochrome P450 2J2Homo sapiens (human)
heme bindingCytochrome P450 2J2Homo 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 2J2Homo sapiens (human)
endopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Notch bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
interleukin-6 receptor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
integrin bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
protein bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
peptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metallopeptidase activityDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
SH3 domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytokine bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
PDZ domain bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
tumor necrosis factor bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metal ion bindingDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
metalloendopeptidase activity involved in amyloid precursor protein catabolic processDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
virus receptor activitySodium/bile acid cotransporterHomo sapiens (human)
protein bindingSodium/bile acid cotransporterHomo sapiens (human)
bile acid:sodium symporter activitySodium/bile acid cotransporterHomo sapiens (human)
inositol-1,3,4,5,6-pentakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol heptakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
protein bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
ATP bindingInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 1-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol hexakisphosphate 3-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol 5-diphosphate pentakisphosphate 5-kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
inositol diphosphate tetrakisphosphate kinase activityInositol hexakisphosphate kinase 1Homo sapiens (human)
serine-type endopeptidase inhibitor activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B3Homo sapiens (human)
protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
organic anion transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ABC-type xenobiotic transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
urate transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
biotin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
efflux transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATP hydrolysis activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
riboflavin transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
ATPase-coupled transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
identical protein bindingBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
protein homodimerization activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
xenobiotic transmembrane transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
sphingolipid transporter activityBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
protein bindingCystine/glutamate transporterHomo sapiens (human)
cystine:glutamate antiporter activityCystine/glutamate transporterHomo sapiens (human)
L-kynurenine transmembrane transporter activityCystine/glutamate transporterHomo sapiens (human)
L-amino acid transmembrane transporter activityCystine/glutamate transporterHomo sapiens (human)
organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
bile acid transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
prostaglandin transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
sodium-independent organic anion transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
thyroid hormone transmembrane transporter activitySolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Ceullar Components (69)

Processvia Protein(s)Taxonomy
plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basal plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
basolateral plasma membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
membraneATP-binding cassette sub-family C member 3Homo sapiens (human)
nucleolusMultidrug resistance-associated protein 4Homo sapiens (human)
Golgi apparatusMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
membraneMultidrug resistance-associated protein 4Homo sapiens (human)
basolateral plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
platelet dense granule membraneMultidrug resistance-associated protein 4Homo sapiens (human)
external side of apical plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneMultidrug resistance-associated protein 4Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
apical plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
apical plasma membraneSolute carrier organic anion transporter family member 2B1 Homo sapiens (human)
basolateral plasma membraneBile salt export pumpHomo sapiens (human)
Golgi membraneBile salt export pumpHomo sapiens (human)
endosomeBile salt export pumpHomo sapiens (human)
plasma membraneBile salt export pumpHomo sapiens (human)
cell surfaceBile salt export pumpHomo sapiens (human)
apical plasma membraneBile salt export pumpHomo sapiens (human)
intercellular canaliculusBile salt export pumpHomo sapiens (human)
intracellular canaliculusBile salt export pumpHomo sapiens (human)
recycling endosomeBile salt export pumpHomo sapiens (human)
recycling endosome membraneBile salt export pumpHomo sapiens (human)
extracellular exosomeBile salt export pumpHomo sapiens (human)
membraneBile salt export pumpHomo sapiens (human)
cytosolCarbonic anhydrase 1Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 1Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
cytosolCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
myelin sheathCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
extracellular exosomeCarbonic anhydrase 2Homo sapiens (human)
cytoplasmCarbonic anhydrase 2Homo sapiens (human)
plasma membraneCarbonic anhydrase 2Homo sapiens (human)
apical part of cellCarbonic anhydrase 2Homo sapiens (human)
extracellular spaceTumor necrosis factorHomo sapiens (human)
phagocytic cupTumor necrosis factorHomo sapiens (human)
extracellular regionTumor necrosis factorHomo sapiens (human)
extracellular spaceTumor necrosis factorHomo sapiens (human)
plasma membraneTumor necrosis factorHomo sapiens (human)
external side of plasma membraneTumor necrosis factorHomo sapiens (human)
cell surfaceTumor necrosis factorHomo sapiens (human)
neuronal cell bodyTumor necrosis factorHomo sapiens (human)
membrane raftTumor necrosis factorHomo sapiens (human)
recycling endosomeTumor necrosis factorHomo sapiens (human)
cell surfaceTumor necrosis factorHomo sapiens (human)
extracellular spaceInterferon betaHomo sapiens (human)
extracellular regionInterferon betaHomo sapiens (human)
Golgi membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
endoplasmic reticulumHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
Golgi apparatusHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
cell surfaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
ER to Golgi transport vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
secretory granule membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
phagocytic vesicle membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
early endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
recycling endosome membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular exosomeHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
lumenal side of endoplasmic reticulum membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
MHC class I protein complexHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular spaceHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
external side of plasma membraneHLA class I histocompatibility antigen, B alpha chain Homo sapiens (human)
extracellular regionInterstitial collagenaseHomo sapiens (human)
extracellular matrixInterstitial collagenaseHomo sapiens (human)
extracellular spaceInterstitial collagenaseHomo sapiens (human)
extracellular regionFibroblast growth factor 1Homo sapiens (human)
extracellular spaceFibroblast growth factor 1Homo sapiens (human)
nucleoplasmFibroblast growth factor 1Homo sapiens (human)
cytosolFibroblast growth factor 1Homo sapiens (human)
cell cortexFibroblast growth factor 1Homo sapiens (human)
extracellular matrixFibroblast growth factor 1Homo sapiens (human)
cytoplasmFibroblast growth factor 1Homo sapiens (human)
extracellular spaceFibroblast growth factor 1Homo sapiens (human)
nucleusFibroblast growth factor 1Homo sapiens (human)
cytoplasmATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
cell surfaceATP-dependent translocase ABCB1Homo sapiens (human)
membraneATP-dependent translocase ABCB1Homo sapiens (human)
apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
extracellular exosomeATP-dependent translocase ABCB1Homo sapiens (human)
external side of apical plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
plasma membraneATP-dependent translocase ABCB1Homo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2C9 Homo sapiens (human)
plasma membraneCytochrome P450 2C9 Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C9 Homo sapiens (human)
cytoplasmCytochrome P450 2C9 Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2C9 Homo sapiens (human)
endoplasmic reticulumThromboxane-A synthase Homo sapiens (human)
endoplasmic reticulum membraneThromboxane-A synthase Homo sapiens (human)
cytosolThromboxane-A synthase Homo sapiens (human)
extracellular regionMitogen-activated protein kinase 1Homo sapiens (human)
nucleusMitogen-activated protein kinase 1Homo sapiens (human)
nucleoplasmMitogen-activated protein kinase 1Homo sapiens (human)
cytoplasmMitogen-activated protein kinase 1Homo sapiens (human)
mitochondrionMitogen-activated protein kinase 1Homo sapiens (human)
early endosomeMitogen-activated protein kinase 1Homo sapiens (human)
late endosomeMitogen-activated protein kinase 1Homo sapiens (human)
endoplasmic reticulum lumenMitogen-activated protein kinase 1Homo sapiens (human)
Golgi apparatusMitogen-activated protein kinase 1Homo sapiens (human)
centrosomeMitogen-activated protein kinase 1Homo sapiens (human)
cytosolMitogen-activated protein kinase 1Homo sapiens (human)
cytoskeletonMitogen-activated protein kinase 1Homo sapiens (human)
plasma membraneMitogen-activated protein kinase 1Homo sapiens (human)
caveolaMitogen-activated protein kinase 1Homo sapiens (human)
focal adhesionMitogen-activated protein kinase 1Homo sapiens (human)
pseudopodiumMitogen-activated protein kinase 1Homo sapiens (human)
azurophil granule lumenMitogen-activated protein kinase 1Homo sapiens (human)
synapseMitogen-activated protein kinase 1Homo sapiens (human)
mitotic spindleMitogen-activated protein kinase 1Homo sapiens (human)
ficolin-1-rich granule lumenMitogen-activated protein kinase 1Homo sapiens (human)
cytoplasmMitogen-activated protein kinase 1Homo sapiens (human)
nucleusMitogen-activated protein kinase 1Homo sapiens (human)
cytoplasmCaspase-1Homo sapiens (human)
cytosolCaspase-1Homo sapiens (human)
nucleolusCaspase-1Homo sapiens (human)
cytoplasmCaspase-1Homo sapiens (human)
cytosolCaspase-1Homo sapiens (human)
microtubuleCaspase-1Homo sapiens (human)
plasma membraneCaspase-1Homo sapiens (human)
canonical inflammasome complexCaspase-1Homo sapiens (human)
NLRP1 inflammasome complexCaspase-1Homo sapiens (human)
NLRP3 inflammasome complexCaspase-1Homo sapiens (human)
AIM2 inflammasome complexCaspase-1Homo sapiens (human)
protein-containing complexCaspase-1Homo sapiens (human)
IPAF inflammasome complexCaspase-1Homo sapiens (human)
protease inhibitor complexCaspase-1Homo sapiens (human)
cytoplasmFlavin reductase (NADPH)Homo sapiens (human)
nucleoplasmFlavin reductase (NADPH)Homo sapiens (human)
cytosolFlavin reductase (NADPH)Homo sapiens (human)
plasma membraneFlavin reductase (NADPH)Homo sapiens (human)
intracellular membrane-bounded organelleFlavin reductase (NADPH)Homo sapiens (human)
extracellular exosomeFlavin reductase (NADPH)Homo sapiens (human)
cytosolBifunctional purine biosynthesis protein ATICHomo sapiens (human)
plasma membraneBifunctional purine biosynthesis protein ATICHomo sapiens (human)
membraneBifunctional purine biosynthesis protein ATICHomo sapiens (human)
extracellular exosomeBifunctional purine biosynthesis protein ATICHomo sapiens (human)
cytosolBifunctional purine biosynthesis protein ATICHomo sapiens (human)
endoplasmic reticulum membraneCytochrome P450 2J2Homo sapiens (human)
extracellular exosomeCytochrome P450 2J2Homo sapiens (human)
cytoplasmCytochrome P450 2J2Homo sapiens (human)
intracellular membrane-bounded organelleCytochrome P450 2J2Homo sapiens (human)
cell-cell junctionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
focal adhesionDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
ruffle membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
Golgi membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytoplasmDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
endoplasmic reticulum lumenDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cytosolDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
cell surfaceDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
actin cytoskeletonDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
apical plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
membrane raftDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneDisintegrin and metalloproteinase domain-containing protein 17Homo sapiens (human)
plasma membraneSodium/bile acid cotransporterHomo sapiens (human)
basolateral plasma membraneSodium/bile acid cotransporterHomo sapiens (human)
fibrillar centerInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
cytosolInositol hexakisphosphate kinase 1Homo sapiens (human)
nucleusInositol hexakisphosphate kinase 1Homo sapiens (human)
cytoplasmInositol hexakisphosphate kinase 1Homo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B3Homo sapiens (human)
nucleoplasmBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
brush border membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
mitochondrial membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
membrane raftBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
external side of apical plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneBroad substrate specificity ATP-binding cassette transporter ABCG2Homo sapiens (human)
plasma membraneCystine/glutamate transporterHomo sapiens (human)
cell surfaceCystine/glutamate transporterHomo sapiens (human)
membraneCystine/glutamate transporterHomo sapiens (human)
brush border membraneCystine/glutamate transporterHomo sapiens (human)
microvillus membraneCystine/glutamate transporterHomo sapiens (human)
apical part of cellCystine/glutamate transporterHomo sapiens (human)
astrocyte projectionCystine/glutamate transporterHomo sapiens (human)
plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basal plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
basolateral plasma membraneSolute carrier organic anion transporter family member 1B1Homo sapiens (human)
[Information is prepared from geneontology information from the June-17-2024 release]

Bioassays (472)

Assay IDTitleYearJournalArticle
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.
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.
AID1347103qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for OHS-50 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
AID1347097qHTS of pediatric cancer cell lines to identify multiple opportunities for drug repurposing: Primary screen for Saos-2 cells2018Oncotarget, Jan-12, Volume: 9, Issue:4
Quantitative high-throughput phenotypic screening of pediatric cancer cell lines identifies multiple opportunities for drug repurposing.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
AID1745845Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
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.
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.
AID651635Viability Counterscreen for Primary qHTS for Inhibitors of ATXN expression
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.
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.
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.
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.
AID977610Experimentally measured binding affinity data (Ki) for protein-ligand complexes derived from PDB1999Journal of molecular biology, Aug-27, Volume: 291, Issue:4
The ligandin (non-substrate) binding site of human Pi class glutathione transferase is located in the electrophile binding site (H-site).
AID1811Experimentally measured binding affinity data derived from PDB1999Journal of molecular biology, Aug-27, Volume: 291, Issue:4
The ligandin (non-substrate) binding site of human Pi class glutathione transferase is located in the electrophile binding site (H-site).
AID1347161Confirmatory screen NINDS Rhodamine qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
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.
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.
AID1347149Furin counterscreen qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347411qHTS to identify inhibitors of the type 1 interferon - major histocompatibility complex class I in skeletal muscle: primary screen against the NCATS Mechanism Interrogation Plate v5.0 (MIPE) Libary2020ACS chemical biology, 07-17, Volume: 15, Issue:7
High-Throughput Screening to Identify Inhibitors of the Type I Interferon-Major Histocompatibility Complex Class I Pathway in Skeletal Muscle.
AID1347169Tertiary RLuc qRT-PCR qHTS assay for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347157Confirmatory screen GU Rhodamine qHTS for Zika virus inhibitors qHTS2020Proceedings 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.
AID588519A screen for compounds that inhibit viral RNA polymerase binding and polymerization activities2011Antiviral research, Sep, Volume: 91, Issue:3
High-throughput screening identification of poliovirus RNA-dependent RNA polymerase inhibitors.
AID540299A screen for compounds that inhibit the MenB enzyme of Mycobacterium tuberculosis2010Bioorganic & medicinal chemistry letters, Nov-01, Volume: 20, Issue:21
Synthesis and SAR studies of 1,4-benzoxazine MenB inhibitors: novel antibacterial agents against Mycobacterium tuberculosis.
AID686947qHTS for small molecule inhibitors of Yes1 kinase: Primary Screen2013Bioorganic & medicinal chemistry letters, Aug-01, Volume: 23, Issue:15
Identification of potent Yes1 kinase inhibitors using a library screening approach.
AID622159Inhibition of xc-cystine-glutamate antiporter-mediated cystine uptake in human U87 cells using L-[14C]cystine as substrate after 15 mins by liquid scintillation counting2011Bioorganic & medicinal chemistry letters, Oct-15, Volume: 21, Issue:20
Inhibition of xc⁻ transporter-mediated cystine uptake by sulfasalazine analogs.
AID231333Ratio of [(apical to basal)/(basal to apical)] (Caco-2 cell monolayer)2001Journal of medicinal chemistry, Jun-07, Volume: 44, Issue:12
Experimental and computational screening models for the prediction of intestinal drug absorption.
AID444055Fraction absorbed in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1211093Tmax in wild-type Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID386623Inhibition of 4-(4-(dimethylamino)styryl)-N-methylpyridinium uptake at human OCT1 expressed in HEK293 cells at 100 uM by confocal microscopy2008Journal of medicinal chemistry, Oct-09, Volume: 51, Issue:19
Structural requirements for drug inhibition of the liver specific human organic cation transport protein 1.
AID1211023Clearance in BCRP knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1079943Malignant tumor, proven histopathologically. Value is number of references indexed. [column 'T.MAL' in source]
AID1129361Unbound fraction in HEK293 cell homogenate at 0.1 uM by equilibrium dialysis based UPLC-MS/MS analysis2014Journal of medicinal chemistry, Apr-10, Volume: 57, Issue:7
A high-throughput cell-based method to predict the unbound drug fraction in the brain.
AID156203Binding to POPC/GMI liposomes using biosensor system2000Journal of medicinal chemistry, Jun-01, Volume: 43, Issue:11
SPR biosensor studies of the direct interaction between 27 drugs and a liposome surface: correlation with fraction absorbed in humans.
AID436239Antiinflammatory activity against trinitrobenzenesulfonic acid-induced colitis in Wistar rat assessed as decrease in colonic myeloperoxidase activity at 100 mg/kg, po measured 24 hrs after last dose on day 11 by spectrometry2009European journal of medicinal chemistry, Oct, Volume: 44, Issue:10
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrugs of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1473740Inhibition of human MRP3 overexpressed in Sf9 insect cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 10 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1757483Anti-colitis activity against DSS-induced BALB/c mouse model of subchronic relapsing colitis assessed as effect on colon length at 100 mg/kg/day, po administered for 7 days in second week during 2 weeks DSS challenge and measured at the end of 2nd week2021European journal of medicinal chemistry, Apr-15, Volume: 2166-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3β).
AID1211167Tmax in BCRP knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211146Volume of distribution at steady state in MRP2-deficient Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211148Half life in MRP2-deficient Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID588217FDA HLAED, serum glutamic pyruvic transaminase (SGPT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1211158AUC (infinity) in MDR1A knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1413411Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in ICAM1 expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by Western blot analysi2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1245316Anti-ulcerative colitis activity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as improvement in number of visible colitis lesions at 300 mg/kg, po qd measured on day 82015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID1272121Antiulcerative colitis activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in severity of inflammation at 300 mg/kg qd for 6 consecutive days measured on 7th day2016European journal of medicinal chemistry, Jan-27, Volume: 108Synthesis, colon-targeted studies and pharmacological evaluation of an anti-ulcerative colitis drug 4-Aminosalicylic acid-β-O-glucoside.
AID1079934Highest frequency of acute liver toxicity observed during clinical trials, expressed as a percentage. [column '% AIGUE' in source]
AID1757471Anti-colitis activity against DSS-induced BALB/c mouse model of subchronic relapsing colitis assessed as increase in body weight at 100 mg/kg/day, po administered for 7 days in second week during 2 weeks DSS challenge and measured at the end of 2nd week2021European journal of medicinal chemistry, Apr-15, Volume: 2166-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3β).
AID509500Antibacterial activity agaisnt Staphylococcus aureus MTCC 3160 by agar diffusion method2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID1209582Unbound volume of distribution in Sprague-Dawley rat brain slices at 100 nM after 5 hrs2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1824207Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as fold decrease in disease activity index at 50 mg/kg, po administered via gavage twice daily for 10 days relative to control2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID236916Percentage of mass balance in hexadecane membranes model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID1245298Toxicity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as change in body weight at 300 mg/kg, po qd (Rvb = -15.3%)2015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID1221977Transporter substrate index of efflux ratio in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID699543Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1824877Anti-colitis activity against DSS-induced BALB/c mouse model assessed as increase in body weight at 100 mg/kg, po administered for 5 to 14 days2022Journal of medicinal chemistry, 01-13, Volume: 65, Issue:1
Discovery of a Series of Pyrimidine Carboxamides as Inhibitors of Vanin-1.
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.
AID296197Antiinflammatory activity against dextran sodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as rectal prolaps2007European journal of medicinal chemistry, Aug, Volume: 42, Issue:8
Antileukotrienic N-arylethyl-2-arylacetamides in the treatment of ulcerative colitis.
AID604025Unbound CSF to plasma concentration ratio in Sprague-Dawley rat administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID625283Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for elevated liver function tests2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID156089Binding to POPC (palmitoyl-oleolyl-phosphatidyl-choline) liposomes using biosensor system2000Journal of medicinal chemistry, Jun-01, Volume: 43, Issue:11
SPR biosensor studies of the direct interaction between 27 drugs and a liposome surface: correlation with fraction absorbed in humans.
AID1221980Transporter substrate index of efflux ratio in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID453204Permeability in human skin after 48 hrs by Franz cell permeability assay2010Bioorganic & medicinal chemistry letters, Jan-01, Volume: 20, Issue:1
Development of an in silico model for human skin permeation based on a Franz cell skin permeability assay.
AID1594519Binding affinity to MERS-CoV papain-like protease by SPR analysis2019Bioorganic & medicinal chemistry, 05-15, Volume: 27, Issue:10
Identification and design of novel small molecule inhibitors against MERS-CoV papain-like protease via high-throughput screening and molecular modeling.
AID1824213Anti-colitis activity against DSS-induced C57BL/6 mouse model of colitis assessed as fold change in disease activity index at 25 to 100 mg/kg, po administered via gavage twice a day for 10 days relative to SASP2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID194538Tested for peak serum concentration in rat 61983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211024Clearance in MRP2 knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID699544Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID588214FDA HLAED, liver enzyme composite activity2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1815672Binding affinity to human N-terminal His6-tagged and thrombin cleavage fused BLVRB expressed in Escherichia coli BL21 (DE3) assessed as change in enthalpy by isothermal titration calorimetry2022Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3
Repositioning Food and Drug Administration-Approved Drugs for Inhibiting Biliverdin IXβ Reductase B as a Novel Thrombocytopenia Therapeutic Target.
AID73470Binding affinity for Fibroblast growth factor 2 (No data)2004Journal of medicinal chemistry, Mar-25, Volume: 47, Issue:7
Validation of molecular docking calculations involving FGF-1 and FGF-2.
AID1221969Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1413403Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as myeloperoxidase level at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by ELISA (Rvb = 456.67 +/- 41.2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID696364Inhibition of NF-kappaB expressed in human HepG2 cells assessed as inhibition of TNFalpha-induced luciferase activity preincubated for 1 hr followed by TNFalpha challenge measured after 1 hr by reporter gene assay2012Bioorganic & medicinal chemistry letters, Nov-01, Volume: 22, Issue:21
Diarylheptanoid glycosides from Tacca plantaginea and their effects on NF-κB activation and PPAR transcriptional activity.
AID1221958Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1404016Permeability of the compound by PAMPA2018European journal of medicinal chemistry, Feb-10, Volume: 145Chameleon-like behavior of indolylpiperidines in complex with cholinesterases targets: Potent butyrylcholinesterase inhibitors.
AID1676588Binding affinity to Zinc ion assessed as performance ratio ratio by measuring product of accounting ratio and retention ratio at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1896148Inhibition of preS1-peptide binding to human HA-tagged NTCP in U2OS expresseing NTCP in incubated for 24 hrs using Myrcludex B as substrate by competitive binding assay2022Journal of medicinal chemistry, 10-13, Volume: 65, Issue:19
Inhibiting Sodium Taurocholate Cotransporting Polypeptide in HBV-Related Diseases: From Biological Function to Therapeutic Potential.
AID1272123Antiulcerative colitis activity in TNBS-induced Sprague-Dawley rat colitis model assessed as myeloperoxidase activity at 300 mg/kg, qd for 6 consecutive days by spectrophotometry (Rvb = 1.44 +/- 0.041 U/g)2016European journal of medicinal chemistry, Jan-27, Volume: 108Synthesis, colon-targeted studies and pharmacological evaluation of an anti-ulcerative colitis drug 4-Aminosalicylic acid-β-O-glucoside.
AID170015Effect of compound on myeloperoxidase activity was evaluated in rat2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID1211151Volume of distribution at steady state in BCRP knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1690379Activation of ABCB1 ATPase activity (unknown origin) expressed in baculovirus infected Sf9 insect cells using ATP as substrate measured after 1 hr by colorimetric assay2020European journal of medicinal chemistry, Apr-01, Volume: 191Tariquidar-related triazoles as potent, selective and stable inhibitors of ABCG2 (BCRP).
AID1392402Inhibition of DSS-induced acute ulcerative colitis C57BL/6J mouse model at 500 mg/kg, po qd administered for 7 days relative to control2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Syntheses and structure-activity relationships on antibacterial and anti-ulcerative colitis properties of quaternary 13-substituted palmatines and 8-oxo-13-substituted dihydropalmatines.
AID614828Binding affinity to dipalmitoyl phosphatidyl choline lipid bilayer assessed as decrease in pre-transition temperature at compound to lipid molar ratio of 1:5 by DSC technique2011European journal of medicinal chemistry, Sep, Volume: 46, Issue:9
In-vitro metabolic inhibition and antifertility effect facilitated by membrane alteration: search for novel antifertility agent using nifedipine analogues.
AID678721Metabolic stability in human liver microsomes assessed as GSH adduct formation at 100 uM after 90 mins by HPLC-MS analysis2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID588215FDA HLAED, alkaline phosphatase increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID588218FDA HLAED, lactate dehydrogenase (LDH) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID444054Oral bioavailability in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID588219FDA HLAED, gamma-glutamyl transferase (GGT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID604021Unbound volume of distribution in Sprague-Dawley rat brain measured per gram of brain tissue administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr b2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID1074029Apparent permeability in pig LLC-PK1 cells by LC-MS/MS analysis2014Journal of medicinal chemistry, Feb-13, Volume: 57, Issue:3
Discovery of 7-tetrahydropyran-2-yl chromans: β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors that reduce amyloid β-protein (Aβ) in the central nervous system.
AID509501Antibacterial activity agaisnt Bacillus subtilis MTCC 1456 by agar diffusion method2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID625292Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) combined score2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID678714Inhibition of human CYP2C19 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 3-butyryl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID152782Inhibitory concentration against growth of LPS stimulated human peripheral blood mononuclear cells2001Bioorganic & medicinal chemistry letters, Feb-26, Volume: 11, Issue:4
Structure-activity relationships of quinazoline derivatives: dual-acting compounds with inhibitory activities toward both TNF-alpha production and T cell proliferation.
AID1211165Tmax in wild-type Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID509504Antiulcerogenic activity against acetic acid-induced ulcerative colitis in albino rat assessed as ulcer area at 12.5 mmol/kg, po2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID194533Tested for peak serum concentration in rat1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211149AUC (infinity) in wild-type Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1676598Binding affinity to cupric ion assessed as retention ratio by measuring compound detected in elution fraction/total compound detected at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1413402Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as recovery in colon weight at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 72018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1221974Fold activity change at MRP2 ATPase (unknown origin) relative to control2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1474166Liver toxicity in human assessed as induction of drug-induced liver injury by measuring severity class index2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID1211152Volume of distribution at steady state in MRP2 knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID179007Fecal recovery in colostomized rats at 2 hr intervals for 48 h1993Journal of medicinal chemistry, Dec-24, Volume: 36, Issue:26
Brush-border-enzyme-mediated intestine-specific drug delivery. Amino acid prodrugs of 5-aminosalicylic acid.
AID1676593Binding affinity to Gallium ion assessed as retention ratio by measuring compound detected in elution fraction/total compound detected at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1079940Granulomatous liver disease, proven histopathologically. Value is number of references indexed. [column 'GRAN' in source]
AID699542Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1676599Binding affinity to cupric ion assessed as accounting ratio by measuring total compound detected/total compound adsorbed at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID152781Inhibitory concentration against TNF-alpha production from human peripheral blood mononuclear cells stimulated by LPS2001Bioorganic & medicinal chemistry letters, Feb-26, Volume: 11, Issue:4
Structure-activity relationships of quinazoline derivatives: dual-acting compounds with inhibitory activities toward both TNF-alpha production and T cell proliferation.
AID1061076Inhibition of TNF-alpha-induced NF-kappaB transcriptional activation in human HepG2 cells preincubated for 1 hr followed by TNF-alpha challenge measured after 1 hr by luciferase reporter gene assay2014Bioorganic & medicinal chemistry letters, Jan-01, Volume: 24, Issue:1
New anti-inflammatory cembranoid diterpenoids from the Vietnamese soft coral Lobophytum crassum.
AID588216FDA HLAED, serum glutamic oxaloacetic transaminase (SGOT) increase2004Current drug discovery technologies, Dec, Volume: 1, Issue:4
Assessment of the health effects of chemicals in humans: II. Construction of an adverse effects database for QSAR modeling.
AID1470760Trypanocidal activity against bloodstream form of Trypanosoma cruzi NINOA infected in NIH mouse assessed as reduction in parasitemia at 100 mg/kg, po measured at 2 to 4 hrs post dose by microscopic method2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID1473739Inhibition of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1211157AUC (infinity) in wild-type Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1824215Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as decrease in MPO level in colon at 50 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID19419Partition coefficient (logD7.4)1998Journal of medicinal chemistry, Mar-26, Volume: 41, Issue:7
Physicochemical high throughput screening: parallel artificial membrane permeation assay in the description of passive absorption processes.
AID1211098Oral bioavailability in MRP2-deficient Wistar rat at 5 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1761236Permeability of compound at pH 7.4 measured after 6 hrs by PAMPA assay2021European journal of medicinal chemistry, Feb-05, Volume: 2112-Propargylamino-naphthoquinone derivatives as multipotent agents for the treatment of Alzheimer's disease.
AID1634677Antiinflammatory activity in DSS-induced C57BL/6 mouse acute colitis model assessed as lowering of IL-6 level at 300 mg/kg administered by oral gavage from day 5 to day 12 measured on day 132016Journal of natural products, Apr-22, Volume: 79, Issue:4
Anti-inflammatory Actions of (+)-3'α-Angeloxy-4'-keto-3',4'-dihydroseselin (Pd-Ib) against Dextran Sulfate Sodium-Induced Colitis in C57BL/6 Mice.
AID1757485Anti-colitis activity against DSS-induced BALB/c mouse model of subchronic relapsing colitis assessed as decrease in colon weight to length ratio at 100 mg/kg/day, po administered for 7 days in second week during 2 weeks DSS challenge and measured at the 2021European journal of medicinal chemistry, Apr-15, Volume: 2166-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3β).
AID425628Antituberculosis activity against Mycobacterium paratuberculosis ATCC 19698 isolated from bovine assessed as effect on average time to detection of growth at >10'2 CFU of inoculum by MGIT 960 susceptibility test2008Antimicrobial agents and chemotherapy, Feb, Volume: 52, Issue:2
Thiopurine drugs azathioprine and 6-mercaptopurine inhibit Mycobacterium paratuberculosis growth in vitro.
AID1824209Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as increase in colon length at 50 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1211097Oral bioavailability in wild-type Wistar rat at 5 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1221964Transporter substrate index ratio of permeability from basolateral to apical side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1221965Transporter substrate index of efflux ratio in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID299084Ulcerogenic activity in Wistar rat assessed as ulcer index at 2290 mg/kg, po2007Bioorganic & medicinal chemistry letters, Apr-01, Volume: 17, Issue:7
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid with D-phenylalanine for colon specific drug delivery in inflammatory bowel disease.
AID1221978Transporter substrate index ratio of permeability from apical to basolateral side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID678722Covalent binding affinity to human liver microsomes assessed per mg of protein at 10 uM after 60 mins presence of NADPH2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1209591Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 10 uM of fumitremorgin-C and 20 uM of MK-5712011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID622107Inhibition of NF-kappaB activation expressed in TNFalpha-stimulated human HepG2 cells co-transfected with PPRE-Luc plasmid pretreated for 1 hr before TNFalpha challenge measured after 24 hrs by luciferase reporter gene assay2011Bioorganic & medicinal chemistry letters, Oct-15, Volume: 21, Issue:20
Oleanane-type triterpene saponins from the bark of Aralia elata and their NF-κB inhibition and PPAR activation signal pathway.
AID1473835Stimulation of human MRP2 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID415827Half life in TNBS-induced po dosed Wistar rat colitis model assessed as assessed as release of 5-aminosalicylic acid2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Colon-specific mutual amide prodrugs of 4-aminosalicylic acid for their mitigating effect on experimental colitis in rats.
AID1221970Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID173949Tested for peak serum concentration in urine after oral administered dose in rat 51983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID625281Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholelithiasis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1470761Trypanocidal activity against bloodstream form of Trypanosoma cruzi NINOA infected in NIH mouse assessed as reduction in parasitemia at 100 mg/kg, po measured at 6 hrs post dose by microscopic method2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID625280Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cholecystitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID80567Tested for weight loss in guinea pig at 60 umol concentration of compound1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211026Volume of distribution at steady state in MDR1A knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1470753Trypanocidal activity against trypomastigote stage of Trypanosoma cruzi NINOA infected in NIH mouse blood assessed as parasite lysis at 50 ug/ml after 24 hrs by optical microscopic method relative to control2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID1413414Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in IL-6 expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by Western blot analysis2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID678717Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-benzyloxyquinoline as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID395170Antiinflammatory activity against dextrane disodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as diseased animal with rectal prolapse at 250 mg/kg administered 1 hr before dextrane disodium sulfate challenge2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Antileukotrienic phenethylamido derivatives of arylalkanoic acids in the treatment of ulcerative colitis.
AID91481Binding constant against human serum albumin (HSA)2001Journal of medicinal chemistry, Dec-06, Volume: 44, Issue:25
Cheminformatic models to predict binding affinities to human serum albumin.
AID173943Tested for peak serum concentration in feces after oral administered dose in rat 61983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1676601Binding affinity to Zinc ion assessed as retention ratio by measuring compound detected in elution fraction/total compound detected at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1211160AUC (infinity) in MRP2 knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID509502Antibacterial activity agaisnt Escherichia coli MTCC 8739 by agar diffusion method2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID1473738Inhibition of human BSEP overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-taurocholate in presence of ATP measured after 15 to 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID395169Antiinflammatory activity against dextrane disodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as diseased animal with stool consistency at 250 mg/kg administered 1 hr before dextrane disodium sulfate challenge2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Antileukotrienic phenethylamido derivatives of arylalkanoic acids in the treatment of ulcerative colitis.
AID1576578Fraction absorbed of the compound by PAMPA2019MedChemComm, Dec-01, Volume: 10, Issue:12
Synthesis of new lophine-carbohydrate hybrids as cholinesterase inhibitors: cytotoxicity evaluation and molecular modeling.
AID1542240Permeability of the compound at 30 to 50 uM at pH 7.4 measured up to 6 hrs by PAMPA-BBB assay method2019European journal of medicinal chemistry, Apr-01, Volume: 167Tackling neuroinflammation and cholinergic deficit in Alzheimer's disease: Multi-target inhibitors of cholinesterases, cyclooxygenase-2 and 15-lipoxygenase.
AID1221976Transporter substrate index ratio of permeability from basolateral to apical side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1230165Anti-colitis activity in Wistar rat assessed as suppression of TNBS-induced body weight reduction at 300 mg/kg, po qd administered for 1 week starting 48 hrs post TNBS induction2015Journal of natural products, Jun-26, Volume: 78, Issue:6
Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel Disease.
AID173944Tested for peak serum concentration in urine after mean oral administered dose in rat1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211164Cmax in MRP2 knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1763266Anti-colitis activity against TNBS-induced rat model of colitis assessed as increase in body weight at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID1211019AUC (infinity) in BCRP knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1079936Choleostatic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is < 2 (see ACUTE). Value is number of references indexed. [column 'CHOLE' in source]
AID1211095Half life in wild-type Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1676591Binding affinity to Nickel cation assessed as accounting ratio by measuring total compound detected/total compound adsorbed at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID209811Inhibitory concentration against T cell proliferation using concanavalin A stimulated mice spleen cells2001Bioorganic & medicinal chemistry letters, Feb-26, Volume: 11, Issue:4
Structure-activity relationships of quinazoline derivatives: dual-acting compounds with inhibitory activities toward both TNF-alpha production and T cell proliferation.
AID433903Hepatotoxicity in mouse assessed as carcinogenic potency2009European journal of medicinal chemistry, Sep, Volume: 44, Issue:9
Development of QSAR models for predicting hepatocarcinogenic toxicity of chemicals.
AID1392398Antiulcerogenic activity in DSS-induced acute ulcerative colitis C57BL/6J mouse model assessed as decrease in body weight at 500 mg/kg, po qd administered for 7 days (Rvb = 23.96%)2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Syntheses and structure-activity relationships on antibacterial and anti-ulcerative colitis properties of quaternary 13-substituted palmatines and 8-oxo-13-substituted dihydropalmatines.
AID655417Inhibition of TNFalpha-induced NFkappaB transcriptional activity in human HepG2 cells pretreated for 1 hr before TNFalpha challenge by luciferase reporter gene analysis2012Bioorganic & medicinal chemistry letters, Apr-01, Volume: 22, Issue:7
Anti-inflammatory and PPAR transactivational effects of secondary metabolites from the roots of Asarum sieboldii.
AID1211120Oral bioavailability in MRP2 knockout Sprague-Dawley rat at 20 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID78212Tested for mean score after quantitative histological evaluation result in guinea pig1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID417730Ulcerogenic effect in rat colon assessed as ulcer index at 3000 mg/kg by Rainsford's cold stress method2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Colon-specific mutual amide prodrugs of 4-aminosalicylic acid for their mitigating effect on experimental colitis in rats.
AID1824210Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as reduction colonic damage at 50 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1824219Antiinflammatory activity in DSS-induced C57BL/6 mouse model of colitis assessed as decrease in TNF-gamma level 25 to 100 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1079937Severe hepatitis, defined as possibly life-threatening liver failure or through clinical observations. Value is number of references indexed. [column 'MASS' in source]
AID1079947Comments (NB not yet translated). [column 'COMMENTAIRES' in source]
AID1824218Antiinflammatory activity in DSS-induced C57BL/6 mouse model of colitis assessed as decrease in IL-1beta level 25 to 100 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1660992Inhibition of AICAR transformylase (unknown origin)2020Journal of medicinal chemistry, 08-13, Volume: 63, Issue:15
The Structural Basis for Nonsteroidal Anti-Inflammatory Drug Inhibition of Human Dihydrofolate Reductase.
AID1211159AUC (infinity) in BCRP knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1824921Anti-colitis activity against DSS-induced BALB/c mouse model assessed as reduction in disease activity index at 100 mg/kg, po administered for 5 to 14 days2022Journal of medicinal chemistry, 01-13, Volume: 65, Issue:1
Discovery of a Series of Pyrimidine Carboxamides as Inhibitors of Vanin-1.
AID1392406Antiulcerogenic activity in DSS-induced acute ulcerative colitis C57BL/6J mouse model assessed as disappearance of inflammatory edema at 500 mg/kg, po qd administered for 7 days by microscopic analysis2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Syntheses and structure-activity relationships on antibacterial and anti-ulcerative colitis properties of quaternary 13-substituted palmatines and 8-oxo-13-substituted dihydropalmatines.
AID1211020AUC (infinity) in MRP2 knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID349141Inhibition of human carbonic anhydrase 2 esterase activity by spectrophotometry2008Bioorganic & medicinal chemistry, Oct-15, Volume: 16, Issue:20
In vitro inhibition of salicylic acid derivatives on human cytosolic carbonic anhydrase isozymes I and II.
AID444051Total clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID604022Fraction unbound in Sprague-Dawley rat plasma administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID1321649Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as inhibition of myeloperoxidase level in colon at 300 mg/kg/day, po administered for 5 days post 1 day of TNBS-challenge by colorimetric method relative to control2016Bioorganic & medicinal chemistry letters, 10-01, Volume: 26, Issue:19
In vitro and in vivo inhibitory activity of 6-amino-2,4,5-trimethylpyridin-3-ols against inflammatory bowel disease.
AID1824220Antiinflammatory activity in DSS-induced C57BL/6 mouse model of colitis assessed as increase in IL-10 level 25 to 100 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID190858Urinary recovery in colostomized rats at 2 hr intervals for 48 h1993Journal of medicinal chemistry, Dec-24, Volume: 36, Issue:26
Brush-border-enzyme-mediated intestine-specific drug delivery. Amino acid prodrugs of 5-aminosalicylic acid.
AID1221971Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID425632Antituberculosis activity against Mycobacterium paratuberculosis ATCC 19698 isolated from bovine assessed as minimum drug level resulting in no detectable growth at 10'6 CFU of inoculum after 56 days by MGIT 960 susceptibility test2008Antimicrobial agents and chemotherapy, Feb, Volume: 52, Issue:2
Thiopurine drugs azathioprine and 6-mercaptopurine inhibit Mycobacterium paratuberculosis growth in vitro.
AID1221961Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1896149Inhibition of human NTCP mediated TCA uptake in U2OS expresseing HA-tagged NTCP cells preincubated for 10 mins followed by substrate addition and measured after 2 mins using [3H]-taurocholate as substrate by liquid scintillation counter analysis2022Journal of medicinal chemistry, 10-13, Volume: 65, Issue:19
Inhibiting Sodium Taurocholate Cotransporting Polypeptide in HBV-Related Diseases: From Biological Function to Therapeutic Potential.
AID1470762Trypanocidal activity against bloodstream form of Trypanosoma cruzi NINOA infected in NIH mouse assessed as reduction in parasitemia at 100 mg/kg, po measured at 4 hrs post dose by microscopic method relative to control2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID1815674Binding affinity to human N-terminal His6-tagged and thrombin cleavage fused BLVRB expressed in Escherichia coli BL21 (DE3) assessed as change in gibbs free energy by isothermal titration calorimetry2022Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3
Repositioning Food and Drug Administration-Approved Drugs for Inhibiting Biliverdin IXβ Reductase B as a Novel Thrombocytopenia Therapeutic Target.
AID455986Permeability across human Caco-2 cells2009Bioorganic & medicinal chemistry, Oct-01, Volume: 17, Issue:19
Computational modeling of novel inhibitors targeting the Akt pleckstrin homology domain.
AID588210Human drug-induced liver injury (DILI) modelling dataset from Ekins et al2010Drug metabolism and disposition: the biological fate of chemicals, Dec, Volume: 38, Issue:12
A predictive ligand-based Bayesian model for human drug-induced liver injury.
AID1600822Inhibition of HA-tagged human NTCP expressed in human U2OS cells assessed as reduction in [14C]taurocholate uptake preincubated for 10 mins followed by [14C] taurocholate addition and further incubation for 10 mins by scintillation counting method2019Bioorganic & medicinal chemistry letters, 10-01, Volume: 29, Issue:19
Design, synthesis and biological evaluation of benzamide derivatives as novel NTCP inhibitors that induce apoptosis in HepG2 cells.
AID1211116Half life in MRP2 knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1221960Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1534338Inhibition of cystine/glutamate antiporter system xc- in human Calu1 cells assessed as reduction in L-[3,3'-14C]-cystine uptake in presence of Na+ free uptake buffer by scintillation counting assay2019European journal of medicinal chemistry, Feb-01, Volume: 163Discovery and development of small molecule modulators targeting glutamine metabolism.
AID1211051Oral bioavailability in BCRP knockout mouse at 20 mg/kg2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID444056Fraction escaping gut-wall elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID173942Tested for peak serum concentration in feces after oral administered dose in rat 51983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211094Tmax in MRP2-deficient Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1245306Anti-ulcerative colitis activity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as colon macroscopic damage index at 300 mg/kg, po qd measured on day 8 (Rvb = 5.69 +/- 1.12 No_unit)2015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID1470755Inhibition of Trypanosoma cruzi trans-sialidase at 1 mM using N-acetyllactosamine as substrate in presence of 3'-sialyllactose measured after 15 mins by HPAEC-PAD relative to control2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID349142Inhibition of human carbonic anhydrase 1 esterase activity by noncompetitive Lineweaver-Burke plot2008Bioorganic & medicinal chemistry, Oct-15, Volume: 16, Issue:20
In vitro inhibition of salicylic acid derivatives on human cytosolic carbonic anhydrase isozymes I and II.
AID143586Tested in vivo for the ability to inhibit myeloperoxidase (MPO) activity in the colon of the TNB/ethanol-induced chronic colitis rats at the dosage of 500 mg/kg/day1994Journal of medicinal chemistry, Sep-16, Volume: 37, Issue:19
Novel dual inhibitors of 5-lipoxygenase and thromboxane A2 synthetase: synthesis and structure-activity relationships of 3-pyridylmethyl-substituted 2-amino-6-hydroxybenzothiazole derivatives.
AID1211145Volume of distribution at steady state in wild-type Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
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.
AID1211161Cmax in wild-type Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1763270Anti-colitis activity against TNBS-induced rat model of colitis assessed as increase in colon length at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID1676590Binding affinity to Nickel cation assessed as retention ratio by measuring compound detected in elution fraction/total compound detected at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1079935Cytolytic liver toxicity, either proven histopathologically or where the ratio of maximal ALT or AST activity above normal to that of Alkaline Phosphatase is > 5 (see ACUTE). Value is number of references indexed. [column 'CYTOL' in source]
AID1221982Fraction absorbed in human2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1499312Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as recovery of colon tissue edematous inflammation at 300 mg/kg, po qd administered for 5 days measured on day 62017European journal of medicinal chemistry, Sep-08, Volume: 137Discovery and structure-activity relationship studies of 2-benzylidene-2,3-dihydro-1H-inden-1-one and benzofuran-3(2H)-one derivatives as a novel class of potential therapeutics for inflammatory bowel disease.
AID977599Inhibition of sodium fluorescein uptake in OATP1B1-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID296200Antiinflammatory activity against dextran sodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as weight loss after 6 days2007European journal of medicinal chemistry, Aug, Volume: 42, Issue:8
Antileukotrienic N-arylethyl-2-arylacetamides in the treatment of ulcerative colitis.
AID1211143Clearance in wild-type Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID509505Antiulcerogenic activity against acetic acid-induced ulcerative colitis in albino rat assessed as ratio of wet weight and length at 12.5 mmol/kg, po2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID1221957Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID625284Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic failure2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079944Benign tumor, proven histopathologically. Value is number of references indexed. [column 'T.BEN' in source]
AID1230183Toxicity in Wistar rat assessed as decrease in Hsp70 level at 300 mg/kg, po qd administered for 1 week starting 48 hrs post TNBS induction by ELISA2015Journal of natural products, Jun-26, Volume: 78, Issue:6
Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel Disease.
AID1413412Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in TNFalpha expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by Western blot anal2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1576577Effective permeability of compound incubated for 8 hrs by PAMPA2019MedChemComm, Dec-01, Volume: 10, Issue:12
Synthesis of new lophine-carbohydrate hybrids as cholinesterase inhibitors: cytotoxicity evaluation and molecular modeling.
AID444053Renal clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1634664Antiinflammatory activity in DSS-induced C57BL/6 mouse acute colitis model assessed as lowering of disease activity index at 300 mg/kg administered by oral gavage from day 5 to day 12 measured on day 13 relative to DSS-treated control2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Anti-inflammatory Actions of (+)-3'α-Angeloxy-4'-keto-3',4'-dihydroseselin (Pd-Ib) against Dextran Sulfate Sodium-Induced Colitis in C57BL/6 Mice.
AID1498652In vivo of inhibition of TNBS-induced decrease in body weight in TNBS-induced colitis Sprague-Dawley rat model at 300 mg/kg/day, po administered on day of TNBS administration and on four consecutive days measured on day 62018Bioorganic & medicinal chemistry letters, 08-01, Volume: 28, Issue:14
Synthesis and biological evaluation of pyridine-linked indanone derivatives: Potential agents for inflammatory bowel disease.
AID28399Cellular permeability (Pc) (Caco-2 cell monolayer)2001Journal of medicinal chemistry, Jun-07, Volume: 44, Issue:12
Experimental and computational screening models for the prediction of intestinal drug absorption.
AID1413410Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in MCP1 expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by ELISA2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1763267Anti-colitis activity against TNBS-induced rat model of colitis assessed as decrease in congestion at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID1815675Binding affinity to human N-terminal His6-tagged and thrombin cleavage fused BLVRB expressed in Escherichia coli BL21 (DE3) assessed as dissociation constant by isothermal titration calorimetry2022Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3
Repositioning Food and Drug Administration-Approved Drugs for Inhibiting Biliverdin IXβ Reductase B as a Novel Thrombocytopenia Therapeutic Target.
AID625279Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for bilirubinemia2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1321643Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as colon weight recovery at 300 mg/kg/day, po administered for 5 days post 1 day of TNBS-challenge relative to control2016Bioorganic & medicinal chemistry letters, 10-01, Volume: 26, Issue:19
In vitro and in vivo inhibitory activity of 6-amino-2,4,5-trimethylpyridin-3-ols against inflammatory bowel disease.
AID417722Antiinflammatory activity against TNBS-induced Wistar rat colitis model assessed as decrease in severity of inflammation treated rectally 3 days after TNBS induction measured on day 72009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Colon-specific mutual amide prodrugs of 4-aminosalicylic acid for their mitigating effect on experimental colitis in rats.
AID1703908Permeability of the compound by PAMPA-TGI assay2020European journal of medicinal chemistry, Oct-15, Volume: 204Discovery of sulfonyl hydrazone derivative as a new selective PDE4A and PDE4D inhibitor by lead-optimization approach on the prototype LASSBio-448: In vitro and in vivo preclinical studies.
AID190239% of rats exhibiting diarrhea2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID781326pKa (acid-base dissociation constant) as determined by Avdeef ref: DOI: 10.1002/047145026X2014Pharmaceutical research, Apr, Volume: 31, Issue:4
Comparison of the accuracy of experimental and predicted pKa values of basic and acidic compounds.
AID28925Highest effective permeability across hexadecane membrane (pH 4-8)2001Journal of medicinal chemistry, Mar-15, Volume: 44, Issue:6
High-throughput permeability pH profile and high-throughput alkane/water log P with artificial membranes.
AID1221979Transporter substrate index ratio of permeability from basolateral to apical side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID678713Inhibition of human CYP2C9 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 7-methoxy-4-trifluoromethylcoumarin-3-acetic acid as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID453203Lipophilicity, log D of the compound2010Bioorganic & medicinal chemistry letters, Jan-01, Volume: 20, Issue:1
Development of an in silico model for human skin permeation based on a Franz cell skin permeability assay.
AID1534336Inhibition of xCT-mediated cystein/glutamate transporter (unknown origin) assessed as reduction in L-[14C]cyctein uptake2019European journal of medicinal chemistry, Feb-01, Volume: 163Discovery and development of small molecule modulators targeting glutamine metabolism.
AID1211155Half life in BCRP knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID625286Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatitis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID678716Inhibition of human CYP3A4 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using diethoxyfluorescein as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID476929Human intestinal absorption in po dosed human2010European journal of medicinal chemistry, Mar, Volume: 45, Issue:3
Neural computational prediction of oral drug absorption based on CODES 2D descriptors.
AID1079945Animal toxicity known. [column 'TOXIC' in source]
AID1824212Anti-colitis activity against DSS-induced C57BL/6 mouse model of colitis assessed as fold change in colon length at 25 to 100 mg/kg, po administered via gavage twice a day for 10 days relative to SASP2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID173950Tested for peak serum concentration in urine after oral administered dose in rat 61983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID509503Antibacterial activity agaisnt Candida albicans MTCC 3541 by agar diffusion method2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID1634676Antiinflammatory activity in DSS-induced C57BL/6 mouse acute colitis model assessed as lowering of IL-17A level at 300 mg/kg administered by oral gavage from day 5 to day 12 measured on day 132016Journal of natural products, Apr-22, Volume: 79, Issue:4
Anti-inflammatory Actions of (+)-3'α-Angeloxy-4'-keto-3',4'-dihydroseselin (Pd-Ib) against Dextran Sulfate Sodium-Induced Colitis in C57BL/6 Mice.
AID237585Tested for fraction of oral dose absorbed orally in humans2005Journal of medicinal chemistry, May-05, Volume: 48, Issue:9
Calculating virtual log P in the alkane/water system (log P(N)(alk)) and its derived parameters deltalog P(N)(oct-alk) and log D(pH)(alk).
AID1824203Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as increase in colon length at 25 mg/kg, po administered via gavage twice daily for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID614829Binding affinity to dipalmitoyl phosphatidyl choline lipid bilayer assessed as decrease in pre-transition temperature at compound to lipid molar ratio of 1:100 by DSC technique2011European journal of medicinal chemistry, Sep, Volume: 46, Issue:9
In-vitro metabolic inhibition and antifertility effect facilitated by membrane alteration: search for novel antifertility agent using nifedipine analogues.
AID173937Tested for peak serum concentration in feces after mean oral administered dose in rat1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1676594Binding affinity to gallium ion assessed as accounting ratio by measuring total compound detected/total compound adsorbed at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID77141Tested for cecal ulceration in diarrhea at 60 umol concentration of compound1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID444057Fraction escaping hepatic elimination in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID1079933Acute liver toxicity defined via clinical observations and clear clinical-chemistry results: serum ALT or AST activity > 6 N or serum alkaline phosphatases activity > 1.7 N. This category includes cytolytic, choleostatic and mixed liver toxicity. Value is
AID1221968Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID188198Effect of compound on LTB4 production was measured in rat2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID293918Antiinflammatory activity in Wistar rat colon assessed as myeloperoxidase activity per 100 mg tissue2007European journal of medicinal chemistry, Jun, Volume: 42, Issue:6
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1824202Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as assessed as recovery of body weight at 25 mg/kg, po administered via gavage twice daily for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1211118Oral bioavailability in MDR1A knockout Sprague-Dawley rat at 20 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID444052Hepatic clearance in human2010Journal of medicinal chemistry, Feb-11, Volume: 53, Issue:3
Physicochemical space for optimum oral bioavailability: contribution of human intestinal absorption and first-pass elimination.
AID625290Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver fatty2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079942Steatosis, proven histopathologically. Value is number of references indexed. [column 'STEAT' in source]
AID1221963Transporter substrate index ratio of permeability from apical to basolateral side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1824217Antiinflammatory activity in DSS-induced C57BL/6 mouse model of colitis assessed as decrease in TNF-alpha level 25 to 100 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1211022Clearance in MDR1A knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211153Half life in wild-type Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID977602Inhibition of sodium fluorescein uptake in OATP1B3-transfected CHO cells at an equimolar substrate-inhibitor concentration of 10 uM2013Molecular pharmacology, Jun, Volume: 83, Issue:6
Structure-based identification of OATP1B1/3 inhibitors.
AID1074028Efflux ratio of permeability in pig LLC-PK1 cells transfected with human MDR1 at 1 uM by LC-MS/MS analysis2014Journal of medicinal chemistry, Feb-13, Volume: 57, Issue:3
Discovery of 7-tetrahydropyran-2-yl chromans: β-site amyloid precursor protein cleaving enzyme 1 (BACE1) inhibitors that reduce amyloid β-protein (Aβ) in the central nervous system.
AID425631Antituberculosis activity against Mycobacterium paratuberculosis ATCC 19698 isolated from bovine assessed as lowest drug level producing inhibition at 10'6 CFU of inoculum by agar counting method2008Antimicrobial agents and chemotherapy, Feb, Volume: 52, Issue:2
Thiopurine drugs azathioprine and 6-mercaptopurine inhibit Mycobacterium paratuberculosis growth in vitro.
AID1499313Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as recovery in body weight decrease at 300 mg/kg, po qd administered for 5 days measured on day 62017European journal of medicinal chemistry, Sep-08, Volume: 137Discovery and structure-activity relationship studies of 2-benzylidene-2,3-dihydro-1H-inden-1-one and benzofuran-3(2H)-one derivatives as a novel class of potential therapeutics for inflammatory bowel disease.
AID1221966Ratio of plasma AUC in po dosed mdr1 knock out mouse to plasma AUC in po dosed wild type mouse2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1221962Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of P-gp inhibitor LY3359792011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID175772Damage to the colon observed after 48 hr after colitis induction in rats2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID293919Antiarthritic activity in Freund's adjuvant-induced arthritis Wistar rat model after 13 days2007European journal of medicinal chemistry, Jun, Volume: 42, Issue:6
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1763269Anti-colitis activity against TNBS-induced rat model of colitis assessed as increase in colon weight at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID77142Tested for cecal ulceration in necropsy at 60 umol concentration of compound1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211117Oral bioavailability in wild-type Sprague-Dawley rat at 20 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1824211Anti-colitis activity against DSS-induced C57BL/6 mouse model of colitis assessed as fold change in body weight recovery at 25 to 100 mg/kg, po administered via gavage twice a day for 10 days relative to SASP2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID1676592Binding affinity to Gallium ion assessed as performance ratio ratio by measuring product of accounting ratio and retention ratio at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID625285Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatic necrosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID625289Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver disease2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID436235Antiinflammatory activity against trinitrobenzenesulfonic acid-induced colitis in Wistar rat at 100 mg/kg, administered rectally2009European journal of medicinal chemistry, Oct, Volume: 44, Issue:10
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrugs of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID194536Tested for peak serum concentration in rat 41983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1230173Anti-colitis activity in Wistar rat assessed as suppression of TNBS-induced reduction of colonic GSH level at 300 mg/kg, po qd administered for 1 week starting 48 hrs post TNBS induction by spectrophotometric analysis2015Journal of natural products, Jun-26, Volume: 78, Issue:6
Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel Disease.
AID1873197Inhibition of ABCG2 (unknown origin) expressed in human HEK cells membrane vesicle assessed as inhibition of BCRP- mediated transport of [3H]-E3S using [3H]-oestrone 3-sulfate as radiolabeled substrate by liquid scintillation counter analysis2022European journal of medicinal chemistry, Jul-05, Volume: 237Targeting breast cancer resistance protein (BCRP/ABCG2): Functional inhibitors and expression modulators.
AID1634667Antiinflammatory activity in DSS-induced C57BL/6 mouse acute colitis model assessed as protection against mucosal injury at 300 mg/kg administered by oral gavage from day 5 to day 12 measured on day 13 by hematoxylin/eosin staining-based microscopic analy2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Anti-inflammatory Actions of (+)-3'α-Angeloxy-4'-keto-3',4'-dihydroseselin (Pd-Ib) against Dextran Sulfate Sodium-Induced Colitis in C57BL/6 Mice.
AID1230169Anti-colitis activity in Wistar rat assessed as reduction of TNBS-induced colon mass index at 300 mg/kg, po qd administered for 1 week starting 48 hrs post TNBS induction2015Journal of natural products, Jun-26, Volume: 78, Issue:6
Bacteria-Derived Compatible Solutes Ectoine and 5α-Hydroxyectoine Act as Intestinal Barrier Stabilizers to Ameliorate Experimental Inflammatory Bowel Disease.
AID349140Inhibition of human carbonic anhydrase 1 esterase activity by spectrophotometry2008Bioorganic & medicinal chemistry, Oct-15, Volume: 16, Issue:20
In vitro inhibition of salicylic acid derivatives on human cytosolic carbonic anhydrase isozymes I and II.
AID395173Antiinflammatory activity against dextrane disodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as length of colon at 250 mg/kg administered 1 hr before dextrane disodium sulfate challenge2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Antileukotrienic phenethylamido derivatives of arylalkanoic acids in the treatment of ulcerative colitis.
AID1534337Inhibition of cystine/glutamate antiporter system xc- in human HT1080 cells assessed as reduction in L-[3,3'-14C]-cystine uptake in presence of Na+ free uptake buffer by scintillation counting assay2019European journal of medicinal chemistry, Feb-01, Volume: 163Discovery and development of small molecule modulators targeting glutamine metabolism.
AID1209589Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 10 uM of fumitremorgin-C2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID73467Dissociation constant for Fibroblast growth factor 2 (None Observed)2004Journal of medicinal chemistry, Mar-25, Volume: 47, Issue:7
Validation of molecular docking calculations involving FGF-1 and FGF-2.
AID1443980Inhibition of human BSEP expressed in fall armyworm sf9 cell plasma membrane vesicles assessed as reduction in vesicle-associated [3H]-taurocholate transport preincubated for 10 mins prior to ATP addition measured after 15 mins in presence of [3H]-tauroch2010Toxicological sciences : an official journal of the Society of Toxicology, Dec, Volume: 118, Issue:2
Interference with bile salt export pump function is a susceptibility factor for human liver injury in drug development.
AID299088Ulcerogenic activity in Wistar rat assessed as ulcer index at 3000 mg/kg, po2007Bioorganic & medicinal chemistry letters, Apr-01, Volume: 17, Issue:7
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid with D-phenylalanine for colon specific drug delivery in inflammatory bowel disease.
AID1211154Half life in MDR1A knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID395171Antiinflammatory activity against dextrane disodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as diseased animal with small intestine bleeding at 250 mg/kg administered 1 hr before dextrane disodium sulfate challenge2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Antileukotrienic phenethylamido derivatives of arylalkanoic acids in the treatment of ulcerative colitis.
AID299841Effect on TNBS-induced experimental colitis in po dosed Sprague-Dawely rat assessed as colon to body weight ratio after 5 days relative to control2007Bioorganic & medicinal chemistry, Jul-15, Volume: 15, Issue:14
Colon-specific, mutual azo prodrug of 5-aminosalicylic acid with L-tryptophan: synthesis, kinetic studies and evaluation of its mitigating effect in trinitrobenzenesulfonic acid-induced colitis in rats.
AID1763268Anti-colitis activity against TNBS-induced rat model of colitis assessed as decrease in adhesion at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID1392404Antiulcerogenic activity in DSS-induced acute ulcerative colitis C57BL/6J mouse model assessed as colon macroscopic damage index at 500 mg/kg, po qd administered for 7 days (Rvb = 4.13 +/- 0.78 No_unit)2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Syntheses and structure-activity relationships on antibacterial and anti-ulcerative colitis properties of quaternary 13-substituted palmatines and 8-oxo-13-substituted dihydropalmatines.
AID1473741Inhibition of human MRP4 overexpressed in Sf9 cell membrane vesicles assessed as uptake of [3H]-estradiol-17beta-D-glucuronide in presence of ATP and GSH measured after 20 mins by membrane vesicle transport assay2013Toxicological sciences : an official journal of the Society of Toxicology, Nov, Volume: 136, Issue:1
A multifactorial approach to hepatobiliary transporter assessment enables improved therapeutic compound development.
AID1211017AUC (infinity) in wild-type Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID296198Antiinflammatory activity against dextran sodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as small intestinal bleeding2007European journal of medicinal chemistry, Aug, Volume: 42, Issue:8
Antileukotrienic N-arylethyl-2-arylacetamides in the treatment of ulcerative colitis.
AID1079941Liver damage due to vascular disease: peliosis hepatitis, hepatic veno-occlusive disease, Budd-Chiari syndrome. Value is number of references indexed. [column 'VASC' in source]
AID1413413Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as decrease in IL1beta expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by Western blot analy2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1470763Solubility of the compound in water2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID1703889Permeability of the compound incubated for 8 hrs by PAMPA-TGI assay2020European journal of medicinal chemistry, Oct-15, Volume: 204Discovery of sulfonyl hydrazone derivative as a new selective PDE4A and PDE4D inhibitor by lead-optimization approach on the prototype LASSBio-448: In vitro and in vivo preclinical studies.
AID436237Antiarthritic activity against Freund's adjuvant-induced arthritis in Wistar rat assessed as reduction in paw volume administered 13 days after Freund's adjuvant challenge measured on day 212009European journal of medicinal chemistry, Oct, Volume: 44, Issue:10
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrugs of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1245317Anti-ulcerative colitis activity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as recovery of each muscle layer structure at 300 mg/kg, po qd measured on day 82015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID1079939Cirrhosis, proven histopathologically. Value is number of references indexed. [column 'CIRRH' in source]
AID1824208Anti-colitis activity against DSS-induced colitis in C57BL/6 mouse model assessed as body weight recovery at 50 mg/kg, po administered via gavage twice a day for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID293916Ulcerogenic effect in Wistar rat at 3000 mg/kg, po by Rainsford's cold stress method relative to contro2007European journal of medicinal chemistry, Jun, Volume: 42, Issue:6
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1211114Cmax in wild-type Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211018AUC (infinity) in MDR1A knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1676589Binding affinity to Nickel cation assessed as performance ratio ratio by measuring product of accounting ratio and retention ratio at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID173959Tested for peak serum concentration in feces after oral administered dose in rat 61983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211162Cmax in MDR1A knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211141AUC (infinity) in wild-type Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211169Half life in wild-type Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1079931Moderate liver toxicity, defined via clinical-chemistry results: ALT or AST serum activity 6 times the normal upper limit (N) or alkaline phosphatase serum activity of 1.7 N. Value is number of references indexed. [column 'BIOL' in source]
AID604020Unbound drug concentration in Sprague-Dawley rat plasma administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID436234Antiinflammatory activity against trinitrobenzenesulfonic acid-induced colitis in Wistar rat assessed as decrease in colon to body weight ratio at 100 mg/kg, po measured 24 hrs after last dose on day 112009European journal of medicinal chemistry, Oct, Volume: 44, Issue:10
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrugs of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID236912Permeability Coefficient in 2/4/A1 cell model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID28392Apparent permeability coefficient (Papp) (Caco-2 cell monolayer)2001Journal of medicinal chemistry, Jun-07, Volume: 44, Issue:12
Experimental and computational screening models for the prediction of intestinal drug absorption.
AID173109Colonic weight was measured in rats2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID1209583Unbound drug partitioning coefficient, Kp of the compound assessed as ratio of unbound concentration in Sprague-Dawley rat brain to unbound concentration in plasma2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1079948Times to onset, minimal and maximal, observed in the indexed observations. [column 'DELAI' in source]
AID296201Antiinflammatory activity against dextran sodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as colon length2007European journal of medicinal chemistry, Aug, Volume: 42, Issue:8
Antileukotrienic N-arylethyl-2-arylacetamides in the treatment of ulcerative colitis.
AID1211156Half life in MRP2 knockout Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
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).
AID1221975Transporter substrate index ratio of permeability from apical to basolateral side in human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 1 uM of BCRP inhibitor Ko1432011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID29844Fraction absorbed after oral administration in humans2001Journal of medicinal chemistry, Jun-07, Volume: 44, Issue:12
Experimental and computational screening models for the prediction of intestinal drug absorption.
AID1404017Permeability of the compound at 500 uM after 8 hrs by PAMPA2018European journal of medicinal chemistry, Feb-10, Volume: 145Chameleon-like behavior of indolylpiperidines in complex with cholinesterases targets: Potent butyrylcholinesterase inhibitors.
AID626970Inhibition of TNF-alpha-induced NFkappaB activation in human HepG2 cells after 1 hr by luciferase reporter assay2011Journal of natural products, Sep-23, Volume: 74, Issue:9
Anti-inflammatory triterpenoid saponins from the stem bark of Kalopanax pictus.
AID236268Fraction absorbed in human intestine after oral administration compound was measured2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID1676595Binding affinity to Ferric ion assessed as performance ratio ratio by measuring product of accounting ratio and retention ratio at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID173948Tested for peak serum concentration in urine after oral administered dose in rat 41983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID425630Antituberculosis activity against Mycobacterium paratuberculosis ATCC 19698 isolated from bovine assessed as lowest drug level producing inhibition at 10'6 CFU of inoculum by MGIT 960 susceptibility test2008Antimicrobial agents and chemotherapy, Feb, Volume: 52, Issue:2
Thiopurine drugs azathioprine and 6-mercaptopurine inhibit Mycobacterium paratuberculosis growth in vitro.
AID1221956Apparent permeability from apical to basolateral side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis2011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID409954Inhibition of mouse brain MAOA2008Journal of medicinal chemistry, Nov-13, Volume: 51, Issue:21
Quantitative structure-activity relationship and complex network approach to monoamine oxidase A and B inhibitors.
AID299838Ulcerogenic activity in Wistar rat at 3000 mg/kg, po by cold stress method relative to control2007Bioorganic & medicinal chemistry, Jul-15, Volume: 15, Issue:14
Colon-specific, mutual azo prodrug of 5-aminosalicylic acid with L-tryptophan: synthesis, kinetic studies and evaluation of its mitigating effect in trinitrobenzenesulfonic acid-induced colitis in rats.
AID293920Antiarthritic activity in Freund's adjuvant-induced arthritis Wistar rat model after 21 days2007European journal of medicinal chemistry, Jun, Volume: 42, Issue:6
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID77143Tested for cecal ulceration with mortality at 60 umol concentration of compound1983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211147Half life in wild-type Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID18849Estimation of fraction absorbed (Fa) in the human intestine using biosensor technology.2000Journal of medicinal chemistry, Jun-01, Volume: 43, Issue:11
SPR biosensor studies of the direct interaction between 27 drugs and a liposome surface: correlation with fraction absorbed in humans.
AID1211144Clearance in MRP2-deficient Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1676596Binding affinity to Ferric ion assessed as retention ratio by measuring compound detected in elution fraction/total compound detected at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID625287Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for hepatomegaly2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID173941Tested for peak serum concentration in feces after oral administered dose in rat 41983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID236913Permeability Coefficient in Caco-2 cell culture model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID1211115Half life in BCRP knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1703888Drug absorption of the compound incubated for 8 hrs by PAMPA-TGI assay2020European journal of medicinal chemistry, Oct-15, Volume: 204Discovery of sulfonyl hydrazone derivative as a new selective PDE4A and PDE4D inhibitor by lead-optimization approach on the prototype LASSBio-448: In vitro and in vivo preclinical studies.
AID625291Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for liver function tests abnormal2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1676602Binding affinity to ferric ion assessed as accounting ratio by measuring total compound detected/total compound adsorbed at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
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.
AID625288Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for jaundice2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1211092Cmax in MRP2-deficient Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1757479Anti-colitis activity against DSS-induced BALB/c mouse model of subchronic relapsing colitis assessed as increase in softening of feces at 100 mg/kg/day, po administered for 7 days in second week during 2 weeks DSS challenge and measured at the end of 2nd2021European journal of medicinal chemistry, Apr-15, Volume: 2166-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3β).
AID316228Inhibition of SGK1 at 33 uM2008Journal of medicinal chemistry, Mar-13, Volume: 51, Issue:5
Kinase-likeness and kinase-privileged fragments: toward virtual polypharmacology.
AID1211142AUC (infinity) in MRP2-deficient Wistar rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1209581Fraction unbound in Sprague-Dawley rat brain homogenates at 5 uM by equilibrium dialysis analysis2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID20050Human absorption A (%)1998Journal of medicinal chemistry, Mar-26, Volume: 41, Issue:7
Physicochemical high throughput screening: parallel artificial membrane permeation assay in the description of passive absorption processes.
AID1470754Trypanocidal activity against trypomastigote stage of Trypanosoma cruzi NINOA infected in NIH mouse blood after 24 hrs by optical microscopic method2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID1392400Antiulcerogenic activity in DSS-induced acute ulcerative colitis C57BL/6J mouse model assessed as colon contracture at 500 mg/kg, po qd administered for 7 days (Rvb = 41.87%)2018Bioorganic & medicinal chemistry, 05-15, Volume: 26, Issue:9
Syntheses and structure-activity relationships on antibacterial and anti-ulcerative colitis properties of quaternary 13-substituted palmatines and 8-oxo-13-substituted dihydropalmatines.
AID1498653In vivo of inhibition of TNBS-induced increase in colon weight in TNBS-induced colitis Sprague-Dawley rat model at 300 mg/kg/day, po administered on day of TNBS administration and on four consecutive days measured on day 62018Bioorganic & medicinal chemistry letters, 08-01, Volume: 28, Issue:14
Synthesis and biological evaluation of pyridine-linked indanone derivatives: Potential agents for inflammatory bowel disease.
AID1211170Half life in MDR1A knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1245312Anti-ulcerative colitis activity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as improvement in colon contracture at 300 mg/kg, po qd measured on day 8 (Rvb = 41.8%)2015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID699539Inhibition of human liver OATP1B1 expressed in HEK293 Flp-In cells assessed as reduction in E17-betaG uptake at 20 uM by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID417725Antiinflammatory activity against TNBS-induced po dosed Wistar rat colitis model assessed as inhibition of MPO activity in neutrophils per 100 mg of tissue2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Colon-specific mutual amide prodrugs of 4-aminosalicylic acid for their mitigating effect on experimental colitis in rats.
AID1209592Dissociation constant, pKa of the basic compound by capillary electrophoresis-mass spectrometry analysis2011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1757475Anti-colitis activity against DSS-induced BALB/c mouse model of subchronic relapsing colitis assessed as reduction in fecal blood at 100 mg/kg/day, po administered for 7 days in second week during 2 weeks DSS challenge and measured at the end of 2nd week2021European journal of medicinal chemistry, Apr-15, Volume: 2166-(methylsulfinyl)hexyl isothiocyanate (6-MITC) from Wasabia japonica alleviates inflammatory bowel disease (IBD) by potential inhibition of glycogen synthase kinase 3 beta (GSK-3β).
AID28679Partition coefficient (logD6.8)2001Journal of medicinal chemistry, Mar-15, Volume: 44, Issue:6
High-throughput permeability pH profile and high-throughput alkane/water log P with artificial membranes.
AID73458Binding affinity for Fibroblast growth factor 12004Journal of medicinal chemistry, Mar-25, Volume: 47, Issue:7
Validation of molecular docking calculations involving FGF-1 and FGF-2.
AID395172Antiinflammatory activity against dextrane disodium sulfate-induced ulcerative colitis in BALB/c mouse assessed as diseased animal with large intestine bleeding at 250 mg/kg administered 1 hr before dextrane disodium sulfate challenge2009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Antileukotrienic phenethylamido derivatives of arylalkanoic acids in the treatment of ulcerative colitis.
AID349145Inhibition of human carbonic anhydrase 2 esterase activity by non-competitive Lineweaver-Burke plot2008Bioorganic & medicinal chemistry, Oct-15, Volume: 16, Issue:20
In vitro inhibition of salicylic acid derivatives on human cytosolic carbonic anhydrase isozymes I and II.
AID28234% absorbed in human GI-tract2001Journal of medicinal chemistry, Mar-15, Volume: 44, Issue:6
High-throughput permeability pH profile and high-throughput alkane/water log P with artificial membranes.
AID249179Permeability Coefficient in hexadecane membranes model2005Journal of medicinal chemistry, Jan-27, Volume: 48, Issue:2
Exploring the role of different drug transport routes in permeability screening.
AID678715Inhibition of human CYP2D6 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using 4-methylaminoethyl-7-methoxycoumarin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID616223Binding affinity to multilamellar vesicles assessed as apparent binding constant after 2 hrs by double reciprocal plot2011European journal of medicinal chemistry, Sep, Volume: 46, Issue:9
In-vitro metabolic inhibition and antifertility effect facilitated by membrane alteration: search for novel antifertility agent using nifedipine analogues.
AID1676597Binding affinity to cupric ion assessed as performance ratio ratio by measuring product of accounting ratio and retention ratio at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID1211025Volume of distribution at steady state in wild-type Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1824205Anti-colitis activity against DSS-induced C57BL/6 mouse model of colitis assessed as assessed as body weight recovery at 50 mg/kg, po administered via gavage DSS stimulation for 5 days followed by compound addition once daily for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID167806Concentration required to inhibit PAF-induced maximum aggregation by 50%2001Journal of medicinal chemistry, Aug-30, Volume: 44, Issue:18
Novel azo derivatives as prodrugs of 5-aminosalicylic acid and amino derivatives with potent platelet activating factor antagonist activity.
AID1245302Anti-ulcerative colitis activity in DSS-induced acute C57Bl/6J mouse ulcerative colitis model assessed as inhibition rate of disease activity index at 300 mg/kg, po qd measured on day 8 relative to control2015Journal of medicinal chemistry, Sep-24, Volume: 58, Issue:18
Synthesis and Structure-Activity Relationships of Quaternary Coptisine Derivatives as Potential Anti-ulcerative Colitis Agents.
AID588209Literature-mined public compounds from Greene et al multi-species hepatotoxicity modelling dataset2010Chemical research in toxicology, Jul-19, Volume: 23, Issue:7
Developing structure-activity relationships for the prediction of hepatotoxicity.
AID699540Inhibition of human liver OATP1B3 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E17-betaG uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID436229Gastrointestinal toxicity in Wistar rat assessed as ulcer index at 3000 mg/kg, po by Rainsford's cold stress method2009European journal of medicinal chemistry, Oct, Volume: 44, Issue:10
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrugs of 5-aminosalicylic acid for colon-specific drug delivery in inflammatory bowel disease.
AID1470752Trypanocidal activity against trypomastigote stage of Trypanosoma cruzi INC-5 infected in NIH mouse blood after 24 hrs by optical microscopic method2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID299085Decrease in inflammation in TNBS-induced Wistar rat colitis model after 24 to 48 hrs2007Bioorganic & medicinal chemistry letters, Apr-01, Volume: 17, Issue:7
Synthesis, kinetic studies and pharmacological evaluation of mutual azo prodrug of 5-aminosalicylic acid with D-phenylalanine for colon specific drug delivery in inflammatory bowel disease.
AID1211166Tmax in MDR1A knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID179008Fecal recovery in non-colostomized rats at 2 hr intervals for 48 h1993Journal of medicinal chemistry, Dec-24, Volume: 36, Issue:26
Brush-border-enzyme-mediated intestine-specific drug delivery. Amino acid prodrugs of 5-aminosalicylic acid.
AID1498655In vivo of inhibition of TNBS-induced increase in myeloperoxidase level in TNBS-induced colitis Sprague-Dawley rat model colon tissue at 300 mg/kg/day, po administered on day of TNBS administration and on four consecutive days measured on day 62018Bioorganic & medicinal chemistry letters, 08-01, Volume: 28, Issue:14
Synthesis and biological evaluation of pyridine-linked indanone derivatives: Potential agents for inflammatory bowel disease.
AID73456Dissociation constant for Fibroblast growth factor 12004Journal of medicinal chemistry, Mar-25, Volume: 47, Issue:7
Validation of molecular docking calculations involving FGF-1 and FGF-2.
AID1211119Oral bioavailability in BCRP knockout Sprague-Dawley rat at 20 mg/kg by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID28924Effective permeability (Pe) across a hexadecane membrane (pH 6.8)2001Journal of medicinal chemistry, Mar-15, Volume: 44, Issue:6
High-throughput permeability pH profile and high-throughput alkane/water log P with artificial membranes.
AID1474167Liver toxicity in human assessed as induction of drug-induced liver injury by measuring verified drug-induced liver injury concern status2016Drug discovery today, Apr, Volume: 21, Issue:4
DILIrank: the largest reference drug list ranked by the risk for developing drug-induced liver injury in humans.
AID604023Ratio of total drug level in brain to plasma in Sprague-Dawley rat administered in casettes of 2/3 drugs at 4 hr constant rate intravenous infusions using flow rate of 1 (ml/kg)/hr corresponding to dosage rate of 2 (umol/kg)/hr by LC-MS/MS method2009Journal of medicinal chemistry, Oct-22, Volume: 52, Issue:20
Structure-brain exposure relationships in rat and human using a novel data set of unbound drug concentrations in brain interstitial and cerebrospinal fluids.
AID699541Inhibition of human liver OATP2B1 expressed in HEK293 Flp-In cells assessed as reduction in [3H]E3S uptake at 20 uM incubated for 5 mins by scintillation counting2012Journal of medicinal chemistry, May-24, Volume: 55, Issue:10
Classification of inhibitors of hepatic organic anion transporting polypeptides (OATPs): influence of protein expression on drug-drug interactions.
AID1079946Presence of at least one case with successful reintroduction. [column 'REINT' in source]
AID1413415Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as increase in IL-10 expression at 300 mg/kg, po administered once daily via gavage for 5 days starting 1 day post TNBS induction measured on day 7 by Western blot analysi2018MedChemComm, Aug-01, Volume: 9, Issue:8
Synthesis and evaluation of 6-heteroarylamino-2,4,5-trimethylpyridin-3-ols as inhibitors of TNF-α-induced cell adhesion and inflammatory bowel disease.
AID1321638Antiinflammatory activity in TNBS-induced Sprague-Dawley rat colitis model assessed as body weight recovery at 300 mg/kg/day, po administered for 5 days post 1 day of TNBS-challenge measured daily during compound dosing relative to control2016Bioorganic & medicinal chemistry letters, 10-01, Volume: 26, Issue:19
In vitro and in vivo inhibitory activity of 6-amino-2,4,5-trimethylpyridin-3-ols against inflammatory bowel disease.
AID184773Tested for the ability to decrease lesion area in the colon of the TNB/ethanol-induced chronic colitis rats at the dosage of 500 mg/kg/day1994Journal of medicinal chemistry, Sep-16, Volume: 37, Issue:19
Novel dual inhibitors of 5-lipoxygenase and thromboxane A2 synthetase: synthesis and structure-activity relationships of 3-pyridylmethyl-substituted 2-amino-6-hydroxybenzothiazole derivatives.
AID194537Tested for peak serum concentration in rat 51983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1211021Clearance in wild-type Sprague-Dawley rat at 5 mg/kg, iv by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1209590Drug uptake in Sprague-Dawley rat brain slices at 100 nM after 5 hrs in presence of 20 uM of MK-5712011Drug metabolism and disposition: the biological fate of chemicals, Mar, Volume: 39, Issue:3
Measurement of unbound drug exposure in brain: modeling of pH partitioning explains diverging results between the brain slice and brain homogenate methods.
AID1079949Proposed mechanism(s) of liver damage. [column 'MEC' in source]
AID1211096Half life in MRP2-deficient Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1211168Tmax in MRP2 knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID678712Inhibition of human CYP1A2 assessed as ratio of IC50 in absence of NADPH to IC50 for presence of NADPH using ethoxyresorufin as substrate after 30 mins2012Chemical research in toxicology, Oct-15, Volume: 25, Issue:10
Preclinical strategy to reduce clinical hepatotoxicity using in vitro bioactivation data for >200 compounds.
AID1824206Anti-colitis activity against DSS-induced C57BL/6 mouse model of colitis assessed as increase in colon length at 50 mg/kg, po administered via gavage DSS stimulation for 5 days followed by compound addition once daily for 10 days2022Journal of medicinal chemistry, 03-24, Volume: 65, Issue:6
Modulation of Naturally Occurring Linear Dipeptide Chirality to Reduce the Affinity for Oligopeptide Transporter 1 and Increase Intestinal Stability for an Enhanced Colon-Targeting Effect in the Treatment of Inflammatory Bowel Disease: An Application of
AID190859Urinary recovery in non-colostomized rats at 2 hr intervals for 48 h1993Journal of medicinal chemistry, Dec-24, Volume: 36, Issue:26
Brush-border-enzyme-mediated intestine-specific drug delivery. Amino acid prodrugs of 5-aminosalicylic acid.
AID18847Percent of drug absorbed by human intestine after oral administration2000Journal of medicinal chemistry, Oct-05, Volume: 43, Issue:20
Fast calculation of molecular polar surface area as a sum of fragment-based contributions and its application to the prediction of drug transport properties.
AID1576576Effective permeability of compound by PAMPA2019MedChemComm, Dec-01, Volume: 10, Issue:12
Synthesis of new lophine-carbohydrate hybrids as cholinesterase inhibitors: cytotoxicity evaluation and molecular modeling.
AID1824922Anti-colitis activity against DSS-induced colitis BALB/c mouse model assessed as effect on colon length at 100 mg/kg, po measured after 14 days2022Journal of medicinal chemistry, 01-13, Volume: 65, Issue:1
Discovery of a Series of Pyrimidine Carboxamides as Inhibitors of Vanin-1.
AID425629Antituberculosis activity against Mycobacterium paratuberculosis ATCC 19698 isolated from bovine assessed as effect on average time to detection of growth at 10'5 CFU of inoculum by MGIT 960 susceptibility test2008Antimicrobial agents and chemotherapy, Feb, Volume: 52, Issue:2
Thiopurine drugs azathioprine and 6-mercaptopurine inhibit Mycobacterium paratuberculosis growth in vitro.
AID1210069Inhibition of human recombinant CYP2J2 assessed as reduction in astemizole O-demethylation by LC-MS/MS method2013Drug metabolism and disposition: the biological fate of chemicals, Jan, Volume: 41, Issue:1
Discovery and characterization of novel, potent, and selective cytochrome P450 2J2 inhibitors.
AID1211163Cmax in BCRP knockout Sprague-Dawley rat at 20 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1676600Binding affinity to zinc ion assessed as accounting ratio by measuring total compound detected/total compound adsorbed at 2.55 umol by immobilized metal-ion affinity chromatography2020Journal of medicinal chemistry, 10-22, Volume: 63, Issue:20
Immobilized Metal Affinity Chromatography as a Drug Discovery Platform for Metalloenzyme Inhibitors.
AID592681Apparent permeability across human Caco2 cell membrane after 2 hrs by LC-MS/MS analysis2011Bioorganic & medicinal chemistry, Apr-15, Volume: 19, Issue:8
QSAR-based permeability model for drug-like compounds.
AID515780Intrinsic solubility of the compound in water2010Bioorganic & medicinal chemistry, Oct-01, Volume: 18, Issue:19
QSAR-based solubility model for drug-like compounds.
AID15120Percent of the drug absorbed after administration to humans was determined1999Journal of medicinal chemistry, May-20, Volume: 42, Issue:10
Molecular hashkeys: a novel method for molecular characterization and its application for predicting important pharmaceutical properties of molecules.
AID1221973Efflux ratio of permeability from apical to basolateral side over basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID442514Inhibition of human H-PGDS expressed in Escherichia coli BL21 assessed as rate of glutathione-chloro-dinitro benzene conjugation2010European journal of medicinal chemistry, Feb, Volume: 45, Issue:2
Identification and characterisation of new inhibitors for the human hematopoietic prostaglandin D2 synthase.
AID442515Inhibition of human H-PGDS expressed in Escherichia coli BL21 assessed as rate of glutathione-chloro-dinitro benzene conjugation at 50 uM2010European journal of medicinal chemistry, Feb, Volume: 45, Issue:2
Identification and characterisation of new inhibitors for the human hematopoietic prostaglandin D2 synthase.
AID614827Binding affinity to dipalmitoyl phosphatidyl choline lipid bilayer assessed as decrease in pre-transition temperature at compound to lipid molar ratio of 1:1 by DSC technique2011European journal of medicinal chemistry, Sep, Volume: 46, Issue:9
In-vitro metabolic inhibition and antifertility effect facilitated by membrane alteration: search for novel antifertility agent using nifedipine analogues.
AID173957Tested for total administered dose in rat 51983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1079938Chronic liver disease either proven histopathologically, or through a chonic elevation of serum amino-transferase activity after 6 months. Value is number of references indexed. [column 'CHRON' in source]
AID1763277Anti-colitis activity against TNBS-induced rat model of colitis assessed as decrease in MPO level in colon at 300 mg/kg, po administered for 5 days and measured on day 52021Bioorganic & medicinal chemistry letters, 07-01, Volume: 43Synthesis and activity of N-(5-hydroxy-3,4,6-trimethylpyridin-2-yl)acetamide analogues as anticolitis agents via dual inhibition of TNF-α- and IL-6-induced cell adhesions.
AID1211150AUC (infinity) in MRP2-deficient Wistar rat at 5 mg/kg, po by LC-MS/MS analysis2012Drug metabolism and disposition: the biological fate of chemicals, Sep, Volume: 40, Issue:9
Characterization of SAGE Mdr1a (P-gp), Bcrp, and Mrp2 knockout rats using loperamide, paclitaxel, sulfasalazine, and carboxydichlorofluorescein pharmacokinetics.
AID1221972Apparent permeability from basolateral to apical side of human Caco2 cells at 10 uM up to 120 mins by HPLC-MC analysis in presence of 10 uM of MRP2 inhibitor MK5712011Drug metabolism and disposition: the biological fate of chemicals, Feb, Volume: 39, Issue:2
Attenuation of intestinal absorption by major efflux transporters: quantitative tools and strategies using a Caco-2 model.
AID1470751Trypanocidal activity against trypomastigote stage of Trypanosoma cruzi INC-5 infected in NIH mouse blood assessed as parasite lysis at 50 ug/ml after 24 hrs by optical microscopic method relative to control2017European journal of medicinal chemistry, May-26, Volume: 132An in vitro and in vivo evaluation of new potential trans-sialidase inhibitors of Trypanosoma cruzi predicted by a computational drug repositioning method.
AID509498Antiulcerogenic activity against acetic acid-induced ulcerative colitis in albino rat assessed as ulcer index at 12.5 mmol/kg, po2010European journal of medicinal chemistry, Sep, Volume: 45, Issue:9
Design, synthesis and anti-ulcerogenic effect of some of furo-salicylic acid derivatives on acetic acid-induced ulcerative colitis.
AID616228Antifertility effect in goat epididymis spermatozoa assessed as decrease in lactate production at 1.25 mm after 2 hrs by NMR analysis2011European journal of medicinal chemistry, Sep, Volume: 46, Issue:9
In-vitro metabolic inhibition and antifertility effect facilitated by membrane alteration: search for novel antifertility agent using nifedipine analogues.
AID173956Tested for total administered dose in rat 41983Journal of medicinal chemistry, Sep, Volume: 26, Issue:9
A polymeric drug for treatment of inflammatory bowel disease.
AID1815673Binding affinity to human N-terminal His6-tagged and thrombin cleavage fused BLVRB expressed in Escherichia coli BL21 (DE3) assessed as change in entropy by isothermal titration calorimetry2022Journal of medicinal chemistry, 02-10, Volume: 65, Issue:3
Repositioning Food and Drug Administration-Approved Drugs for Inhibiting Biliverdin IXβ Reductase B as a Novel Thrombocytopenia Therapeutic Target.
AID417721Antiinflammatory activity against TNBS-induced Wistar rat colitis model assessed as decrease in severity of inflammation treated po 3 days after TNBS induction measured on day 72009European journal of medicinal chemistry, Jan, Volume: 44, Issue:1
Colon-specific mutual amide prodrugs of 4-aminosalicylic acid for their mitigating effect on experimental colitis in rats.
AID625282Drug Induced Liver Injury Prediction System (DILIps) training set; hepatic side effect (HepSE) score for cirrhosis2011PLoS computational biology, Dec, Volume: 7, Issue:12
Translating clinical findings into knowledge in drug safety evaluation--drug induced liver injury prediction system (DILIps).
AID1079932Highest frequency of moderate liver toxicity observed during clinical trials, expressed as a percentage. [column '% BIOL' in source]
AID504749qHTS profiling for inhibitors of Plasmodium falciparum proliferation2011Science (New York, N.Y.), Aug-05, Volume: 333, Issue:6043
Chemical genomic profiling for antimalarial therapies, response signatures, and molecular targets.
AID1347163384 well plate NINDS AMC confirmatory qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347158ZIKV-mCherry secondary qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347164384 well plate NINDS Rhodamine confirmatory qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1347156DAPI mCherry counterscreen qHTS for Zika virus inhibitors2020Proceedings of the National Academy of Sciences of the United States of America, 12-08, Volume: 117, Issue:49
Therapeutic candidates for the Zika virus identified by a high-throughput screen for Zika protease inhibitors.
AID1159607Screen for inhibitors of RMI FANCM (MM2) intereaction2016Journal of biomolecular screening, Jul, Volume: 21, Issue:6
A High-Throughput Screening Strategy to Identify Protein-Protein Interaction Inhibitors That Block the Fanconi Anemia DNA Repair Pathway.
AID1634957Antiulcerative activity in DSS-induced C57BL/6J mouse model of acute ulcerative colitis assessed as partial disappearance of inflammatory edema at 200 mg/kg, po measured over 7 days by microscopic analysis2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Synthesis and Structure-Activity Relationships of N-Dihydrocoptisine-8-ylidene Aromatic Amines and N-Dihydrocoptisine-8-ylidene Aliphatic Amides as Antiulcerative Colitis Agents Targeting XBP1.
AID1634949Antiulcerative activity in DSS-induced C57BL/6J mouse model of acute ulcerative colitis assessed as body weight loss at 300 mg/kg, po measured over 7 days (Rvb = 18%)2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Synthesis and Structure-Activity Relationships of N-Dihydrocoptisine-8-ylidene Aromatic Amines and N-Dihydrocoptisine-8-ylidene Aliphatic Amides as Antiulcerative Colitis Agents Targeting XBP1.
AID1634951Antiulcerative activity in DSS-induced C57BL/6J mouse model of acute ulcerative colitis assessed as colon contracture at 300 mg/kg, po measured over 7 days (Rvb = 37 %)2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Synthesis and Structure-Activity Relationships of N-Dihydrocoptisine-8-ylidene Aromatic Amines and N-Dihydrocoptisine-8-ylidene Aliphatic Amides as Antiulcerative Colitis Agents Targeting XBP1.
AID1634955Antiulcerative activity in DSS-induced C57BL/6J mouse model of acute ulcerative colitis assessed as colon macroscopic damage index at 300 mg/kg, po measured over 7 days (Rvb = 4.63 +/- 0.52 No_unit)2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Synthesis and Structure-Activity Relationships of N-Dihydrocoptisine-8-ylidene Aromatic Amines and N-Dihydrocoptisine-8-ylidene Aliphatic Amides as Antiulcerative Colitis Agents Targeting XBP1.
AID1634953Antiulcerative activity in DSS-induced C57BL/6J mouse model of acute ulcerative colitis assessed as inhibition of disease activity index at 300 mg/kg, po measured over 7 days relative to control2016Journal of natural products, Apr-22, Volume: 79, Issue:4
Synthesis and Structure-Activity Relationships of N-Dihydrocoptisine-8-ylidene Aromatic Amines and N-Dihydrocoptisine-8-ylidene Aliphatic Amides as Antiulcerative Colitis Agents Targeting XBP1.
AID1345155Human Proton-coupled folate transporter (SLC46 family of folate transporters)2006Cell, Dec-01, Volume: 127, Issue:5
Identification of an intestinal folate transporter and the molecular basis for hereditary folate malabsorption.
AID1159550Human Phosphogluconate dehydrogenase (6PGD) Inhibitor Screening2015Nature cell biology, Nov, Volume: 17, Issue:11
6-Phosphogluconate dehydrogenase links oxidative PPP, lipogenesis and tumour growth by inhibiting LKB1-AMPK signalling.
AID1802828Surface Plasmon Resonance (SPR) Assay from Article 10.1074/jbc.M113.521708: \\A novel small-molecule tumor necrosis factor a inhibitor attenuates inflammation in a hepatitis mouse model.\\2014The Journal of biological chemistry, May-02, Volume: 289, Issue:18
A novel small-molecule tumor necrosis factor α inhibitor attenuates inflammation in a hepatitis mouse model.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (4,151)

TimeframeStudies, This Drug (%)All Drugs %
pre-19901388 (33.44)18.7374
1990's927 (22.33)18.2507
2000's808 (19.47)29.6817
2010's777 (18.72)24.3611
2020's251 (6.05)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 109.18

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 Index109.18 (24.57)
Research Supply Index8.52 (2.92)
Research Growth Index4.49 (4.65)
Search Engine Demand Index205.47 (26.88)
Search Engine Supply Index2.00 (0.95)

This Compound (109.18)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials585 (13.18%)5.53%
Reviews631 (14.22%)6.00%
Case Studies932 (21.01%)4.05%
Observational24 (0.54%)0.25%
Other2,265 (51.05%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Clinical Trials (67)

Trial Overview

TrialPhaseEnrollmentStudy TypeStart DateStatus
The Effect of Sulfasalazine on CRH Levels in Pregnant Women With a History of Pre-Term Birth: A Randomized Controlled Trial [NCT05703425]Phase 250 participants (Anticipated)Interventional2023-03-01Recruiting
IL-7 and IL-7R Expression in Peripheral Blood Mononuclear Cells, Peripheral Blood Monocytes or Differentiated Macrophages of Rheumatoid Arthritis Patients With Active vs. Inactive Disease Treated With DMARD and/or CIMZIA [NCT02451748]Phase 432 participants (Actual)Interventional2015-08-31Completed
A Prospective, Single-centre, Randomised Study Evaluating the Clinical, Imaging and Immunological Depth of Remission Achieved by Very Early Versus Delayed Etanercept in Patients With Rheumatoid Arthritis [NCT02433184]Phase 4120 participants (Actual)Interventional2011-07-31Completed
Comparison of Sulfasalazine Versus Leflunomide Based Combination Disease Modifying Anti-rheumatic Drug Therapy (DMARD) in Patients With Rheumatoid Arthritis Failing Methotrexate Monotherapy : A Randomized Control Trial [NCT02930343]Phase 3136 participants (Actual)Interventional2016-09-30Terminated(stopped due to Due to time constraints, the study was halted prematurely)
Gastrointestinal Nutrient Transit and Enteroendocrine Function After Upper Gastrointestinal Surgery [NCT03734627]40 participants (Actual)Observational2016-07-01Completed
On the Impact of Therapeutic Tumor Necrosis Factor-alpha Inhibition on Anogenital Human Papillomavirus Infection [NCT02376478]222 participants (Actual)Observational2009-12-31Completed
Targeted Treatment Early With Etanercept Plus Methotrexate Versus T2T Care for DMARD-naïve Early RA Patients. A Prospective, Longitudinal Cohort Study With Embedded Pilot Randomised Controlled Trial to Assess Treatment Rationalisation Based on naïve T-cel [NCT03813771]Phase 4106 participants (Anticipated)Interventional2019-03-31Not yet recruiting
Prospective Randomized Study to Compare Clinical Outcomes in Patients With Osteomyelitis Treated With Intravenous Antibiotics Versus Intravenous Antibiotics With an Early Switch to Oral Antibiotics [NCT02099240]Early Phase 111 participants (Actual)Interventional2014-03-06Terminated(stopped due to Not enough patient enrollment and lack of staffing)
CSP #551 - Rheumatoid Arthritis: Comparison of Active Therapies in Patients With Active Disease Despite Methotrexate Therapy [NCT00405275]353 participants (Actual)Interventional2007-07-31Completed
Effect of Sarilumab on Patient-reported Outcomes in Patients With Moderately to Severely Active Rheumatoid Arthritis and With Inadequate Response or Intolerance to Current Conventional Synthetic DMARDs or Tumor Necrosis Factor Inhibitors [NCT03449758]Phase 484 participants (Actual)Interventional2018-03-05Completed
A Prospective, Randomized, Controlled, Open Label, Assessor-blinded, Parallel-group Phase III Clinical Trial to Evaluate the Impact of Tapering Systemic Immunosuppressive Therapy in a Treat-to-target Approach on Maintaining Minimal Disease Activity in Adu [NCT04610476]Phase 3270 participants (Anticipated)Interventional2020-10-19Recruiting
A Phase Ib/II Randomized, Open Label Drug Repurposing Trial of Glutamate Signaling Inhibitors in Combination With Chemoradiotherapy in Patients With Newly Diagnosed Glioblastoma [NCT05664464]Phase 1/Phase 2120 participants (Anticipated)Interventional2023-01-01Recruiting
Clinical Effectiveness of Standard Step up Care (Methotrexate) Compared to Early Combination DMARD Therapy With Standard Step up Care Compared to Early Use of TNF Inhibitors With Standard Step up Care for the Treatment of Moderate to Severe Psoriatic Arth [NCT03739853]Phase 4315 participants (Anticipated)Interventional2019-05-14Recruiting
An Open Label, Randomised Study to Compare the Efficacy of Certolizumab Pegol (CZP) Plus a Dynamic or Fixed Dose Treatment Strategy in Patients With Rheumatoid Arthritis, a Phase II Study [NCT02293590]Phase 243 participants (Actual)Interventional2013-11-30Completed
Treatment of Early Aggressive Rheumatoid Arthritis (TEAR) [NCT00259610]Phase 4755 participants (Actual)Interventional2004-05-31Completed
Phase I/II Clinical Trial Assessing the Combination of Sulfasalazine With Standard of Care Induction Therapy in Newly Diagnosed Acute Myeloid Leukemias (AML) Patients 60 Years or Older- the SALMA Study [NCT05580861]Phase 1/Phase 264 participants (Anticipated)Interventional2023-05-17Recruiting
Treatment of Rheumatoid Arthritis With DMARDs: Predictors of Response [NCT03414502]Phase 3400 participants (Anticipated)Interventional2007-12-10Recruiting
A Prospective Randomized, Open, Multi-Center Trial Comparing TNF-Blockade + MTX to MTX+SSZ+HCQ in Patients With Early RA With an Inadequate Response to MTX [NCT00764725]Phase 4487 participants (Actual)Interventional2002-12-31Completed
Double Blind Trial Investigating the Role of Sulfasalazine in Decreasing Opioids Requirements in Breast Cancer Patients [NCT03847311]Phase 240 participants (Anticipated)Interventional2021-05-03Recruiting
A Randomized, Double-blind, Multicenter Study Evaluating the Safety and Efficacy of Sarilumab Added to Non-MTX DMARDs or as Monotherapy in Japanese Patients With Active Rheumatoid Arthritis [NCT02373202]Phase 391 participants (Actual)Interventional2015-02-28Completed
Clinical Study Evaluating the Efficacy and Safety of Sulfasalazine in Patients With Metastatic Colorectal Cancer [NCT06134388]Phase 350 participants (Anticipated)Interventional2023-09-01Recruiting
Use of TNF-blocking Therapy in Combination With DMARDs in Patients With Early Rheumatoid Arthritis [NCT00908089]Phase 4100 participants (Actual)Interventional2003-03-31Active, not recruiting
Efficacy and Safety of Etanercept Dose Reduction in Patients With Ankylosing Spondylitis [NCT02638896]Phase 4100 participants (Anticipated)Interventional2016-01-31Not yet recruiting
Longitudinal Observational Study on Rheumatoid Arthritis Patients: Effects of Antirheumatic Treatment on Serum Levels of Survivin [NCT03440892]2,500 participants (Anticipated)Observational2017-11-01Recruiting
Treat-to-target Strategy in Ankylosing Spondylitis Using Etanercept and Conventional Synthetic DMARDs, a Prospective Randomized Controlled Study [NCT04077957]Phase 4100 participants (Anticipated)Interventional2019-10-07Not yet recruiting
Triple III Comparison of Leflunomide Alone Versus Two DMARD Combinations (Leflunomide-Hydroxychloroquine-Sulfasalazine or Methotrexate-Hydroxychloroquine-Sulfasalazine) in the Treatment of Rheumatoid Arthritis [NCT00579878]Phase 369 participants (Actual)Interventional2001-03-27Completed
A Randomized, Open-Label Study in the Asia-Pacific Region Comparing the Safety and Efficacy of Etanercept With Usual DMARD Therapy in Subjects With Rheumatoid Arthritis [NCT00422227]Phase 4300 participants (Actual)Interventional2007-06-30Completed
Randomized Controlled Clinical Trial Evaluating Methotrexate or Leflunomide + Targeted Therapy Versus Methotrexate or Leflunomide + Sulfasalazine + Hydroxychloroquine in Patients With Rheumatoid Arthritis and Insufficient Response to Methotrexate or Leflu [NCT02714634]Phase 4286 participants (Anticipated)Interventional2016-03-30Recruiting
Phase I Trial Combining Sulfasalazine and Gamma Knife Radiosurgery for Recurrent Glioblastoma [NCT04205357]Phase 124 participants (Actual)Interventional2020-03-01Completed
A Phase 1, Open-label Study in Healthy Adult Subjects to Evaluate Effects of Cytochrome P450 Inhibition and Induction on the Pharmacokinetics of CC-99677 and the Effects of CC-99677 on the Pharmacokinetics of Digoxin, Metformin, Methotrexate, Midazolam, R [NCT04268394]Phase 148 participants (Actual)Interventional2020-03-13Completed
CHronic Nonbacterial Osteomyelitis International Registry (CHOIR) [NCT04725422]2,000 participants (Anticipated)Observational2018-08-01Recruiting
Comparison of Anti-TNF Therapy Plus Methotrexate, Combination Therapy of DMARDs, and Methotrexate Alone in Very Early Polyarticular Juvenile Idiopathic Arthritis. A National Randomized Multicenter Clinical Trial. [NCT01015547]Phase 360 participants (Actual)Interventional2003-05-31Completed
Pilot Study of the Safety and Efficacy of Sulfasalazine in Pulmonary Arterial Hypertension [NCT04528056]Phase 1/Phase 280 participants (Anticipated)Interventional2020-08-01Recruiting
Phase III, Randomized, Study of Sulfasalazine Versus Placebo in the Prevention of Acute Diarrhea in Patients Receiving Pelvic Radiation Therapy [NCT01198145]Phase 387 participants (Actual)Interventional2011-04-30Completed
A 2 Year Prospective Multicentre Randomised Controlled Trial Comparing Effectiveness in Daily Practice of Different Treatment Strategies for Early Rheumatoid Arthritis. [NCT01172639]Phase 4400 participants (Actual)Interventional2009-02-28Completed
Randomized Controlled 12 Months Trial With Etanercept (Enbrel ®) vs. Sulfasalazine in Early Axial Spondyloarthritis With Focus on Improvement of Acute Inflammatory Lesions as Detected by MRI. Amendment 4: 1-Year Extension of Study [NCT00844142]Phase 280 participants (Anticipated)Interventional2005-11-30Recruiting
Clinical Study of Tripterygium Capsule to Treat Early Ankylosing Spondylitis: a 12-Week, Multiple Centers, Randomized Double-Blind, Positive Drug and Placebo Controlled Clinical Trial [NCT00889694]Phase 2/Phase 380 participants (Anticipated)Interventional2008-10-31Enrolling by invitation
Effect of Sulfasalazine on Endothelial Function [NCT00554203]60 participants (Anticipated)Interventional2003-07-31Completed
Comparison of Three Different Treatment Regimes in Early Rheumatoid Arthritis: A Randomized Open-labelled Trial [NCT01870128]Phase 360 participants (Actual)Interventional2009-08-31Completed
A Randomized, Double-Blind Study Evaluating the Safety and Efficacy of Etanercept and Sulphasalazine in Subjects With Ankylosing Spondylitis [NCT00247962]Phase 4566 participants (Actual)Interventional2005-12-31Completed
A Phase 1, Fixed Sequence, Open-label, Drug-drug Interaction Study to Evaluate the Effect of GLPG3970 on the Pharmacokinetics of Sulfasalazine in Adult, Healthy Subjects [NCT04720183]Phase 18 participants (Actual)Interventional2021-01-11Completed
Effects of Sulfasalazine on BOLD Response to Alcohol Cues [NCT01312129]23 participants (Actual)Interventional2010-03-31Completed
Leflunomide Versus Sulfasalazine/Methotrexate in Rheumatoid Arthritis Patients With Active Disease Despite Methotrexate: an Ultrasound and Magnetic Resonance Imaging Study [NCT01659242]Phase 41 participants (Actual)Interventional2012-07-31Terminated
A Phase 1, Three-Part, Open-label Study in Healthy Adult Volunteers to Assess Vadadustat as a Perpetrator in Drug-Drug Interactions With Rosuvastatin, Sulfasalazine, Pravastatin, Atorvastatin and Simvastatin [NCT03801733]Phase 1134 participants (Actual)Interventional2018-06-17Completed
A Single-center, Randomized, Double-blind Clinical Study to Evaluate the Effect of Sulfasalazine on Painful Neuropathy [NCT01667029]Phase 28 participants (Actual)Interventional2013-05-31Terminated(stopped due to poor enrollment)
A Pilot Study to Determine the Effect of Sulfasalazine on Glutamate Levels Detected by Magnetic Resonance Spectroscopy(MRS) in Patients With Glioma [NCT01577966]9 participants (Actual)Interventional2012-01-31Completed
An Open Label, Single Dose, Three Part Study to Assess the Effects of Rolapitant (1.8 mg/mL Rolapitant IV Solution) on the Pharmacokinetics of Digoxin (P-gp); Sulfasalazine (BCRP); and the Cooperstown Cocktail (Midazolam [CYP3A4], Omeprazole [CYP2C19], Wa [NCT02434861]Phase 1102 participants (Actual)Interventional2015-05-31Completed
A Randomized, Double-Blind, Double-Dummy Study Assessing The Safety and Tolerability of Sarilumab and Tocilizumab In Patients With Rheumatoid Arthritis Who Are Inadequate Responders to or Intolerant of TNF Antagonists [NCT01768572]Phase 3202 participants (Actual)Interventional2013-03-31Completed
Pharmacokinetics of Sulfasalazine, Paracetamol, Fexofenadine and Valsartan After Oral Administration Using 240 ml Non-caloric Water, a Carbohydrate Enriched Drink and Grapefruit Juice in Correlation to the Intestinal Availability of Water as Quantified by [NCT03012763]Phase 19 participants (Actual)Interventional2016-04-30Completed
Clinical Effectiveness of Symptomatic Therapy Compared to Standard Step up Care for the Treatment of Low Impact Psoriatic Oligoarthritis: a 2 Arm Parallel Group Feasibility Study [NCT03797872]Phase 41 participants (Actual)Interventional2019-04-17Completed
Effects of Extended Release Methylnaltrexone Bromide (150 mg b.i.d.) in Comparison to Extended Release Naloxone Hydrochloride (20 mg b.i.d.) on Loperamide-induced Delay of the Oro-cecal, Whole-gut and Colon Transit Time in Healthy Subjects. [NCT01596764]Phase 116 participants (Actual)Interventional2011-05-31Completed
Effects of 500 mg Immediate Release and Extended Release Methylnaltrexone on Loperamide-induced Delay of the Oro-cecal and Whole-gut Transit Time in Healthy Subjects [NCT01596777]Phase 115 participants (Actual)Interventional2010-01-31Completed
Sequential Application of Yisaipu® and Disease Modifying Anti-Rheumatic Drugs (DMARDs) in Treating Mild-to-Moderate Ankylosing Spondylitis: the Mid-term Follow-up Result [NCT03411798]Phase 476 participants (Actual)Interventional2017-12-15Completed
Induction of Remission in RA Patients at Low Disease Activity by Additional Infliximab-therapy [NCT00521924]Phase 38 participants (Actual)Interventional2007-06-30Terminated(stopped due to Slow Enrollment)
Treatments Against RA and Effect on FDG-PET/CT (The TARGET Trial) [NCT02374021]Phase 4159 participants (Actual)Interventional2016-07-31Completed
A Multicenter, Randomized, Open-Label, Parallel-Group Usability Study Of The Sarilumab Auto-Injector Device And A Prefilled Syringe In Patients With Moderate To Severe Active Rheumatoid Arthritis Who Are Candidates For Anti-IL6R Therapy [NCT02057250]Phase 3217 participants (Actual)Interventional2014-03-31Completed
A Multicenter, Randomized, Open-label, Blinded-assessor, Follow-up, Phase 4 Study in Patients With Rheumatoid Arthritis Who Have Completed the Initial Treatment Part in the NORD-STAR Study and Have Reached Stable Low Disease Activity [NCT02466581]Phase 425 participants (Actual)Interventional2015-02-03Active, not recruiting
A Phase 1, Two-part, Open-label, Drug-drug Interaction Study in Healthy Male Adult Participants to Evaluate the Effects of BMS-986371 on the Pharmacokinetics of Methotrexate in the Presence and Absence of Sulfasalazine [NCT05445440]Phase 130 participants (Actual)Interventional2022-09-06Completed
A Randomized, Placebo-controlled Pilot Study of Sulfasalazine for the Treatment of Primary Sclerosing Cholangitis (PSC) [NCT03561584]Phase 242 participants (Anticipated)Interventional2018-07-01Recruiting
Anti-Tumor Necrosis Factor Therapy In Patients With Ankylosing Spondylitis-A Registry Project [NCT02456363]Phase 2300 participants (Anticipated)Interventional2009-11-30Recruiting
Adjunctive Effect of Topical Sulfasalazine for Oral Lichen Planus Management: A Randomized Clinical Trial [NCT06060301]Phase 346 participants (Actual)Interventional2023-03-01Active, not recruiting
An Open Label Non-randomized Study To Characterize The Steady State Pharmacokinetics Of Sulfasalazine Delayed Release Tablets In Children With Juvenile Idiopathic Arthritis [NCT00637780]Phase 42 participants (Actual)Interventional2010-06-30Terminated(stopped due to Study terminated on 13 April 2016 for business reasons. No safety and/or efficacy concerns contributed to the termination of the study)
Multicenter, Open Label, Phase IIIb Study to Evaluate the Safety and Tolerability of Subcutaneous Tocilizumab as Monotherapy and/or in Combination With Methotrexate or Other Non-Biologic Disease-Modifying Antirheumatic Drugs in Patients With Rheumatoid Ar [NCT01941095]Phase 3100 participants (Actual)Interventional2013-11-20Completed
Methotrexate, Blood Pressure and Arterial Function in Rheumatoid Arthritis [NCT03254589]Phase 4124 participants (Anticipated)Interventional2017-10-01Recruiting
Anti-TNF Therapy and Nerve Conduction Studies in Patients With Ankylosing Spondylitis [NCT04943237]60 participants (Actual)Observational2019-07-01Completed
Comparison of Infliximab With Sulfasalazine/Hydroxychloroquine Initiated After Methotrexate by Rheumatoid Arthritis Patients Treated in Clinical Practice (Real-World Emulation of SWEFOT Trial) [NCT05051137]509 participants (Actual)Observational2006-01-12Completed
A Randomized, Double-blind, Parallel, Placebo-controlled Study Assessing the Efficacy and Safety of Sarilumab Added to Non-biologic DMARD Therapy in Patients With Rheumatoid Arthritis Who Are Inadequate Responders to or Intolerant of TNF-α Antagonists [NCT01709578]Phase 3546 participants (Actual)Interventional2012-10-31Completed
[information is prepared from clinicaltrials.gov, extracted Sep-2024]

Trial Outcomes

TrialOutcome
NCT00247962 (2) [back to overview]Number of Patients Achieving Assessment in Ankylosing Spondylitis (ASAS 20)
NCT00247962 (2) [back to overview]Ankylosing Spondylitis Quality of Life (ASQoL) Total Score Change From Baseline
NCT00259610 (2) [back to overview]Disease Activity Score Erythrocyte Sedimentation Rate(DAS28-ESR)
NCT00259610 (2) [back to overview]Radiographic Disease Progression Between Baseline and Week 102 as Assessed by Van Der Heijde Modified Sharp Scores.
NCT00405275 (1) [back to overview]Mean 48-week Change in DAS28
NCT00422227 (10) [back to overview]Percentage of Participants Achieving ACR 20, 50, and 70 Responses
NCT00422227 (10) [back to overview]Percent Change From Baseline in Painful and Swollen Joint Counts
NCT00422227 (10) [back to overview]Percent Change From Baseline in General Health, Pain, and Fatigue, Visual Analog Scales
NCT00422227 (10) [back to overview]Percent Change From Baseline in Duration (Minutes) of Morning Stiffness
NCT00422227 (10) [back to overview]Percentage of Participants Achieving European League Against Rheumatism (EULAR) Moderate or Good Response
NCT00422227 (10) [back to overview]Percent Change From Baseline in DAS28 at Week 16
NCT00422227 (10) [back to overview]Change From Baseline in Adjusted Mean of American College of Rheumatology Response (ACR-N) Area Under Curve (AUC) Over 16 Weeks
NCT00422227 (10) [back to overview]Percent Change From Baseline in Physician And Subject Global Assessments
NCT00422227 (10) [back to overview]Percentage of Participants With DAS28 Improvement of ≥0.6 and ≥1.2
NCT00422227 (10) [back to overview]Percentage of Participants Achieving DAS28 <3.2 (Low Disease Activity) and <2.6 (Remission)
NCT00579878 (1) [back to overview]Measuring the Safety and Efficacy of a New DMARD, Leflunomide Alone or in Combination With Traditional DMARD's. Participants Reaching ACR 20 Response. at 48 Weeks
NCT00637780 (12) [back to overview]Sulfasalazine Steady State Maximum Plasma Concentration (Cmax) and Predose Concentration (Cmin)
NCT00637780 (12) [back to overview]Sulfasalazine Area Under the Concentration-time Profile From Time 0 to Time Tau, the Dosing Interval (AUCtau) at Steady State
NCT00637780 (12) [back to overview]Sulfapyridine Tmax at Steady State
NCT00637780 (12) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and Withdrawals Due to TEAEs
NCT00637780 (12) [back to overview]5-aminosalicylic Acid (5-ASA) AUCtau at Steady State
NCT00637780 (12) [back to overview]Sulfapyridine AUCtau at Steady State
NCT00637780 (12) [back to overview]5-aminosalicylic Acid (5-ASA) Tmax at Steady State
NCT00637780 (12) [back to overview]5-aminosalicylic Acid (5-ASA) Steady State Cmax and Cmin
NCT00637780 (12) [back to overview]Number of Participants With Vital Signs Values Meeting Categorical Summarization Criteria
NCT00637780 (12) [back to overview]Number of Participants With Laboratory Test Abnormalities
NCT00637780 (12) [back to overview]Sulfapyridine Steady State Cmax and Cmin
NCT00637780 (12) [back to overview]Sulfasalazine Time for Cmax (Tmax) at Steady State
NCT01172639 (7) [back to overview]Remission According to DAS28-CRP at Week 16
NCT01172639 (7) [back to overview]Remission According to SDAI at Week 104
NCT01172639 (7) [back to overview]Remission According to SDAI at Week 52
NCT01172639 (7) [back to overview]Clinically Significant Change in HAQ Score
NCT01172639 (7) [back to overview]Remission According to DAS28-CRP at Week 104
NCT01172639 (7) [back to overview]Remission According to DAS28-CRP at Week 52
NCT01172639 (7) [back to overview]Remission According to SDAI (Simple Disease Activity Index) at Week 16
NCT01198145 (8) [back to overview]Percentage of Patients in Each Arm That Experience Clinically Significant Deficits in Overall Quality of Life and Fatigue
NCT01198145 (8) [back to overview]Percentage of Patients in Each Arm That Experience Tenesmus, Abdominal Pain, Constipation, Diarrhea and Rectal Bleeding During and After RT
NCT01198145 (8) [back to overview]"Percent of Patients in Each Arm That Recorded Yes to Each of Questions 2-10 on the Bowel Function Questionnaire"
NCT01198145 (8) [back to overview]Area Under the Curve That Combines the Individual Severity of Diarrhea Toxicity as Measured by the CTCAE v4.0 During and After RT
NCT01198145 (8) [back to overview]Average Graded Severity for Tenesmus, Abdominal Pain, Constipation, Diarrhea and Hemorrhage During and After RT as Graded by CTCAE v4.0
NCT01198145 (8) [back to overview]Maximum Severity of Each Outcome Variable (Rectal Bleeding, Abdominal Cramping, Tenesmus, Constipation, and Diarrhea) Measured During and After RT
NCT01198145 (8) [back to overview]Maximum Severity of Diarrhea Toxicity as Measured by the CTCAE v4.0 During and After Radiotherapy (RT)
NCT01198145 (8) [back to overview]Percentage of Patients in Each Arm That Require Any Type of Antidiarrheal Medications.
NCT01312129 (1) [back to overview]% BOLD Response Increase Above Baseline
NCT01577966 (1) [back to overview]Percent Decrease in Central Nervous System Bioavailability of Sulfasalazine
NCT01667029 (18) [back to overview]Categorical Rating of Pain Intensity (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Pain Score (First Treatment Period)
NCT01667029 (18) [back to overview]Categorical Rating of Pain Intensity (First Treatment Period Only)
NCT01667029 (18) [back to overview]Pain Score (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Physical Functioning Score Assessed Using the Euroquality of Life (EQ-5D) Metrics (First Treatment Period Only)
NCT01667029 (18) [back to overview]Physical Functioning Score Assessed Using the Euroquality of Life (EQ-5D) (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Physical Functioning Score Assessed Using the Brief Pain Inventory (BPI) Interference Scale (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Missed Medication Doses (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Missed Medication Dose (First Treatment Period Only)
NCT01667029 (18) [back to overview]Emotional Functioning (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Emotional Functioning (First Treatment Period Only)
NCT01667029 (18) [back to overview]Overall Improvement (First Treatment Period Only)
NCT01667029 (18) [back to overview]Breakthrough Treatment (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Breakthrough Treatment (First Treatment Period Only)
NCT01667029 (18) [back to overview]Number of Patients With >=50% Pain Reduction (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Overall Improvement (Using the Crossover Comparison Structure of the Study)
NCT01667029 (18) [back to overview]Number of Patients With >=50% Pain Reduction (First Treatment Period)
NCT01667029 (18) [back to overview]Physical Functioning Score Assessed Using the Brief Pain Inventory (BPI) Interference Scale (First Treatment Period Only)
NCT01709578 (41) [back to overview]Change From Baseline in Work Productivity Survey - Rheumatoid Arthritis (WPS-RA) at Week 24: Work Days Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: Days With Family/Social/Leisure Activities Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: Days With Household Work Productivity Reduced by ≥ 50% Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: Days With Outside Help Hired Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: House Work Days Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: RA Interference With Household Work Productivity
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: RA Interference With Work Productivity
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: Work Days Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: Days With Family/Social/Leisure Activities Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: Days With Household Work Productivity Reduced by ≥ 50% Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: Days With Outside Help Hired Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: Days With Work Productivity Reduced by ≥ 50% Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: House Work Days Missed Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: RA Interference With Household Work Productivity
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 24: RA Interference With Work Productivity
NCT01709578 (41) [back to overview]Percentage of Participants Achieving ACR50 Criteria at Week 24
NCT01709578 (41) [back to overview]Percentage of Participants Achieving ACR70 Criteria at Week 24
NCT01709578 (41) [back to overview]Percentage of Participants Achieving Clinical Remission Score (DAS28--CRP <2.6) at Week 12
NCT01709578 (41) [back to overview]Percentage of Participants Achieving Clinical Remission Score (DAS28-CRP) <2.6 at Week 24
NCT01709578 (41) [back to overview]Percentage of Participants Who Achieved at Least 20% Improvement in the American College of Rheumatology (ACR20) Criteria at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Individual ACR Component - CRP Level at Week 12 and Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Individual ACR Component - HAQ-DI at Week 12 and Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Individual ACR Component - Physician Global VAS, Participant Global VAS and Pain VAS at Week 12 and Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Individual ACR Components - TJC and SJC at Week 12 and Week 24
NCT01709578 (41) [back to overview]Change From Baseline in SF-36 at Week 12
NCT01709578 (41) [back to overview]Percentage of Participants Achieving ACR20, ACR50 and ACR70 Criteria at Week 12
NCT01709578 (41) [back to overview]Change From Baseline in WPS-RA at Week 12: Days With Work Productivity Reduced by ≥ 50% Due to RA
NCT01709578 (41) [back to overview]Change From Baseline in 36-Item Short-Form Health Survey (SF-36) Physical Component Summary Scores (PCS) at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in DAS28-CRP at Week 12
NCT01709578 (41) [back to overview]Change From Baseline in Disease Activity Score for 28 Joints -C-Reactive Protein (DAS28--CRP) Score at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in EQ-5D-3L VAS Scores at Week 12
NCT01709578 (41) [back to overview]Change From Baseline in European Quality of Life-5 Dimension 3 Level (EQ-5D-3L) VAS Scores at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in HAQ-DI at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in Morning Stiffness VAS at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in RAID Scores at Week 12
NCT01709578 (41) [back to overview]Change From Baseline in Rheumatoid Arthritis Impact of Disease (RAID) Scores at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in SF-36 MCS at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in the FACIT-fatigue at Week 12
NCT01709578 (41) [back to overview]Change From Baseline in the Functional Assessment of Chronic Illness Therapy Fatigue (FACIT-fatigue) Score at Week 24
NCT01709578 (41) [back to overview]Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 12
NCT01768572 (1) [back to overview]Number of Participants With Treatment Emergent Adverse Events (TEAEs)
NCT01941095 (19) [back to overview]Number of Participants by Reasons (Categories) for Corticosteroid Dose Reduction or Discontinuation
NCT01941095 (19) [back to overview]HAQ-DI Score
NCT01941095 (19) [back to overview]Functional Assessment of Chronic Illness Therapy (FACIT)-Fatigue Total Score
NCT01941095 (19) [back to overview]Change From Baseline in TJC28 up to Week 52
NCT01941095 (19) [back to overview]Change From Baseline in SJC28 up to Week 52
NCT01941095 (19) [back to overview]Percentage of Participants Who Achieved DAS28-ESR Remission/Low Disease Activity (LDA) From Week 28 up to Week 52 Among Participants With Intensification of Methotrexate/Other Non-Biologic DMARDs in Combination With Tocilizumab Since Week 24
NCT01941095 (19) [back to overview]Percentage of Participants Who Maintained DAS28-ESR Remission From Week 24 up to Week 52 Among Participants on Tocilizumab Monotherapy Since Week 24
NCT01941095 (19) [back to overview]Percentage of Participants Who Received All Planned Study Medication (Compliance)
NCT01941095 (19) [back to overview]Change From Baseline in DAS28-ESR up to Week 52
NCT01941095 (19) [back to overview]Percentage of Participants With Good, Moderate, or No Response According to European League Against Rheumatism (EULAR) Response Criteria
NCT01941095 (19) [back to overview]PGA, Using VAS Score
NCT01941095 (19) [back to overview]Soluble Interleukin-6 Receptor (sIL-6R) Levels
NCT01941095 (19) [back to overview]Tocilizumab Serum Levels
NCT01941095 (19) [back to overview]Percentage of Participants With Corticosteroid Dose Reduction or Discontinuation
NCT01941095 (19) [back to overview]Percentage of Participants Who Achieved Disease Activity Score Based on 28 Joint Count and Erythrocyte Sedimentation Rate (DAS28-ESR) Remission at Week 24
NCT01941095 (19) [back to overview]Change From Baseline in Simplified Disease Activity Index (SDAI) Score up to Week 52
NCT01941095 (19) [back to overview]Patient Assessment of Pain, Using VAS Score
NCT01941095 (19) [back to overview]Number of Participants With Anti-Tocilizumab Antibodies (ATA)
NCT01941095 (19) [back to overview]Number of Participants With American College of Rheumatology 20 (ACR20) Response
NCT02057250 (2) [back to overview]Number of Validated AID Associated Product Technical Failures (PTFs)
NCT02057250 (2) [back to overview]Area Under the Serum Concentration Versus Time Curve Calculated Using the Trapezoidal Method During a Dose Interval (AUC[0-tau]) for Sarilumab
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Renal Function Parameters
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Liver Function Parameters
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Hematological Parameters
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Metabolic Parameters
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Electrolytes
NCT02373202 (11) [back to overview]Change From Baseline in Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 52
NCT02373202 (11) [back to overview]Change From Baseline at Week 52 in Disease Activity Score for 28 Joints Based on C-Reactive Protein (DAS28-CRP)
NCT02373202 (11) [back to overview]Number of Participants With Potentially Clinically Significant Vital Signs Abnormalities
NCT02373202 (11) [back to overview]Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT02373202 (11) [back to overview]Percentage of Participants Achieving American College of Rheumatology (ACR) 20, 50 and 70 Responses at Week 52
NCT02374021 (5) [back to overview]Change From Baseline in the Average TBR of the Bilateral Carotids
NCT02374021 (5) [back to overview]Change From Baseline in the Average TBR of the Aorta
NCT02374021 (5) [back to overview]Change From Baseline in the Average TBR of the Index Vessel
NCT02374021 (5) [back to overview]Change From Baseline in the MDS of the Aorta
NCT02374021 (5) [back to overview]Change From Baseline in Vascular Inflammation as Measured by FDG-PET/CT at 6 Months
NCT02930343 (4) [back to overview]Indian Health Assessment Questionnaire (iHAQ)
NCT02930343 (4) [back to overview]Number of Patients Achieving Good EULAR Response at the End of 12 Weeks
NCT02930343 (4) [back to overview]Number of Participants With Adverse Drug Reactions
NCT02930343 (4) [back to overview]Disease Activity as Per Ultrasound-7 (US-7) Score
NCT03449758 (30) [back to overview]Change From Baseline in Multidimensional Assessment of Thymic States Scale Total Score at Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Change From Baseline in Number of Swelling Joints at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Number of Tender Joints at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Patient Global Assessment of Disease Activity Score by Visual Analog Scale at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Rheumatoid Arthritis Impact of Disease Total Score at Weeks 4 and 12
NCT03449758 (30) [back to overview]Change From Baseline in Disease Activity Score-28 for Rheumatoid Arthritis With Erythrocyte Sedimentation Rate at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Rheumatoid Arthritis Impact of Disease Total Score at Week 24
NCT03449758 (30) [back to overview]Change From Baseline in Clinical Disease Activity Index Total Score at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Duration of Morning Stiffness at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Stanford Health Assessment Questionnaire Disability Index (HAQ-DI) Total Score at Baseline, Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Rheumatoid Arthritis Impact of Disease Total Score at Baseline, Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Erythrocyte Sedimentation Rate (ESR) at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Number of Tender Joints at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Number of Swollen Joints at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)
NCT03449758 (30) [back to overview]Number of Participants Achieving Low Disease Activity (DAS28 ESR Score <=3.2) and Remission (DAS28 ESR Score <2.6) at Weeks 12, and 24
NCT03449758 (30) [back to overview]Number of Participants Achieving Clinical Disease Activity Index: Low Disease Activity (CDAI Score <=10.0) and Remission (CDAI Score <=2.8) Weeks 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Erythrocyte Sedimentation Rate at Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Hospital Anxiety and Depression Scale: Anxiety (HADS-A) and Depression (HADS-D) Subscale Scores at Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Change From Baseline in International Physical Activity Questionnaire Total Score at Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Change From Baseline in Functional Assessment of Chronic Illness Therapy - Fatigue Total Scores at Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Multidimensional Assessment of Thymic States (MAThyS) Scale Total Score at Baseline, Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]International Physical Activity Questionnaire (IPAQ) Total Score at Baseline, Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Hospital Anxiety and Depression Scale (HADS): Anxiety (HADS-A) and Depression (HADS-D) Subscale Scores at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-F) Total Scores at Baseline, Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Duration of Morning Stiffness at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Disease Activity Score-28 for Rheumatoid Arthritis With Erythrocyte Sedimentation Rate (DAS28-ESR) at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Clinical Disease Activity Index (CDAI) Total Score at Baseline, Weeks 4, 12, and 24
NCT03449758 (30) [back to overview]Change From Baseline in Stanford Health Assessment Questionnaire Disability Index Total Score at Weeks 4, 12 and 24
NCT03449758 (30) [back to overview]Patient Global Assessment (PtGA) of Disease Activity Score by Visual Analog Scale (VAS) at Baseline, Weeks 4, 12 and 24
NCT03797872 (1) [back to overview]Number of Participants Who Are Eligible, Consent, and Complete the 48 Weeks Study

Number of Patients Achieving Assessment in Ankylosing Spondylitis (ASAS 20)

ASAS measures symptomatic improvement in Ankylosing Spondylitis (AS) participants ASAS = 4 domains: participant global assessment of disease activity, pain, function, inflammation. ASAS 20 = 20% improvement from baseline and an improvement ≥ 10 units on a 0-100 scale (0=no disease activity; 100=high disease activity) for ≥ 3 domains, and no worsening in remaining domain. (NCT00247962)
Timeframe: 16 weeks

Interventionparticipants (Number)
Etanercept287
Sulphasalazine99

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Ankylosing Spondylitis Quality of Life (ASQoL) Total Score Change From Baseline

"ASQoL is a questionnaire to assess disease specific quality of life. It consists of 18 statements that are relevant to the physical and mental conditions for a patient with Ankylosing Spondylitis (AS). Each statement is answered by the patients as a Yes (scored as 1) or No (scored as 0). All item scores are summed to give a total score. Scores can range from 0 (good QoL) to 18 (poor QoL)." (NCT00247962)
Timeframe: Baseline and 16 Weeks

,
Interventionunits on a scale (Mean)
BaselineWeek 16
Etanercept11.036.21
Sulphasalazine11.329.06

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Disease Activity Score Erythrocyte Sedimentation Rate(DAS28-ESR)

"Outcome measured was the observed-group analysis of the DAS28-ESR between weeks 48 and 102. DAS28 is a calculated scale using a formula that includes the number of tender joints and swollen joints (28 joints maximum). The following is the calculation: DAS28 = 0.56 * sqrt(tender28) + 0.28 * sqrt(swollen28) + 0.70 * ln(ESR) + 0.014 * GH. The ESR is the rate at which red blood cells sediment in a period of one hour.~The total range for the DAS28ESR goes from 0.0 to 9.2; this indicates the current activity of the rheumatoid arthritis of a subject. A DAS28 above 5.1 means high disease activity whereas a DAS28 below 3.2 indicates low disease activity." (NCT00259610)
Timeframe: Change of the Mean of DAS28-ESR between weeks 48 - 102.

InterventionScores on a scale (Mean)
MTX + Immediate Etanercept3.0
MTX+ Immediate SSZ +HCQ2.9
MTX + Step-up Etanercept3.1
MTX + Step-up SSZ + HCQ(ST)2.8

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Radiographic Disease Progression Between Baseline and Week 102 as Assessed by Van Der Heijde Modified Sharp Scores.

Changes in disease progression between treatment groups will be described by the mean score at two years as assessed after adjustment for the baseline radiographic score. Radiographs were observed of hands, wrists, and feet. The range of scores available for the modified Sharp Score is 0 to 448. The erosion score per joint of the hands can range from 0 to 5. The maximal erosion score for each hand is thus 80, considering the 16 areas for erosions per hand. Joint space narrowing and joint subluxation or luxation are combined in a single score with a range of 0 to 4 with a max score of 60. The erosion score per joint can range from 0 to 10, with each side of the joint independently scored from 0 to 5. The maximal erosion score per foot is thus 60. The joint space narrowing and joint (sub)luxation are combined in a single score with a range of 0 to 4. The maximal narrowing/(sub)luxation score per foot is thus 24. (NCT00259610)
Timeframe: Year 2, Week 102

InterventionScores on a scale (Mean)
MTX + Immediate Etanercept7.0
MTX+ Immediate SSZ +HCQ7.3
MTX + Step-up Etanercept4.8
MTX + Step-up SSZ + HCQ(ST)6.2

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Mean 48-week Change in DAS28

"Average difference between 48-week and Baseline DAS28.~The Disease Activity Score for 28 Joints (DAS28) is a well-validated composite outcome measure ranging from 2-10 (higher scores indicating more disease) that incorporates a tender and swollen joint count of 28 joints, a laboratory measure of systemic inflammation (ESR) and a patient-reported general assessment of health on a visual analog scale (ranging from 0-10cm) all into one measure.~Low disease activity is defined as DAS28 ≤ 3.2 units." (NCT00405275)
Timeframe: 48 weeks after baseline assessment

Interventionunits on a scale (Mean)
Triple-2.12
Etanercept-2.29

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Percentage of Participants Achieving ACR 20, 50, and 70 Responses

Response includes improvement in tender or swollen joints as well as 20 percent improvement in three of the other five criteria. Required: ≥ 20%, 50% or 70% improvement in tender joint count ≥ 20% , 50% or 70% improvement in swollen joint count and at least 20%, 50%, 70% improvement in 3 of the following 5:Patient pain assessment , Patient global assessment ,Physician global assessment, Patient self-assessed disability. (NCT00422227)
Timeframe: Week 16

,
InterventionPercentage of Participants (Number)
ACR 20ACR 50ACR 70
DMARD/MTX58.1634.697.14
ETN/MTX78.8756.7019.07

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Percent Change From Baseline in Painful and Swollen Joint Counts

Participant's assessment of pain - A horizontal pain visual analog scale (VAS) (0-100 mm) is used to assess the participants current level of pain; 0 = no pain and 100 = worst pain. Swollen joint count - ACR swollen joint count, an assessment of 28 joints. Joints are classified as either swollen or not swollen. (NCT00422227)
Timeframe: Week 2, 4, 8, 12, 16

,
InterventionPercent change (Number)
Painful Joints - Week 2Painful Joints - Week 4Painful Joints - Week 8Painful Joints - Week 12Painful Joints - Week 16Swollen Joints - Week 2Swollen Joints - Week 4Swollen Joints - Week 8Swollen Joints - Week 12Swollen Joints - Week 16
DMARD/MTX27.6836.7149.7155.5557.3121.3227.7244.1950.4856.32
ETN/MTX34.1746.1155.4865.6568.9938.5949.3359.9167.9773.83

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Percent Change From Baseline in General Health, Pain, and Fatigue, Visual Analog Scales

"VAS, participant indicates by marking a vertical line at an appropriate position through a horizontal line. The length of the line measures from left (in mm) and the value (in mm) is recorded. General Health VAS, in general how would you rate your heath over the last 2-3 weeks, 0mm equals very well and 100mm equals extremely bad. Pain VAS: indicate the amount of pain experienced during the last 2-3 days, 0 mm equals no pain and 100 mm equals pain as bad as it can be. Fatigue VAS: how fatigued or tired have you been over the last week, range =No Fatigue - Extremely Fatigued." (NCT00422227)
Timeframe: Week 2, 4, 8, 12, 16

,
InterventionPercent change (Number)
General Health - Week 2General Health - Week 4General Health - Week 8General Health - Week 12General Health - Week 16Pain - Week 2Pain - Week 4Pain - Week 8Pain - Week 12Pain - Week 16Fatigue - Week 2Fatigue - Week 4Fatigue - Week 8Fatigue - Week 12Fatigue - Week 16
DMARD/MTX8.8822.7827.8630.2633.899.9922.9829.1433.9736.456.6319.0021.8228.6530.04
ETN/MTX21.1430.6138.5742.1050.4927.5934.7342.9748.4654.4220.9030.8735.9239.6546.92

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Percent Change From Baseline in Duration (Minutes) of Morning Stiffness

The duration of morning stiffness on the day of examination should be determined by asking the following two questions: When did you awaken this morning? When were you able to resume your normal activities without stiffness? Duration of morning stiffness is equal to the time elapsed between the above two times in minutes; If none is present enter 0, If morning stiffness is still continuing, please indicate average of duration of stiffness over the past 3 days. If stiffness persists the entire day 1440 minutes (24h x 60 minutes) should be recorded. (NCT00422227)
Timeframe: Week 2, 4, 8, 12, 16

,
InterventionPercent change (Number)
Week 2Week 4Week 8Week 12Week 16
DMARD/MTX16.4333.2237.3552.7646.77
ETN/MTX54.9263.8573.4179.7680.55

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Percentage of Participants Achieving European League Against Rheumatism (EULAR) Moderate or Good Response

EULAR Response Criteria DAS28) improvement at week 16. Good response was defined as >1.2 improvement in DAS from Baseline and DAS attained during follow-up of ≤2.4. Non-responders were participants with improvement of ≤0.6 or participants with improvement of >0.6 but ≤1.2 and DAS attained during follow-up of >3.7. Remaining participants were classified as moderate. Scores of good and moderate were considered to have therapeutic response. (NCT00422227)
Timeframe: Week 16

InterventionPercentage of Participants (Number)
ETN/MTX87.82
DMARD/MTX73.79

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Percent Change From Baseline in DAS28 at Week 16

Disease Activity Score 28 based on 28 Joints (DAS28) is the calculation of DAS28: DAS28 = 0.56 sqrt (28 painful joint count) + 0.28 sqrt (28 swollen joint count) + 0.70 (ln erythrocyte sedimentation rate (ESR)) + 0.014 (General Health) (GH). GH = Subject general health visual analog scale (0-10 mm). (NCT00422227)
Timeframe: Week 16

InterventionPercent change (Number)
ETN/MTX38.32
DMARD/MTX27.46

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Change From Baseline in Adjusted Mean of American College of Rheumatology Response (ACR-N) Area Under Curve (AUC) Over 16 Weeks

"ACR-N = the lowest of 3 values (percent change in the number of swollen joints, percent change in the number of tender joints, and median of the other 5 measures in the ACR core data set). Negative numbers indicate worsening.~The ACR-N AUC was calculated using the trapezoidal rule as the ACR-N multiplied by the duration of the assessment period (in weeks) and was presented as %-weeks." (NCT00422227)
Timeframe: 16 weeks

InterventionUnits on a scale (Mean)
ETN/MTX434.83
DMARD/MTX289.54

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Percent Change From Baseline in Physician And Subject Global Assessments

The Physician Global Assessment of Disease Activity: The participant's disease activity is estimated over the last two - three days by the physician; A zero (0) means no disease activity and a ten (10) means extreme disease activity. The Subject Global Assessment of Disease Activity: The participant assesses overall arthritis activity. A zero (0) means no disease activity and a ten (10) means extreme disease activity. (NCT00422227)
Timeframe: Week 2, 4, 8, 12, 16

,
InterventionPercent change (Number)
Physician Global Assessment - Week 2Physician Global Assessment - Week 4Physician Global Assessment - Week 8Physician Global Assessment - Week 12Physician Global Assessment - Week 16Subject Global Assessment - Week 2Subject Global Assessment - Week 4Subject Global Assessment - Week 8Subject Global Assessment - Week 12Subject Global Assessment - Week 16
DMARD/MTX11.8322.8135.4138.6745.047.2419.2226.0830.1030.55
ETN/MTX30.4039.5845.8655.0062.0521.8428.9434.9243.1850.76

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Percentage of Participants With DAS28 Improvement of ≥0.6 and ≥1.2

Disease Activity Score 28 based on 28 Joints (DAS28) is the calculation of DAS28: DAS28 = 0.56 sqrt (28 painful joint count) + 0.28 sqrt (28 swollen joint count) + 0.70 (ln erythrocyte sedimentation rate (ESR) + 0.014 (General Health) (GH). GH = Subject general health visual analog scale (0-10 mm). (NCT00422227)
Timeframe: Week 16

,
InterventionPercentage of Participants (Number)
≥0.6≥1.2
DMARD/MTX78.6466.02
ETN/MTX91.3782.74

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Percentage of Participants Achieving DAS28 <3.2 (Low Disease Activity) and <2.6 (Remission)

Disease Activity Score 28 based on 28 Joints (DAS28) is the calculation of DAS28: DAS28 = 0.56 sqrt (28 painful joint count) + 0.28 sqrt (28 swollen joint count) + 0.70 (ln erythrocyte sedimentation rate (ESR)) + 0.014 (General Health) (GH). GH = Subject general health visual analog scale (0-10 mm). (NCT00422227)
Timeframe: Week 16

,
InterventionPercentage of Participants (Number)
Low Disease (DAS28 <3.2)Remission (DAS28 <2.6)
DMARD/MTX18.457.77
ETN/MTX39.0915.74

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Measuring the Safety and Efficacy of a New DMARD, Leflunomide Alone or in Combination With Traditional DMARD's. Participants Reaching ACR 20 Response. at 48 Weeks

"The combination of Methotrexate-Sulfasalazine-Hydroxychloroquine has been shown to be more effective than Methotrexate alone or the double combination of Methotrexate-Hydroxychloroquine. Primary outcome is ACR 20 response at 48 weeks.~An ACR 20 Response is a measure of at least 20% improvement in the number of tender and swollen joints. and a 20% improvement in at least 3 of the following:~the patient's global assessment of disease status; the patient's assessment of pain; the patient's assessment of function; the physician's global assessment of disease status; serum C-reactive protein levels." (NCT00579878)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
1 Leflunomide Alone vs Combination Therapy8
Methotrexate-Sulfasalazine-Hydroxychloroquine20
Leflunomide-Sulfasalazine-Hydroxychloroquine12

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Sulfasalazine Steady State Maximum Plasma Concentration (Cmax) and Predose Concentration (Cmin)

(NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmicrograms (mcg)/milliliter (mL) (Number)
Cmax - Value 1Cmax - Value 2Cmin - Value 1Cmin - Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis17.64.514.280.988

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Sulfasalazine Area Under the Concentration-time Profile From Time 0 to Time Tau, the Dosing Interval (AUCtau) at Steady State

(NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmcg*hr/mL (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis11034.7

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Sulfapyridine Tmax at Steady State

Sulfapyridine and 5-ASA are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionhr (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis4.0011.9

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Number of Participants With Treatment-emergent Adverse Events (TEAEs), Serious Adverse Events (SAEs), and Withdrawals Due to TEAEs

An adverse event (AE) was any untoward medical occurrence attributed to study drug in a participant who received study drug. TEAEs are defined as newly occurring AEs or those worsening after first dose. AEs comprised both SAEs and non-SAEs. An SAE was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly. (NCT00637780)
Timeframe: Screening through to and including 28 calendar days after the last administration of the investigational product

Interventionparticipants (Number)
TEAEsSAEsWithdrawals due to TEAEs
Sulfasalazine in Juvenile Idiopathic Arthritis000

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5-aminosalicylic Acid (5-ASA) AUCtau at Steady State

Sulfapyridine and 5-ASA are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmcg*hr/mL (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis1.631.04

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Sulfapyridine AUCtau at Steady State

Sulfapyridine and 5-ASA are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmcg*hr/mL (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis23267.3

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5-aminosalicylic Acid (5-ASA) Tmax at Steady State

Sulfapyridine and 5-ASA are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionhr (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis0.00011.9

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5-aminosalicylic Acid (5-ASA) Steady State Cmax and Cmin

Sulfapyridine and 5-ASA are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmcg/mL (Number)
Cmax - Value 1Cmax - Value 2Cmin - Value 1Cmin - Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis0.2080.09820.04390.0816

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Number of Participants With Vital Signs Values Meeting Categorical Summarization Criteria

Vital sign values which met categorical summarization criteria included: supine/sitting pulse rate less than (<) 40 or more than (>) 120 beats per minute (bpm); erect pulse rate <40 or >140 bpm; changes from baseline in same posture of systolic blood pressure (SBP) more than or equal to (>=) 30 millimeters of mercury (mm Hg) or diastolic blood pressure (DBP) >=20 mm Hg; SBP <90 mm Hg; and DBP <50 mm Hg. (NCT00637780)
Timeframe: Screening, Day 0, and Day 7

Interventionparticipants (Number)
Sulfasalazine in Juvenile Idiopathic Arthritis0

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Number of Participants With Laboratory Test Abnormalities

Number of participants with laboratory test abnormalities without regard to baseline abnormality. Laboratory test parameters included hematology, coagulation, liver function, renal function, electrolytes,clinical chemistry, and urinalysis (dipstick and microscopy). (NCT00637780)
Timeframe: Screening, Day 0, and Day 7

Interventionparticipants (Number)
Sulfasalazine in Juvenile Idiopathic Arthritis1

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Sulfapyridine Steady State Cmax and Cmin

Sulfapyridine and 5-aminosalicylic acid (5-ASA) are primary metabolites of sulfasalazine, the study drug. (NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionmcg/mL (Number)
Cmax - Value 1Cmax - Value 2Cmin - Value 1Cmin - Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis21.77.6814.74.79

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Sulfasalazine Time for Cmax (Tmax) at Steady State

(NCT00637780)
Timeframe: Day 7 predose, and 2, 4, 6, 10, and 12 hours postdose

Interventionhours (hr) (Number)
Value 1Value 2
Sulfasalazine in Juvenile Idiopathic Arthritis2.025.92

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Remission According to DAS28-CRP at Week 16

"Number of patients in remission according to DAS28-CRP (Disease Activity Score based on 28 joint count and C-reactive Protein) at week 16.~DAS28-CRP is calculated with the following formula : 0.56*SQRT TJC28+0.28*SQRT SJC28+0.36*ln (CRP+1)+0.014*GH+0.96 in which TJC is the tender joint count, SJC the Swollen Joint Count and GH the general health estimated by the patient on a Visual Analogue Scale (VAS).~A value below 2.6 is indicating remission, below or equal to 3.2 low disease activity, between 3.2 and 5.1 moderate disease activity and above 5.1 high disease activity." (NCT01172639)
Timeframe: week 16

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group69
CoBRA Slim High Risk Group72
CoBRA Avant-garde High Risk Group61
CoBRA Slim Low Risk Group25
Tight Step Up Low Risk Group23

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Remission According to SDAI at Week 104

"Number of patients in remission according to SDAI (Simplified Disease Activity Index) at week 104.~SDAI is calculated with the following formula : TJC28+SJC28+GH+GA ph in which TJC is the number of tender joints, SJC the number of Swollen Joint and GH the general health assessed by the patient on a Visual Analogue Scale (VAS) and GA ph the general assessment of the physician on a VAS.~A value below 3.3 is indicating remission, between 3.4 and 11.0 low disease activity, between 11.1 and 26.0 moderate disease activity and above 26.0 high disease activity." (NCT01172639)
Timeframe: week 104

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group31
CoBRA Slim High Risk Group28
CoBRA Avant-garde High Risk Group41
CoBRA Slim Low Risk Group20
Tight Step Up Low Risk Group13

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Remission According to SDAI at Week 52

"Number of patients in remission according to SDAI (Simplified Disease Activity Index) at week 52.~SDAI is calculated with the following formula : TJC28+SJC28+GH+GA ph in which TJC is the number of tender joints, SJC the number of Swollen Joint and GH the general health assessed by the patient on a Visual Analogue Scale (VAS) and GA ph the general assessment of the physician on a VAS.~A value below 3.3 is indicating remission, between 3.4 and 11.0 low disease activity, between 11.1 and 26.0 moderate disease activity and above 26.0 high disease activity." (NCT01172639)
Timeframe: week 52

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group36
CoBRA Slim High Risk Group27
CoBRA Avant-garde High Risk Group39
CoBRA Slim Low Risk Group20
Tight Step Up Low Risk Group15

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Clinically Significant Change in HAQ Score

"Number of patients with a change of > 0.22 in the Health Assessment Questionnaire (HAQ) score over the period between baseline and week 104.~A change of > 0.22 in this score is considered as clinical relevant for rheumatoid arthritis patients." (NCT01172639)
Timeframe: Baseline-week104

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group71
CoBRA Slim High Risk Group62
CoBRA Avant-garde High Risk Group64
CoBRA Slim Low Risk Group25
Tight Step Up Low Risk Group26

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Remission According to DAS28-CRP at Week 104

"Number of patients in remission according to DAS28-CRP (Disease Activity Score based on 28 joint count and C-reactive Protein) at week 104. (co-primary endpoints)~DAS28-CRP is calculated with the following formula : 0.56*SQRT TJC28+0.28*SQRT SJC28+0.36*ln (CRP+1)+0.014*GH+0.96 in which TJC is the tender joint count, SJC the Swollen Joint Count and GH the general health estimated by the patient on a Visual Analogue Scale (VAS).~A value below 2.6 is indicating remission, below or equal to 3.2 low disease activity, between 3.2 and 5.1 moderate disease activity and above 5.1 high disease activity." (NCT01172639)
Timeframe: week 104

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group64
CoBRA Slim High Risk Group71
CoBRA Avant-garde High Risk Group69
CoBRA Slim Low Risk Group29
Tight Step Up Low Risk Group34

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Remission According to DAS28-CRP at Week 52

"Number of patients in remission according to DAS28-CRP (Disease Activity Score based on 28 joint count and C-reactive Protein) at week 52. (co-primary end point)~DAS28-CRP is calculated with the following formula : 0.56*SQRT TJC28+0.28*SQRT SJC28+0.36*ln (CRP+1)+0.014*GH+0.96 in which TJC is the tender joint count, SJC the Swollen Joint Count and GH the general health estimated by the patient on a Visual Analogue Scale (VAS).~A value below 2.6 is indicating remission, below or equal to 3.2 low disease activity, between 3.2 and 5.1 moderate disease activity and above 5.1 high disease activity." (NCT01172639)
Timeframe: week 52

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group63
CoBRA Slim High Risk Group57
CoBRA Avant-garde High Risk Group57
CoBRA Slim Low Risk Group29
Tight Step Up Low Risk Group29

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Remission According to SDAI (Simple Disease Activity Index) at Week 16

"Number of patients in remission according to SDAI (Simplified Disease Activity Index) at week 16.~SDAI is calculated with the following formula : TJC28+SJC28+GH+GA ph in which TJC is the number of tender joints, SJC the number of Swollen Joint and GH the general health assessed by the patient on a Visual Analogue Scale (VAS) and GA ph the general assessment of the physician on a VAS.~A value below 3.3 is indicating remission, between 3.4 and 11.0 low disease activity, between 11.1 and 26.0 moderate disease activity and above 26.0 high disease activity." (NCT01172639)
Timeframe: week 16

InterventionParticipants (Count of Participants)
CoBRA Classic High Risk Group42
CoBRA Slim High Risk Group33
CoBRA Avant-garde High Risk Group44
CoBRA Slim Low Risk Group12
Tight Step Up Low Risk Group12

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Percentage of Patients in Each Arm That Experience Clinically Significant Deficits in Overall Quality of Life and Fatigue

For each arm, the percentage of patients experience clinically significant deficits in overall QOL and fatigue as indicated by a score of 5 or lower on the 0-10 scale. The analysis was done using the questionnaire that was completed during the first week of radiotherapy (RT) and 6 weeks after RT. (NCT01198145)
Timeframe: Up to 6 weeks post radiotherapy

,
Interventionpercentage of participants (Number)
During RTAfter RT
Arm I: Sulfasalazine17.926.9
Arm II: Placebo7.527.6

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Percentage of Patients in Each Arm That Experience Tenesmus, Abdominal Pain, Constipation, Diarrhea and Rectal Bleeding During and After RT

The number of patients that reported any grade 1 or higher adverse event was divided by the total number of patients evaluated. The analysis was done separately for each of the 5 outcomes and separately during RT and after RT. (NCT01198145)
Timeframe: During radiation therapy and up to 6 weeks post radiation therapy

,
Interventionpercentage of participants (Number)
Tenesmus during RTTenesmus after RTAbdominal pain during RTAbdominal pain after RTConstipation during RTConstipation after RTDiarrhea during RTDiarrhea after RTRectal bleeding during RTRectal bleeding after RT
Arm I: Sulfasalazine35.711.947.619.138.114.376.233.338.111.9
Arm II: Placebo28.619.138.111.935.716.773.835.747.64.8

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"Percent of Patients in Each Arm That Recorded Yes to Each of Questions 2-10 on the Bowel Function Questionnaire"

"Questions that were used in this analysis:~2. Have you had a problem causing you to get up at night to have a bowel movement? 3. Have you had a problem causing you to lose control of your bowel movements? 4. Have you had a problem causing you to have a bowel movement within 30 minutes of a prior bowel movement? 5. Have you had to wear protective clothing or a pad in case you lost control of a bowel movement? 6. Have you had a problem causing you to be unable to tell the difference between stool and gas? 7. Have you had a problem causing you to have stools that are liquid? 1=yes 2=no q08 8. Have you found that once you feel the urge to have a bowel movement, you must do so within 15 minutes to avoid an accident? 9. Have you had cramping with a bowel movement? 10. Have you had blood in your bowel movement?" (NCT01198145)
Timeframe: Up to 6 weeks post radiation therapy

,
Interventionpercentage of participants (Number)
During RT : Q2During RT : Q3During RT : Q4During RT : Q5During RT : Q6During RT : Q7During RT : Q8During RT : Q9During RT : Q10After RT : Q2After RT : Q3After RT : Q4After RT : Q5After RT : Q6After RT : Q7After RT : Q8After RT : Q9After RT : Q10
Arm I: Sulfasalazine191133726114447392455183737703450
Arm II: Placebo1010330232043177272256124637613429

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Area Under the Curve That Combines the Individual Severity of Diarrhea Toxicity as Measured by the CTCAE v4.0 During and After RT

For each patient, an Area Under the Curve (AUC) summary statistic will be calculated taking into account the individual severity of diarrhea toxicity over time. Severity of diarrhea was graded using the terminology and grading categories defined in the NCI's Common Toxicity Criteria (CTCAE), Version 4.0. Grade 0 = None; 1=Mild; Grade 2=Moderate, Grade 3=Severe, Grade 4=Life-threatening. The curve was constructed using weekly assessments during and after RT. A separate analysis was done during the course of RT and every week for 6 weeks following RT. (NCT01198145)
Timeframe: During radiation therapy and up to 6 weeks post radiation therapy

,
Interventiongrade*week (Mean)
During RTAfter RT
Arm I: Sulfasalazine4.01.2
Arm II: Placebo3.31.3

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Average Graded Severity for Tenesmus, Abdominal Pain, Constipation, Diarrhea and Hemorrhage During and After RT as Graded by CTCAE v4.0

Tenesmus, Abdominal pain, constipation, diarrhea and hemorrhaging were assessed during RT and up to 6 weeks after RT. Severity of these events were graded using the terminology and grading categories defined in the NCI's Common Toxicity Criteria (CTCAE), Version 4.0. Grade 0 = None; 1=Mild; Grade 2=Moderate, Grade 3=Severe, Grade 4=Life-threatening. For each patient, an average score for each outcome variable during and after RT calculated as follows: The sum of all severity scores for that variable divided by the number of severity scores for that variable recorded for the patient during the course of RT and for 6 weeks following RT. (NCT01198145)
Timeframe: During radiation therapy and up to 6 weeks post radiation therapy

,
InterventionAverage Grade of Event (Mean)
Tenesmus during RTTenesmus after RTAbdominal pain during RTAbdominal pain after RTConstipation during RTConstipation after RTDiarrhea during RTDiarrhea after RTRectal bleeding during RTRectal bleeding after RT
Arm I: Sulfasalazine0.20.10.30.20.20.10.80.30.20.1
Arm II: Placebo0.10.10.20.20.20.10.60.30.20.1

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Maximum Severity of Each Outcome Variable (Rectal Bleeding, Abdominal Cramping, Tenesmus, Constipation, and Diarrhea) Measured During and After RT

"The maximal severity of each of 5 different adverse even types (Tenesmus, Abdominal Pain, Constipation, Diarrhea, and Rectal Bleeding) were collected as a secondary endpoint. Severity of the events was graded using the terminology and grading categories defined in the NCI's Common Toxicity Criteria (CTCAE), Version 4.0. Grade 0 = None; 1=Mild; Grade 2=Moderate, Grade 3=Severe, Grade 4=Life-threatening. Adverse events were assessed during the course of RT and for 6 weeks following RT. The table below represents the worst grade for each patient for each type.~Two-sided chi-square tests will be used to compare each percentage variable between treatment arms for each event type." (NCT01198145)
Timeframe: During radiation therapy and up to 6 weeks post radiation therapy

InterventionParticipants (Count of Participants)
Tenesmus during RT72333267Tenesmus during RT72333269Tenesmus after RT72333267Tenesmus after RT72333269Abdominal pain during RT72333267Abdominal pain during RT72333269Abdominal pain after RT72333269Abdominal pain after RT72333267Constipation during RT72333267Constipation during RT72333269Constipation after RT72333269Constipation after RT72333267Diarrhea during RT72333267Diarrhea during RT72333269Diarrhea after RT72333269Diarrhea after RT72333267Rectal bleeding during RT72333267Rectal bleeding during RT72333269Rectal bleeding after RT72333267Rectal bleeding after RT72333269
Grade 0Grade 1Grade 4Grade 2Grade 3
Arm I: Sulfasalazine27
Arm II: Placebo30
Arm II: Placebo9
Arm I: Sulfasalazine7
Arm I: Sulfasalazine18
Arm II: Placebo21
Arm I: Sulfasalazine5
Arm II: Placebo7
Arm II: Placebo1
Arm I: Sulfasalazine0
Arm I: Sulfasalazine22
Arm II: Placebo26
Arm I: Sulfasalazine14
Arm II: Placebo12
Arm II: Placebo4
Arm I: Sulfasalazine3
Arm II: Placebo0
Arm I: Sulfasalazine17
Arm II: Placebo24
Arm I: Sulfasalazine8
Arm II: Placebo2
Arm II: Placebo3
Arm I: Sulfasalazine12
Arm I: Sulfasalazine4
Arm I: Sulfasalazine19
Arm II: Placebo22
Arm I: Sulfasalazine6
Arm II: Placebo6
Arm I: Sulfasalazine10
Arm II: Placebo11
Arm I: Sulfasalazine13
Arm II: Placebo14
Arm I: Sulfasalazine9
Arm II: Placebo13
Arm I: Sulfasalazine1
Arm I: Sulfasalazine11
Arm II: Placebo10
Arm I: Sulfasalazine2
Arm I: Sulfasalazine26
Arm I: Sulfasalazine16
Arm II: Placebo20
Arm I: Sulfasalazine20
Arm II: Placebo27

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Maximum Severity of Diarrhea Toxicity as Measured by the CTCAE v4.0 During and After Radiotherapy (RT)

"The primary endpoint for this study is the maximal severity of diarrhea toxicity. Severity of diarrhea was graded using the terminology and grading categories defined in the NCI's Common Toxicity Criteria (CTCAE), Version 4.0. Grade 0 = None; 1=Mild; Grade 2=Moderate, Grade 3=Severe, Grade 4=Life-threatening as measured by the CTCAE version 4.0. Assessments were recorded during the course of RT and for 6 weeks following RT. The table below represents the worst graded diarrhea for each patient.~A two-sided Wilcoxon rank-sum test will be used to test the equality of the distributions of maximum diarrhea severity grades between the two treatment arms." (NCT01198145)
Timeframe: During radiation therapy and up to 6 weeks post radiation therapy

,
InterventionParticipants (Count of Participants)
Grade 0Grade 1Grade 2Grade 3Grade 4
Arm I: Sulfasalazine10138101
Arm II: Placebo10151340

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Percentage of Patients in Each Arm That Require Any Type of Antidiarrheal Medications.

The number of patients reporting the use of anti-diarrheal medications divided by the number of patients evaluated for this endpoint. (NCT01198145)
Timeframe: Up to 24 months post radiotherapy

Interventionpercentage of participants (Number)
Arm I: Sulfasalazine48.7
Arm II: Placebo28.6

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% BOLD Response Increase Above Baseline

Test whether Sulfasalazine, as compared to placebo, diminishes blood-oxygen-level dependent (BOLD) response to alcohol cues in the striatum and prefrontal cortex (PFC). BOLD response refers to brain activation in response to the presence of oxygen in a particular part of the brain. To test the hypothesis, we will compare Sulfasalazine treatment with placebo treatment. During the fMRI scan session, participants will be presented with the alcohol cue task. We will compare the difference in BOLD response during the presence of alcohol vs. a novel substance during the alcohol cue task. Outcome data collected during the alcohol cue task will provide us with BOLD response data for each intervention period. We will analyze the outcome data using FSL (Oxford Centre for Functional MRI of the Brain (FMRIB) Software - a collection of functional and structural brain image analysis tools). (NCT01312129)
Timeframe: Over two weeks

,
Intervention% BOLD Response increase above baseline (Mean)
Control CueAlcohol Cue
Placebo.106.074
Sulfasalazine.082.097

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Percent Decrease in Central Nervous System Bioavailability of Sulfasalazine

To determine the ability of sulfasalazine to alter glioma glutamate levels. These levels will be measured by Magnetic Resonance Spectroscopy (MRS). The percent change is noted per subject. The measure is a % decrease of glioma glutamate levels (NCT01577966)
Timeframe: up to 2 years post baseline

Interventionpercentage of change (Number)
GBM Pt 2GBM Pt 1GBM Pt 4Astro Pt 3Astro Pt 9Astro Pt 5Oligo Pt 8Oligo Pt 6Oligo Pt 7
Sulfasalazine17232855558121842

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Categorical Rating of Pain Intensity (Using the Crossover Comparison Structure of the Study)

Assessed using number of days rated as none, mild, moderate, or severe in pain diary (NCT01667029)
Timeframe: Assessed at end of two week treatment period

,
Interventiondays (Mean)
"None rating""Mild rating""Moderate rating""Severe rating"
Placebo1.171.833.830.17
Sulfasalazine02.004.330.67

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Pain Score (First Treatment Period)

Average pain score will be the average of daily pain scores (0-10) recorded by the subject in a pain diary during the second week of the two week treatment period. Higher scores are worse (0=no pain, 10=pain as bad as you can imagine). (NCT01667029)
Timeframe: second week of two week treatment period

Interventionunits on a scale (Mean)
Sulfasalazine5.60
Placebo4.20

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Categorical Rating of Pain Intensity (First Treatment Period Only)

Assessed using number of days rated as none, mild, moderate, or severe in pain diary (NCT01667029)
Timeframe: Assessed at end of two week treatment period

,
Interventiondays (Mean)
"None rating""Mild rating""Moderate rating""Severe rating"
Placebo01.755.250
Sulfasalazine01.674.331.00

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Pain Score (Using the Crossover Comparison Structure of the Study)

Average pain score will be the average of daily pain scores (0-10) recorded by the subject in a pain diary during the second week of the two week treatment period. Higher scores are worse (0=no pain, 10=pain as bad as you can imagine). (NCT01667029)
Timeframe: Assessed at end of two week treatment period

Interventionunits on a scale (Mean)
Sulfasalazine4.91
Placebo3.93

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Physical Functioning Score Assessed Using the Euroquality of Life (EQ-5D) Metrics (First Treatment Period Only)

The EQ-5D physical functioning items are mobility self-care, and usual activities. These three items are rated from 1 (no problems) to 5 (unable). (NCT01667029)
Timeframe: Assessed at end of two week treatment period

InterventionParticipants (Count of Participants)
EQ-5D mobility72173110EQ-5D mobility72173111EQ-5D self-care72173110EQ-5D self-care72173111EQ-5D usual activities72173110EQ-5D usual activities72173111
12345
Sulfasalazine3
Placebo4
Sulfasalazine1
Sulfasalazine0
Placebo0
Sulfasalazine2
Placebo1
Placebo2

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Physical Functioning Score Assessed Using the Euroquality of Life (EQ-5D) (Using the Crossover Comparison Structure of the Study)

The EQ-5D physical functioning items are mobility self-care, and usual activities. These three items are rated from 1 (no problems) to 5 (unable). (NCT01667029)
Timeframe: Assessed at end of two week treatment period

InterventionParticipants (Count of Participants)
EQ-5D mobility72173110EQ-5D mobility72173111EQ-5D self-care72173111EQ-5D self-care72173110EQ-5D usual activities72173110EQ-5D usual activities72173111
41235
Sulfasalazine4
Sulfasalazine1
Placebo1
Sulfasalazine5
Placebo7
Sulfasalazine2
Placebo0
Sulfasalazine0
Placebo2
Placebo3

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Physical Functioning Score Assessed Using the Brief Pain Inventory (BPI) Interference Scale (Using the Crossover Comparison Structure of the Study)

The BPI interference items are general activity, mood, walking ability, normal work (including housework), relations with other people, sleep, and enjoyment of life. The seven items are rated from 0 (pain does not interfere) to 10 (pain completely interferes). (NCT01667029)
Timeframe: Assessed at end of two week treatment period

,
Interventionunits on a scale (Mean)
General activityMoodWalking abilityNormal workRelations with other peopleSleepEnjoyment of life
Placebo3.714.004.574.142.574.434.00
Sulfasalazine4.003.573.574.141.434.864.57

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Missed Medication Doses (Using the Crossover Comparison Structure of the Study)

Number of missed medication doses (NCT01667029)
Timeframe: Assessed during two week treatment period

Interventiondoses (Mean)
Sulfasalazine0.43
Placebo0

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Missed Medication Dose (First Treatment Period Only)

Number of missed medication doses (NCT01667029)
Timeframe: Assessed during two week treatment period

Interventiondose (Mean)
Sulfasalazine0
Placebo0

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Emotional Functioning (Using the Crossover Comparison Structure of the Study)

Will be assessed by the Beck Depression Inventory (BDI) total score. The BDI has 21 items, each scored 0-3. Higher values are worse. The total score is the sum of the 21 items and ranges from 0-63. (NCT01667029)
Timeframe: Assessed at end of two week treatment period

Interventionunits on a scale (Mean)
Sulfasalazine7.29
Placebo8.29

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Emotional Functioning (First Treatment Period Only)

Will be assessed by the Beck Depression Inventory (BDI) total score. The BDI has 21 items, each scored 0-3. Higher values are worse. The total score is the sum of the 21 items and ranges from 0-63. (NCT01667029)
Timeframe: Assessed at end of two week treatment period

Interventionunits on a scale (Mean)
Sulfasalazine8.25
Placebo10.50

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Overall Improvement (First Treatment Period Only)

The Patient Global Impression of Change (PGIC) reflects a patient's belief about the efficacy of treatment. Item 1 is as follows: Since beginning treatment at this clinic, how would you describe the change (if any) in ACTIVITY LIMITATIONS, SYMPTOMS, EMOTIONS, and OVERALL QUALITY OF LIFE, related to your painful condition? (tick ONE box) (1=No change (or condition has gotten worse), 2=Almost the same, hardly any change at all, 3=A little better, but no noticeable change, 4=Somewhat better, but the change has not made any real difference, 5=Moderately better, and a slight but noticeable change, 6=Better, and a definite improvement that has made a real and worthwhile difference, 7=A great deal better, and a considerable improvement that has made all the difference). Item 2 is as follows: In a similar way, please circle the number below that matches your degree of change since beginning care at this clinic (0-10 scale): 0= Much better, 5= No change, 10= Much worse. (NCT01667029)
Timeframe: Will be assessed at end of two week treatment period

,
Interventionunits on a scale (Mean)
PGIC Item 1PGIC Item 2
Placebo1.754.50
Sulfasalazine1.505.00

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Breakthrough Treatment (Using the Crossover Comparison Structure of the Study)

Number of days breakthrough pain medication was taken (NCT01667029)
Timeframe: Assessed during two week treatment period

Interventiondays (Mean)
Sulfasalazine1.29
Placebo1.14

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Breakthrough Treatment (First Treatment Period Only)

Number of days breakthrough pain medication was taken (NCT01667029)
Timeframe: Assessed during two week treatment period

Interventiondays (Mean)
Sulfasalazine0.75
Placebo2.00

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Number of Patients With >=50% Pain Reduction (Using the Crossover Comparison Structure of the Study)

Average pain score will be the average of daily pain scores (0-10) recorded by the subject in a pain diary during baseline and the second week of each of the two week treatment periods. Higher scores are worse (0=no pain, 10=pain as bad as you can imagine). Percent pain reduction will be calculated from BL to end of treatment period 1 (2 weeks) and from end of treatment period 1 to end of treatment period 2 (2 weeks), based on average pain scores at each time point. (NCT01667029)
Timeframe: Assessed at end of two week treatment period

InterventionParticipants (Count of Participants)
Sulfasalazine0
Placebo1

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Overall Improvement (Using the Crossover Comparison Structure of the Study)

The Patient Global Impression of Change (PGIC) reflects a patient's belief about the efficacy of treatment. Item 1 is as follows: Since beginning treatment at this clinic, how would you describe the change (if any) in ACTIVITY LIMITATIONS, SYMPTOMS, EMOTIONS, and OVERALL QUALITY OF LIFE, related to your painful condition? (tick ONE box) (1=No change (or condition has gotten worse), 2=Almost the same, hardly any change at all, 3=A little better, but no noticeable change, 4=Somewhat better, but the change has not made any real difference, 5=Moderately better, and a slight but noticeable change, 6=Better, and a definite improvement that has made a real and worthwhile difference, 7=A great deal better, and a considerable improvement that has made all the difference). Item 2 is as follows: In a similar way, please circle the number below that matches your degree of change since beginning care at this clinic (0-10 scale): 0= Much better, 5= No change, 10= Much worse. (NCT01667029)
Timeframe: Will be assessed at end of two week treatment period

,
Interventionunits on a scale (Mean)
PGIC item 1PGIC item 2
Placebo3.003.56
Sulfasalazine2.804.00

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Number of Patients With >=50% Pain Reduction (First Treatment Period)

Average pain score will be the average of daily pain scores (0-10) recorded by the subject in a pain diary at baseline and during the second week of the two week treatment period. Higher scores are worse (0=no pain, 10=pain as bad as you can imagine). Percent pain reduction will be calculated from BL to end of treatment period 1 (2 weeks), based on average pain scores at each time point. (NCT01667029)
Timeframe: second week of two week treatment period

InterventionParticipants (Count of Participants)
Sulfasalazine0
Placebo0

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Physical Functioning Score Assessed Using the Brief Pain Inventory (BPI) Interference Scale (First Treatment Period Only)

The BPI interference items are general activity, mood, walking ability, normal work (including housework), relations with other people, sleep, and enjoyment of life. The seven items are rated from 0 (pain does not interfere) to 10 (pain completely interferes). (NCT01667029)
Timeframe: Assessed at end of two week treatment period

,
Interventionunits on a scale (Mean)
General activityMoodWalking abilityNormal workRelations with other peopleSleepEnjoyment of life
Placebo4.005.005.504.753.755.254.75
Sulfasalazine5.253.754.505.251.255.005.75

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Change From Baseline in Work Productivity Survey - Rheumatoid Arthritis (WPS-RA) at Week 24: Work Days Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of work days missed in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-2.01
Sarilumab 150 mg q2w-2.87
Sarilumab 200 mg q2w-3.19

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Change From Baseline in WPS-RA at Week 12: Days With Family/Social/Leisure Activities Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days missed of family/social/leisure activities in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-2.23
Sarilumab 150 mg q2w-2.53
Sarilumab 200 mg q2w-3.26

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Change From Baseline in WPS-RA at Week 12: Days With Household Work Productivity Reduced by ≥ 50% Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with reduced household work productivity by ≥ 50% in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-2.60
Sarilumab 150 mg q2w-3.97
Sarilumab 200 mg q2w-3.98

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Change From Baseline in WPS-RA at Week 12: Days With Outside Help Hired Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with outside help hired in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-0.77
Sarilumab 150 mg q2w-3.07
Sarilumab 200 mg q2w-2.94

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Change From Baseline in WPS-RA at Week 12: House Work Days Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with no household work in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-2.10
Sarilumab 150 mg q2w-5.52
Sarilumab 200 mg q2w-5.54

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Change From Baseline in WPS-RA at Week 12: RA Interference With Household Work Productivity

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). The RA interference in the last month with household work productivity was measured on a scale that ranges from 0 (no interference) to 10 (complete interference). LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.210
Sarilumab 150 mg q2w-2.772
Sarilumab 200 mg q2w-2.404

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Change From Baseline in WPS-RA at Week 12: RA Interference With Work Productivity

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Interference in the last month with work productivity was measured on a scale that ranges from 0 (no interference) to 10 (complete interference). LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.043
Sarilumab 150 mg q2w-1.924
Sarilumab 200 mg q2w-1.873

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Change From Baseline in WPS-RA at Week 12: Work Days Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of work days missed in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-1.20
Sarilumab 150 mg q2w-1.97
Sarilumab 200 mg q2w-2.98

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Change From Baseline in WPS-RA at Week 24: Days With Family/Social/Leisure Activities Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days missed of family/social/leisure activities in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-1.97
Sarilumab 150 mg q2w-3.51
Sarilumab 200 mg q2w-4.12

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Change From Baseline in WPS-RA at Week 24: Days With Household Work Productivity Reduced by ≥ 50% Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with reduced household work productivity by ≥ 50% in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-3.36
Sarilumab 150 mg q2w-4.60
Sarilumab 200 mg q2w-4.88

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Change From Baseline in WPS-RA at Week 24: Days With Outside Help Hired Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with outside help hired in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-1.60
Sarilumab 150 mg q2w-3.87
Sarilumab 200 mg q2w-3.86

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Change From Baseline in WPS-RA at Week 24: Days With Work Productivity Reduced by ≥ 50% Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of work days with reduced productivity by ≥ 50% in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-3.64
Sarilumab 150 mg q2w-4.26
Sarilumab 200 mg q2w-4.34

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Change From Baseline in WPS-RA at Week 24: House Work Days Missed Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of days with no household work in the last month by the participant was reported. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

InterventionDays (Least Squares Mean)
Placebo q2w-3.50
Sarilumab 150 mg q2w-6.13
Sarilumab 200 mg q2w-6.18

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Change From Baseline in WPS-RA at Week 24: RA Interference With Household Work Productivity

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). The RA interference in the last month with household work productivity was measured on a scale that ranges from 0 (no interference) to 10 (complete interference). LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.970
Sarilumab 150 mg q2w-3.096
Sarilumab 200 mg q2w-3.269

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Change From Baseline in WPS-RA at Week 24: RA Interference With Work Productivity

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Interference in the last month with work productivity is measured on a scale that ranges from 0 (no interference) to 10 (complete interference). LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.632
Sarilumab 150 mg q2w-2.422
Sarilumab 200 mg q2w-2.727

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Percentage of Participants Achieving ACR50 Criteria at Week 24

ACR responses are assessed with a composite rating scale that includes 7 variables: TJC; SJC; levels of an acute phase reactant (CRP level); participant's assessment of pain; participant's global assessment of disease activity; physician's global assessment of disease activity; participant's assessment of physical function by HAQ--DI. ACR50 is defined as achieving at least 50% improvement in both TJC and SJC, and at least 50% improvement in at least 3 of the 5 other assessments of the ACR. (NCT01709578)
Timeframe: Week 24

InterventionPercentage of participants (Number)
Placebo q2w18.2
Sarilumab 150 mg q2w37.0
Sarilumab 200 mg q2w40.8

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Percentage of Participants Achieving ACR70 Criteria at Week 24

ACR responses are assessed with a composite rating scale of the American College of Rheumatology that includes 7 variables: TJC; SJC; levels of an acute phase reactant (CRP level); participant's assessment of pain; participant's global assessment of disease activity; physician's global assessment of disease activity; participant's assessment of physical function by HAQ--DI. ACR70 is defined as achieving at least 70% improvement in both TJC and SJC, and at least 70% improvement in at least 3 of the 5 other assessments of the ACR. (NCT01709578)
Timeframe: Week 24

InterventionPercentage of participants (Number)
Placebo q2w7.2
Sarilumab 150 mg q2w19.9
Sarilumab 200 mg q2w16.3

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Percentage of Participants Achieving Clinical Remission Score (DAS28--CRP <2.6) at Week 12

DAS28 is a composite score that includes 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); GH by the participant assessed from the ACR RA core set questionnaire (participant global assessment) in 100 mm VAS; marker of inflammation assessed by hs-CRP in mg/L. The DAS28 provides a number indicating the current activity of the RA. DAS28 total score ranges from 2-10. A DAS28 score above 5.1 means high disease activity, whereas a DAS28 score below 3.2 indicates low disease activity and a DAS28 score below 2.6 means disease remission. (NCT01709578)
Timeframe: Week 12

InterventionPercentage of participants (Number)
Placebo q2w3.9
Sarilumab 150 mg q2w17.1
Sarilumab 200 mg q2w17.9

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Percentage of Participants Achieving Clinical Remission Score (DAS28-CRP) <2.6 at Week 24

DAS28 is a composite score that includes 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); GH by the participant assessed from the ACR rheumatoid arthritis core set questionnaire (participant global assessment) in 100 mm VAS; marker of inflammation assessed by hs-CRP in mg/L. The DAS28 provides a number indicating the current activity of the RA. DAS28 total score ranges from 2-10. A DAS28 score above 5.1 means high disease activity, whereas a DAS28 score below 3.2 indicates low disease activity and a DAS28 score below 2.6 means disease remission. (NCT01709578)
Timeframe: Week 24

InterventionPercentage of participants (Number)
Placebo q2w7.2
Sarilumab 150 mg q2w24.9
Sarilumab 200 mg q2w28.8

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Percentage of Participants Who Achieved at Least 20% Improvement in the American College of Rheumatology (ACR20) Criteria at Week 24

ACR responses are assessed with a composite rating scale of the American College of Rheumatology that includes 7 variables: tender joint count (TJC); swollen joint count (SJC); levels of an acute phase reactant (C-reactive Protein levels [CRP]); participant's assessment of pain; participant's global assessment of disease activity; physician's global assessment of disease activity; participant's assessment of physical function by (health assessment questionnaire disability index [HAQ-DI]). ACR20 is defined as achieving at least 20% improvement in both TJC and SJC, and at least 20% improvement in at least 3 of the 5 other assessments of the ACR. (NCT01709578)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Placebo q2w33.7
Sarilumab 150 mg q2w55.8
Sarilumab 200 mg q2w60.9

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Change From Baseline in Individual ACR Component - CRP Level at Week 12 and Week 24

"ACR components were: TJC, SJC, physician global VAS, participant global VAS, pain VAS, HAQ-DI & CRP. An elevated CRP level was considered a non-specific marker for RA. A reduction level indicates improvement. LS mean and SE at Week 12 & 24 by MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline ACR components as a covariate." (NCT01709578)
Timeframe: Baseline, Week 12 and Week 24

,,
Interventionmg/L (Least Squares Mean)
CRP at week 12CRP at week 24
Placebo q2w-3.63-3.60
Sarilumab 150 mg q2w-15.08-15.24
Sarilumab 200 mg q2w-22.98-23.27

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Change From Baseline in Individual ACR Component - HAQ-DI at Week 12 and Week 24

ACR components were: TJC, SJC, physician global VAS, participant global VAS, pain VAS,HAQ-DI & CRP. HAQ-DI consisted of at least 2 questions per category, participant reported assessment of ability to perform tasks in 8 categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week rated on a 4-point scale where 0 = no difficulty; 1 = some difficulty; 2 = much difficulty; 3 = unable to do. Overall score was computed as the sum of category scores and divided by the number of categories answered, ranging from 0 to 3, where 0 = no disability and 3 = unable to do, high-dependency disability. LS mean and SE at Week 12 & 24 by MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline ACR components as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12 and Week 24

,,
Interventionunits on a scale (Least Squares Mean)
HAQ-DI at week 12HAQ-DI at week 24
Placebo q2w-0.26-0.34
Sarilumab 150 mg q2w-0.46-0.52
Sarilumab 200 mg q2w-0.47-0.58

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Change From Baseline in Individual ACR Component - Physician Global VAS, Participant Global VAS and Pain VAS at Week 12 and Week 24

"ACR components were: TJC, SJC, physician global VAS, participant global VAS, pain VAS, HAQ-DI & CRP. Physician global VAS & participant global VAS was done by 100 mm non-anchored VAS, from no arthritis (0) activity to maximal arthritis (100) activity. Pain VAS by 100 mm VAS ranging from 0 no pain to 100 worst pain. LS mean and SE at Week 12 & 24 by MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline ACR components as a covariate." (NCT01709578)
Timeframe: Baseline, Week 12 and Week 24

,,
Interventionmm (Least Squares Mean)
Physician global VAS at week 12Participant global VAS at week 12Pain VAS at week 12Physician global VAS at week 24Participant global VAS at week 24Pain VAS at week 24
Placebo q2w-22.74-13.75-15.13-28.55-19.76-21.27
Sarilumab 150 mg q2w-33.64-25.28-26.93-40.65-29.59-31.90
Sarilumab 200 mg q2w-35.44-27.38-30.56-43.22-31.28-33.65

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Change From Baseline in Individual ACR Components - TJC and SJC at Week 12 and Week 24

ACR components were: TJC, SJC, physician global VAS, participant global VAS, pain VAS,HAQ-DI & CRP. 68 joints were assessed for tenderness (TJC scoring 0-68) and 66 joints for swelling (SJC scoring 0-66). The 66 SJC evaluated the following joints: temporomandibular, sternoclavicular, acromioclavicular, shoulder, elbow, wrist, metacarpophalangeal, interphalangeal of thumb, distal interphalangeal, proximal interphalangeal, knee, ankle mortise, ankle tarsus, metatarsophalangeal, interphalangeal of great toe, and proximal/distal interphalangeal of the toes. The TJC examined hip joints, in addition to the joints assessed for SJC. Increase in number of tender joints/swollen joints indicated severity. LS mean and SE at Week 12 & 24 by MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline ACR components as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12 and Week 24

,,
Interventionjoints (Least Squares Mean)
TJC at week 12SJC at week 12TJC at week 24SJC at week 24
Placebo q2w-8.55-6.75-10.55-8.19
Sarilumab 150 mg q2w-13.74-10.54-14.44-11.56
Sarilumab 200 mg q2w-14.87-10.59-16.95-11.94

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Change From Baseline in SF-36 at Week 12

SF-36 is a generic 36-item questionnaire measuring HRQL covering 2 summary measures: PCS and MCS. The SF-36 consists of 8 subscales. The PCS is represented by 4 subscales: physical function, role limitations due to physical problems, pain, and general health perception. The MCS is represented by 4 subscales: vitality, social function, role limitations due to emotional problems, and mental health. Participants self-report on items in a subscale that have between 2-6 choices per item using Likert-type responses (e.g. none of the time, some of the time, etc.). Summations of item scores of the same subscale give the subscale scores, which are transformed into a range from 0 to 100; 0= worst HRQL, 100=best HRQL. Higher scores indicate better health and well-being. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline SF-36 as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

,,
Interventionunits on a scale (Least Squares Mean)
Physical Component Summary Score at Week 12Mental Component Summary Score at Week 12
Placebo q2w3.743.50
Sarilumab 150 mg q2w6.935.14
Sarilumab 200 mg q2w6.846.47

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Percentage of Participants Achieving ACR20, ACR50 and ACR70 Criteria at Week 12

ACR responses are assessed with a composite rating scale of the American College of Rheumatology that includes 7 variables: TJC; SJC; levels of an acute phase reactant (CRP level); participant's assessment of pain; participant's global assessment of disease activity; physician's global assessment of disease activity; participant's assessment of physical function by HAQ--DI. ACR20 is defined as achieving at least 20% improvement in both TJC and SJC, and at least 20% improvement in at least 3 of the 5 other assessments of the ACR. ACR50 is defined as achieving at least 50% improvement in both TJC and SJC, and at least 50% improvement in at least 3 of the 5 other assessments of the ACR. ACR70 is defined as achieving at least 70% improvement in both TJC and SJC, and at least 70% improvement in at least 3 of the 5 other assessments of the ACR. (NCT01709578)
Timeframe: Week 12

,,
InterventionPercentage of participants (Number)
ACR20ACR50ACR70
Placebo q2w37.613.32.2
Sarilumab 150 mg q2w54.130.413.8
Sarilumab 200 mg q2w62.533.214.7

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Change From Baseline in WPS-RA at Week 12: Days With Work Productivity Reduced by ≥ 50% Due to RA

The WPS-RA is a validated questionnaire that evaluates productivity limitations within work and within home associated with RA over the previous month. The questionnaire was interviewer-administered and was based on participant self-report. It contains 9 questions addressing employment status (1 item), productivity at work (3 items), and within and outside the home (5 items). Number of work days with reduced productivity by ≥ 50% in the last month by the participant was reported. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline WPS-RA as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

InterventionDays (Least Squares Mean)
Placebo q2w-1.69
Sarilumab 150 mg q2w-4.24
Sarilumab 200 mg q2w-3.20

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Change From Baseline in 36-Item Short-Form Health Survey (SF-36) Physical Component Summary Scores (PCS) at Week 24

SF-36 is a generic 36-item questionnaire measuring health-related quality of life (HRQL) covering 2 summary measures: PCS and mental component summary (MCS). The SF-36 consists of 8 subscales. The PCS had 4 subscales: physical function, role limitations due to physical problems, pain, and general health perception. The MCS had 4 subscales: vitality, social function, role limitations due to emotional problems, and mental health. Participants self-report on items in a subscale that have between 2-6 choices per item using Likert-type responses (e.g. none of the time, some of the time, etc.). Summations of item scores of the same subscale give the subscale scores, which are transformed into a range from 0 to 100; 0= worst HRQL, 100=best HRQL. Higher scores indicate better health and well-being. LS mean and SE at Week 24 by MMRM with treatment,region,number of previous anti TNFs,visit,and treatment-by-visit interaction as fixed effects and baseline SF-36 (PCS) as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w4.40
Sarilumab 150 mg q2w7.65
Sarilumab 200 mg q2w8.48

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Change From Baseline in Clinical Disease Activity Index (CDAI) at Week 24

CDAI is a composite index constructed to measure clinical remission in RA that does not include a laboratory test, and is a numerical summation of 4 components: TJC (28 joints), SJC (28 joints), Participant's Global Assessment of Disease Activity VAS (in cm), and Physician's Global Assessment of Disease VAS (in cm). Total scores ranges from 0 to 76 with a negative change in CDAI score indicating an improvement in disease activity and a positive change in score indicating a worsening of disease activity. LS means and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline CDAI as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-16.35
Sarilumab 150 mg q2w-23.65
Sarilumab 200 mg q2w-26.08

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Change From Baseline in DAS28-CRP at Week 12

DAS28 is a composite score that includes 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); GH by the participant assessed from the ACR rheumatoid arthritis core set questionnaire (participant global assessment) in 100 mm VAS; marker of inflammation assessed by hs-CRP in mg/L. The DAS28 provides a number indicating the current activity of the RA. DAS28 total score ranges from 2-10. A DAS28 score above 5.1 means high disease activity, whereas a DAS28 score below 3.2 indicates low disease activity and a DAS28 score below 2.6 means disease remission. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline DAS score as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-0.97
Sarilumab 150 mg q2w-2.13
Sarilumab 200 mg q2w-2.45

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Change From Baseline in Disease Activity Score for 28 Joints -C-Reactive Protein (DAS28--CRP) Score at Week 24

DAS28 is a composite score that includes 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); General health (GH) assessment by the participant assessed from the ACR rheumatoid arthritis (RA) core set questionnaire (participant global assessment) in 100 mm visual analog scale (VAS). Marker of inflammation assessed by the high sensitivity C-reactive protein (hs-CRP) in mg/L. The DAS28 score provides a number indicating the current disease activity of the RA. DAS28 total score ranges from 2-10. A DAS28 score above 5.1 means high disease activity, whereas a DAS28 score below 3.2 indicates low disease activity and a DAS28 score below 2.6 means disease remission. LS means and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline DAS28-CRP score as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.38
Sarilumab 150 mg q2w-2.35
Sarilumab 200 mg q2w-2.82

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Change From Baseline in EQ-5D-3L VAS Scores at Week 12

The EQ-5D-3L is a standardized, generic measure of health outcome. EQ-5D was designed for self-completion by participants. The EQ-5D was specifically included to address concerns regarding the health economic impact of RA. The EQ-5D-3L comprises 5 questions on mobility, self-care, pain, usual activities, and psychological status with 3 possible answers for each item (1=no problem, 2=moderate problems, 3=severe problems) and a vertical VAS that allows the participants to indicate their health state today that can range from 0 (worst imaginable) to 100 (best imaginable). LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline EQ-5D-3L scores as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w8.39
Sarilumab 150 mg q2w17.16
Sarilumab 200 mg q2w15.23

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Change From Baseline in European Quality of Life-5 Dimension 3 Level (EQ-5D-3L) VAS Scores at Week 24

The EQ-5D-3L is a standardized, generic measure of health outcome. It was designed for self-completion by participants. It was specifically included to address concerns regarding the health economic impact of RA. The EQ-5D-3L comprises 5 questions on mobility, self-care, pain, usual activities, and psychological status with 3 possible answers for each item (1=no problem, 2=moderate problems, 3=severe problems) and a vertical VAS that allows the participants to indicate their health state today that can range from 0 (worst imaginable) to 100 (best imaginable). LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline EQ-5D-3L Scores as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w14.85
Sarilumab 150 mg q2w20.06
Sarilumab 200 mg q2w18.40

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Change From Baseline in HAQ-DI at Week 24

Physical function was assessed by HAQ-DI. It consisted of at least 2 questions per category, participant reported assessment of ability to perform tasks in 8 categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week rated on a 4-point scale where 0 = no difficulty; 1 = some difficulty; 2 = much difficulty; 3 = unable to do. Overall score was computed as the sum of category scores and divided by the number of categories answered, ranging from 0 to 3, where 0 = no disability and 3 = unable to do, high-dependency disability. LS means and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline HAQ-DI as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-0.34
Sarilumab 150 mg q2w-0.52
Sarilumab 200 mg q2w-0.58

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Change From Baseline in Morning Stiffness VAS at Week 24

RA is associated with stiffness of joints, especially in the morning after prolonged stationery state. The degree of stiffness can be an indicator of disease severity. The severity of morning stiffness was assessed on a VAS scale from 0 mm (no problem) to 100 mm (major problem). LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline Morning Stiffness as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionmm (Least Squares Mean)
Placebo q2w-21.66
Sarilumab 150 mg q2w-32.30
Sarilumab 200 mg q2w-33.79

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Change From Baseline in RAID Scores at Week 12

RAID score is a composite measure of the impact of RA on participants that takes into account 7 domains: pain, functional disability, fatigue, physical and emotional well being, quality of sleep, and coping. The RAID is calculated based on 7 NRS questions. Range of the final RAID value is 0-10 where 0= not affected, very good and 10 = most affected weighted and calculated with a total score range of 0 (not affected, very good) to 10 (most affected). A higher RAID value indicates worse status and lower indicates not affected. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline RAID scores as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Mean)
Placebo q2w-1.34
Sarilumab 150 mg q2w-2.27
Sarilumab 200 mg q2w-2.47

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Change From Baseline in Rheumatoid Arthritis Impact of Disease (RAID) Scores at Week 24

RAID is a composite measure of the impact of RA on participants that takes into account 7 domains: pain, functional disability, fatigue, physical and emotional well being, quality of sleep, and coping. The RAID is calculated based on 7 numerical rating scales (NRS) questions. Range of the final RAID value is 0-10 where 0= not affected, very good and 10 = most affected weighted and calculated with a total score range of 0 (not affected, very good) to 10 (most affected). A higher RAID value indicate worse status and lower indicate not affected. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline RAID as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-1.80
Sarilumab 150 mg q2w-2.55
Sarilumab 200 mg q2w-2.80

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Change From Baseline in SF-36 MCS at Week 24

SF-36 is a generic 36-item questionnaire measuring HRQL covering 2 summary measures: PCS and MCS. The SF-36 consists of 8 subscales. The PCS is represented by 4 subscales: physical function, role limitations due to physical problems, pain, and general health perception. The MCS is represented by 4 subscales: vitality, social function, role limitations due to emotional problems, and mental health. Participants self-report on items in a subscale that have between 2-6 choices per item using Likert-type responses (e.g. none of the time, some of the time, etc.). Summations of item scores of the same subscale give the subscale scores, which are transformed into a range from 0 to 100; 0= worst HRQL, 100=best HRQL. Higher scores indicate better health and well-being. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline SF-36 MCS as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w4.74
Sarilumab 150 mg q2w6.26
Sarilumab 200 mg q2w6.76

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Change From Baseline in the FACIT-fatigue at Week 12

The FACIT-Fatigue is a 13-item questionnaire assessing fatigue where participants scored each item on a 5-point scale (0-4): 0=not at all, 1=a little bit, 2=somewhat, 3=quite a bit, 4=very much. A total score ranging from 0 to 52. A higher score corresponded to a lower level of fatigue. A positive change from baseline score indicates an improvement. LS mean and SE at Week 12 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline FACIT-fatigue as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w5.56
Sarilumab 150 mg q2w8.02
Sarilumab 200 mg q2w9.45

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Change From Baseline in the Functional Assessment of Chronic Illness Therapy Fatigue (FACIT-fatigue) Score at Week 24

The FACIT-Fatigue is a 13-item questionnaire assessing fatigue where participants scored each item on a 5-point scale (0-4): 0=not at all, 1=a little bit, 2=somewhat, 3=quite a bit, 4=very much. A total score ranging from 0 to 52. A higher score corresponded to a lower level of fatigue. A positive change from baseline score indicates an improvement. LS mean and SE at Week 24 were obtained from a MMRM with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline FACIT-fatigue as a covariate. (NCT01709578)
Timeframe: Baseline, Week 24

Interventionunits on a scale (Least Squares Mean)
Placebo q2w6.82
Sarilumab 150 mg q2w9.86
Sarilumab 200 mg q2w10.06

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Change From Baseline in the Health Assessment Questionnaire-Disability Index (HAQ-DI) at Week 12

Physical function was assessed by HAQ-DI. It consisted of at least 2 questions per category, participant reported assessment of ability to perform tasks in 8 categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week rated on a 4-point scale where 0 = no difficulty; 1 = some difficulty; 2 = much difficulty; 3 = unable to do. Overall score was computed as the sum of category scores and divided by the number of categories answered, ranging from 0 to 3, where 0 = no disability and 3 = unable to do, high-dependency disability. Least-squares (LS) means and standard errors (SE) at Week 12 were obtained from a mixed-effect model with repeated measures (MMRM) with treatment, region, number of previous anti-TNFs, visit, and treatment-by-visit interaction as fixed effects and baseline HAQ-DI as a covariate. (NCT01709578)
Timeframe: Baseline, Week 12

Interventionunits on a scale (Least Squares Mean)
Placebo q2w-0.26
Sarilumab 150 mg q2w-0.46
Sarilumab 200 mg q2w-0.47

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Number of Participants With Treatment Emergent Adverse Events (TEAEs)

Adverse event (AE) was defined as any untoward medical occurrence in a participant who received study drug and does not necessary have to have a causal relationship with treatment. All adverse events that occurred from the first dose of the study drug administration up to 60 days after the end of treatment visit were considered as TEAEs. Serious AE (SAE) was an AE resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly or a medically important event. A summary of SAEs, all other non-serious AEs, regardless of causality, are reported in AE section. (NCT01768572)
Timeframe: Up to 211 days

,,
Interventionparticipants (Number)
Any TEAEAny treatment-emergent SAEAny TEAE leading to deathAny TEAE leading to discontinuation
Sarilumab 150 mg q2w33106
Sarilumab 200 mg q2w36308
Tocilizumab q4w68714

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Number of Participants by Reasons (Categories) for Corticosteroid Dose Reduction or Discontinuation

Reasons for corticosteroid dose reduction included: Safety Reasons (including elevated liver function test results, respiratory infections, infections and infestations, gastrointestinal disorders etc.); Other Reasons (disease remission, improvement etc.); and Unknown Reasons (including no reason). Number of participants by reasons (Safety, Other, Unknown) for corticosteroid dose reduction or discontinuation were reported. (NCT01941095)
Timeframe: From Baseline up to Week 52

Interventionparticipants (Number)
SafetyOtherUnknown
Tocilizumab6102

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HAQ-DI Score

"The Stanford HAQ-DI is a patient-reported questionnaire specific for rheumatoid arthritis. It consists of 20 questions referring to 8 component sets: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and activities. Responses in each component set were scored from 0 (without any difficulty) to 3 (unable to do). The highest score recorded for any question in a category determines the score for the category, unless aids, devices, or help from another person was required. The HAQ-DI score was calculated as the sum of the category scores divided by the number of categories scored, giving a possible range of scores from 0 to 3. Scores of 0 to 1 are generally considered to represent mild to moderate difficulty, 1 to 2 as moderate to severe disability, and 2 to 3 as severe to very severe disability." (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionunits on a scale (Mean)
Week 1Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab1.311.221.090.910.820.720.680.660.660.590.630.600.590.560.54

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Functional Assessment of Chronic Illness Therapy (FACIT)-Fatigue Total Score

FACIT-Fatigue total score is sum of FACIT-General subscale score and FACIT-Fatigue (additional concerns) subscale score. FACT-General consists of 27 questions grouped in 4 domains of general health-related quality of life: physical well-being, social/family well-being, emotional well-being, and functional well-being; each item ranges from 0 (not at all) to 4 (very much). FACT-General score ranges between 0-108. FACIT-Fatigue subscale is a 13-item questionnaire that evaluates self-reported fatigue and its impact upon daily activities. Each item ranges from 0 (Not at all) to 4 (Very much). For all items, except for the 2 negatively stated ones, the code was reversed and a new score was calculated as 4 minus the participant's response. The sum of all responses resulted in the FACIT-Fatigue subscale score for a total possible score of 0 (worse score) to 52 (better score). FACIT-Fatigue total score (FACT-G plus FACT-F subscale scores) ranges from 0 (better score) to 160 (worse score). (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionunits on a scale (Mean)
Week 1Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab89.6891.83100.38103.16106.39110.17112.60114.21114.85117.01116.50116.59119.67119.83121.82

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Change From Baseline in TJC28 up to Week 52

28 joints were assessed for tenderness and joints were classified as tender/not tender giving a total possible tender joint count score of 0 to 28. A negative change from baseline indicated improvement. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventiontender joints (Mean)
Change at Week 2Change at Week 4Change at Week 8Change at Week 12Change at Week 16Change at Week 20Change at Week 24Change at Week 28Change at Week 32Change at Week 36Change at Week 40Change at Week 44Change at Week 48Change at Week 52
Tocilizumab-1.30-3.26-4.97-5.82-6.39-7.03-7.72-7.91-8.38-8.28-8.22-8.63-8.26-8.75

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Change From Baseline in SJC28 up to Week 52

28 joints were assessed for swelling and joints were classified as swollen/not swollen giving a total possible swollen joint count score of 0 to 28. A negative change from baseline indicated improvement. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionswollen joints (Mean)
Change at Week 2Change at Week 4Change at Week 8Change at Week 12Change at Week 16Change at Week 20Change at Week 24Change at Week 28Change at Week 32Change at Week 36Change at Week 40Change at Week 44Change at Week 48Change at Week 52
Tocilizumab-1.82-3.08-4.71-5.24-5.79-6.06-6.60-6.65-6.73-6.76-6.91-6.82-6.63-6.98

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Percentage of Participants Who Achieved DAS28-ESR Remission/Low Disease Activity (LDA) From Week 28 up to Week 52 Among Participants With Intensification of Methotrexate/Other Non-Biologic DMARDs in Combination With Tocilizumab Since Week 24

DAS28-ESR score is a measure of participant's disease activity calculated using TJC28, SJC28, PGA using VAS 0 mm=no disease activity to 100 mm=maximum disease activity, displayed on the 100 mm horizontal VAS, and acute phase response (ESR in mm/hr) for a total possible score of 0 to 10. The score is calculated using the following formula: DAS28-ESR = [0.56 * √TJC28 + [0.28*√SJC28]+[0.70*ln ESR]+[0.014*GH]. DAS28-ESR score varies from 0 to 10, where higher scores represent greater disease activity. DAS28-ESR score <2.6 represents DAS28-ESR remission. DAS28-ESR score greater than or equal to (>/=) 2.6 and <3.2 represents LDA. (NCT01941095)
Timeframe: Weeks 28, 32, 36, 40, 44, 48, 52

Interventionpercentage of participants (Number)
Week 28: RemissionWeek 32: RemissionWeek 36: RemissionWeek 40: RemissionWeek 44: RemissionWeek 48: RemissionWeek 52: RemissionWeek 28: LDAWeek 32: LDAWeek 36: LDAWeek 40: LDAWeek 44: LDAWeek 48: LDAWeek 52: LDA
Tocilizumab5.18.14.19.56.98.567.61.46.86.86.94.29

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Percentage of Participants Who Maintained DAS28-ESR Remission From Week 24 up to Week 52 Among Participants on Tocilizumab Monotherapy Since Week 24

DAS28-ESR score is a measure of participant's disease activity calculated using TJC28, SJC28, PGA using VAS 0 mm=no disease activity to 100 mm=maximum disease activity, displayed on the 100 mm horizontal VAS, and acute phase response (ESR in mm/hr) for a total possible score of 0 to 10. The score is calculated using the following formula: DAS28-ESR = [0.56 * √TJC28 + [0.28*√SJC28]+[0.70*ln ESR]+[0.014*GH]. DAS28-ESR score varies from 0 to 10, where higher scores represent greater disease activity. DAS28-ESR score <2.6 represents DAS28-ESR remission. The percentage reported for Week 24 is based on confirmation on switching to SC tocilizumab monotherapy. (NCT01941095)
Timeframe: Weeks 24, 28, 32, 36, 40, 44, 48, 52

Interventionpercentage of participants (Number)
Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab38.734.236.536.536.535.235.738.8

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Percentage of Participants Who Received All Planned Study Medication (Compliance)

Compliance (in terms of percentage of participants who received all planned study medication) was assessed on the basis of participant diary cards and return records. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionpercentage of participants (Number)
Week 1Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab6697.910010098.997.698.8100100100100100100100100

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Change From Baseline in DAS28-ESR up to Week 52

DAS28-ESR score is a measure of participant's disease activity calculated using TJC28, SJC28, PGA using VAS 0 mm=no disease activity to 100 mm=maximum disease activity, displayed on the 100 mm horizontal VAS, and acute phase response (ESR in mm/hr) for a total possible score of 0 to 10. The score is calculated using the following formula: DAS28-ESR = [0.56 * √TJC28 + [0.28*√SJC28]+[0.70*ln ESR]+[0.014*GH]. DAS28-ESR score varies from 0 to 10, where higher scores represent greater disease activity. A negative change from baseline indicates an improvement. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionunits on a scale (Mean)
Change at Week 2Change at Week 4Change at Week 8Change at Week 12Change at Week 16Change at Week 20Change at Week 24Change at Week 28Change at Week 32Change at Week 36Change at Week 40Change at Week 44Change at Week 48Change at Week 52
Tocilizumab-0.99-1.70-2.20-2.56-2.59-2.93-3.14-3.22-3.34-3.32-3.40-3.45-3.42-3.40

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Percentage of Participants With Good, Moderate, or No Response According to European League Against Rheumatism (EULAR) Response Criteria

Response to treatment was determined using EULAR criteria based upon DAS28 absolute scores at the assessment visit and the DAS28 reduction from the baseline visit. Participants with a score lesser than or equal to () 1.2 points were assessed as having a 'good' response. Participants with a score >3.2 with reduction of >1.2 points, or a score 0.6 to 5.1 with reduction of >0.6 to NCT01941095)
Timeframe: Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionpercentage of participants (Number)
Week 2: Good responseWeek 2: Moderate responseWeek 2: No responseWeek 4: Good responseWeek 4: Moderate responseWeek 4: No responseWeek 8: Good responseWeek 8: Moderate responseWeek 8: No responseWeek 12: Good responseWeek 12: Moderate responseWeek 12: No responseWeek 16: Good responseWeek 16: Moderate responseWeek 16: No responseWeek 20: Good responseWeek 20: Moderate responseWeek 20: No responseWeek 24: Good responseWeek 24: Moderate responseWeek 24: No responseWeek 28: Good responseWeek 28: Moderate responseWeek 28: No responseWeek 32: Good responseWeek 32: Moderate responseWeek 32: No responseWeek 36: Good responseWeek 36: Moderate responseWeek 36: No responseWeek 40: Good responseWeek 40: Moderate responseWeek 40: No responseWeek 44: Good responseWeek 44: Moderate responseWeek 44: No responseWeek 48: Good responseWeek 48: Moderate responseWeek 48: No responseWeek 52: Good responseWeek 52: Moderate responseWeek 52: No response
Tocilizumab9.444.845.89.538.951.610.823.665.69.220.770.15.915.378.86.126.867.16.221.272.66.311.482.3018.981.11.314.983.85.417.6772.813.983.35.711.482.99460

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PGA, Using VAS Score

"PGA was assessed on a 0 to 100 mm horizontal VAS. The extreme left end of the line = 0 mm, and was described as no disease activity (symptom-free and no arthritis symptoms) and the extreme right end = 100 mm, and was described as maximum disease activity (maximum arthritis disease activity). Higher values correspond to worst state of participant (high disease activity)." (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionmm (Mean)
Week 1Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab28.2627.5728.3632.2828.7324.4028.1532.6326.0227.0830.7930.5025.7923.8623.08

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Soluble Interleukin-6 Receptor (sIL-6R) Levels

(NCT01941095)
Timeframe: Baseline (Week 1), Weeks 12, 24, 36, 52, and 8 weeks after Week 52 dose (Week 60)

Interventionnanograms per milliliter (ng/mL) (Mean)
Week 1Week 12Week 24Week 36Week 52Week 60
Tocilizumab39450553.43572.03570.78537.7342850

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Tocilizumab Serum Levels

(NCT01941095)
Timeframe: Baseline (Week 1), Weeks 12, 24, 36, 52, and 8 weeks after Week 52 dose (Week 60)

Interventionmicrogrms per milliliter (mcg/mL) (Mean)
Week 1Week 12Week 24Week 36Week 52Week 60
Tocilizumab0.3841.9844.6747.9045.376.46

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Percentage of Participants With Corticosteroid Dose Reduction or Discontinuation

(NCT01941095)
Timeframe: From Baseline up to Week 52

Interventionpercentage of participants (Number)
Tocilizumab48.6

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Percentage of Participants Who Achieved Disease Activity Score Based on 28 Joint Count and Erythrocyte Sedimentation Rate (DAS28-ESR) Remission at Week 24

DAS28-ESR score is a measure of participant's disease activity calculated using tender joint count in 28 joints (TJC28), swollen joint count in 28 joints (SJC28), patient global assessment of disease activity (PGA) (general health [GH]) using visual analog scale (VAS): 0 millimeter (mm)=no disease activity to 100 mm=maximum disease activity, displayed on the 100 mm horizontal VAS, and acute phase response (ESR in millimeters per hour [mm/hr]). The score is calculated using the following formula: DAS28-ESR = [0.56 multiplied by (*) square root (√) of TJC28] plus (+) [0.28*√SJC28]+[0.70*the natural logarithm (ln) ESR]+[0.014*GH]. DAS28-ESR score varies from 0 to 10, where higher scores represent greater disease activity. DAS28-ESR score of less than (<) 2.6 represents DAS28-ESR remission. (NCT01941095)
Timeframe: Week 24

Interventionpercentage of participants (Number)
Tocilizumab40

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Change From Baseline in Simplified Disease Activity Index (SDAI) Score up to Week 52

SDAI is an index for measuring disease activity. SDAI is the numerical sum of five outcome parameters: TJC28 and SJC28, PGA and physician global assessment of disease activity assessed on VAS (0 centimeter [cm]-10 cm); 0 cm= no disease activity and 10 cm= worst disease activity, and CRP (in milligrams per deciliter [mg/dL]). SDAI total score ranges from 0 to 86, with higher scores indicating increased (or severe) disease activity. SDAI score 3.4 to 11 = low disease activity, >11 to 26 = moderate disease activity, and >26 = high (or severe) disease activity. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionunits on a scale (Mean)
Change at Week 2Change at Week 4Change at Week 8Change at Week 12Change at Week 16Change at Week 20Change at Week 24Change at Week 28Change at Week 32Change at Week 36Change at Week 40Change at Week 44Change at Week 48Change at Week 52
Tocilizumab-3.41-6.54-8.72-11.07-13.47-13.88-14.08-15.37-16.09-15.61-14.86-16.31-16.47-17.35

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Patient Assessment of Pain, Using VAS Score

"The participant's level of pain was assessed on a 0 to 100 mm horizontal VAS. The extreme left end of the line = 0 mm, and was described as no pain and the extreme right end = 100 mm, and was described as unbearable pain. Higher values correspond to worst state of participant (higher level of pain)." (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionmm (Mean)
Week 1Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab46.4052.0449.8742.7237.2134.2431.0029.5729.6325.5026.7827.5026.8823.6123.98

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Number of Participants With Anti-Tocilizumab Antibodies (ATA)

All samples were tested using a screening assay and, if positive, by a confirmation assay to determine specificity and a neutralizing assay to test for the ability to inhibit the activity of tocilizumab. Number of participants with a positive assay result for screening assay (ATA - Screen), confirmatory assay (ATA - Confirmatory), and neutralizing assay (ATA - Neutralizing) was reported separately. (NCT01941095)
Timeframe: Baseline (Week 1), Weeks 12, 24, 36, 52, and 8 weeks after Week 52 dose (Week 60)

Interventionparticipants (Number)
Week 1: ATA - ScreenWeek 1: ATA - ConfirmatoryWeek 1: ATA - NeutralizingWeek 12: ATA - ScreenWeek 12: ATA - ConfirmatoryWeek 12: ATA - NeutralizingWeek 24: ATA - ScreenWeek 24: ATA - ConfirmatoryWeek 24: ATA - NeutralizingWeek 36: ATA - ScreenWeek 36: ATA - ConfirmatoryWeek 36: ATA - NeutralizingWeek 52: ATA - ScreenWeek 52: ATA - ConfirmatoryWeek 52: ATA - NeutralizingWeek 60: ATA - ScreenWeek 60: ATA - ConfirmatoryWeek 60: ATA - Neutralizing
Tocilizumab740300311200200110

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Number of Participants With American College of Rheumatology 20 (ACR20) Response

ACR20 response was defined as >/=20% improvement from baseline in both TJC28 and SJC28 as well as in 3 out of 5 additional parameters: Separate patient and physician's global assessment of disease activity on VAS (0 mm=no disease activity to 100 mm=maximum disease activity, displayed on the 100 mm horizontal VAS), patient's assessment of pain on VAS (0 mm=no pain to 100 mm=unbearable pain, displayed on the 100 mm horizontal VAS), Health Assessment Questionnaire - Disability Index (HAQ-DI) (20 questions, 8 components: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and activities, 0=without any difficulty to 3=unable to do), and acute phase response (ESR in mm/hr, for a total possible score of 0 to 10). (NCT01941095)
Timeframe: Weeks 2, 4, 8, 12, 16, 20, 24, 28, 32, 36, 40, 44, 48, 52

Interventionparticipants (Number)
Week 2Week 4Week 8Week 12Week 16Week 20Week 24Week 28Week 32Week 36Week 40Week 44Week 48Week 52
Tocilizumab19192391316913101110121315

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Number of Validated AID Associated Product Technical Failures (PTFs)

"A PTF was defined as any product technical complaint (PTC) related to the use of the AID that had a validated technical cause. Each participant was given a diary having questions related to participant's ability to remove the cap, to start the injection, to complete the injection and regarding confirmation of completing the injection. Participants were asked to answer the questions each time they self-inject the sarilumab. If the response was no to any of the first 3 questions, this was considered as a PTC. The used AID, for which PTC was reported, was sent to sponsor, examined and evaluated for the occurrence of a PTF." (NCT02057250)
Timeframe: Baseline up to Week 12

InterventionPTFs (Number)
Sarilumab 150 mg by AID (AID Assessment Phase)0
Sarilumab 200 mg by AID (AID Assessment Phase)0

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Area Under the Serum Concentration Versus Time Curve Calculated Using the Trapezoidal Method During a Dose Interval (AUC[0-tau]) for Sarilumab

AUC(0-tau) is defined as area under the serum concentration versus time curve calculated using the trapezoidal method during a dose interval, where dose interval was 2 weeks. Serum concentrations of sarilumab were analyzed using validated enzyme linked immunosorbent assay (ELISA). (NCT02057250)
Timeframe: Week 0-2: pre-dose on Day 1, anytime post-dose on Day 3, Day 5, Day 8, Day 12, Day 15; Week 10-12: pre-dose on Day 71, anytime post-dose on Day 73, Day 75, Day 78, Day 82, Day 85

,,,
Interventionmg*day/L (Mean)
Week 0-2Week 10-12
Sarilumab 150 mg by AID (AID Assessment Phase)131205
Sarilumab 150 mg by PFS (AID Assessment Phase)152220
Sarilumab 200 mg by AID (AID Assessment Phase)235455
Sarilumab 200 mg by PFS (AID Assessment Phase)227405

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Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Renal Function Parameters

"Criteria for potentially clinically significant abnormalities:~Creatinine: >=150 micromol/L (adults); >=30% change from baseline, >=100% change from baseline~Creatinine clearance: <15 mL/min; >=15 to <30 mL/min; >=30 to <60 mL/min; >=60 to <90 mL/min~Blood urea nitrogen: >=17 mmol/L~Uric acid: <120 micromol/L; >408 micromol/L" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
Creatinine >=150 micromol/L (Adults)Creatinine >=30% change from baselineCreatinine >=100% change from baselineCreatinine Clearance <15 mL/minCreatinine clearance >=15 to <30 mL/minCreatinine clearance >=30 to <60 mL/minCreatinine clearance >=60 to <90 mL/minBlood Urea Nitrogen >=17 mmol/LUric acid <120 micromol/LUric acid >408 micromol/L
Sarilumab 150 mg q2w06000615002
Sarilumab 150 mg q2w + DMARDs0300068001
Sarilumab 200 mg q2w15000517004
Sarilumab 200 mg q2w + DMARDs0300067011

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Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Liver Function Parameters

"Criteria for potentially clinically significant abnormalities:~Alanine Aminotransferase (ALT): >1 ULN and <=1.5 ULN; >1.5 ULN and <=3 ULN; >3 ULN and <=5 ULN; >5 ULN and <=10 ULN; >10 ULN and <=20 ULN; >20 ULN~Aspartate aminotransferase (AST): >1 ULN and <=1.5 ULN; >1.5 ULN and <=3 ULN; >3 ULN and <=5 ULN; >5 ULN and <=10 ULN; >10 ULN and <=20 ULN; >20 ULN~Alkaline phosphatase: >1.5 ULN~Total bilirubin (TBILI): >1.5 ULN; >2 ULN~Conjugated bilirubin(CBILI): >1.5 ULN~Unconjugated bilirubin: >1.5 ULN~ALT >3 ULN and TBILI >2 ULN~CBILI >35% TBILI and TBILI >1.5 ULN~Albumin: <=25 g/L" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
ALT >1 ULN and <=1.5 ULNALT >1.5 ULN and <=3 ULNALT >3 ULN and <=5 ULNALT >5 ULN and <=10 ULNALT >10 ULN and <=20 ULNALT >20 ULNAST >1 ULN and <=1.5 ULNAST >1.5 ULN and <=3 ULNAST >3 ULN and <=5 ULNAST >5 ULN and <=10 ULNAST >10 ULN and <=20 ULNAST >20 ULNAlkaline Phosphatase >1.5 ULNTBILI >1.5 ULNTBILI >2 ULNCBILI >1.5 ULNUnconjugated Bilirubin >1.5 ULNALT> 3 ULN and TBILI >2ULNCBILI >35% TBILI and TBILI >1.5 ULNAlbumin <=25 g/L
Sarilumab 150 mg q2w73100082000000000000
Sarilumab 150 mg q2w + DMARDs32110061100001000000
Sarilumab 200 mg q2w62400043100000000000
Sarilumab 200 mg q2w + DMARDs41000050000001000000

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Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Hematological Parameters

"Criteria for potentially clinically significant abnormalities:~Hemoglobin: <=115 g/L (Male[M]) or <=95 g/L (Female[F]); >=185 g/L (M) or >=165 g/L (F); DFB >=20 g/L~Hematocrit: <=0.37 v/v (M) or <=0.32 v/v (F); >=0.55 v/v (M) or >=0.5 v/v (F)~Red blood cells (RBC): >=6 Tera/L~Platelets: <50 Giga/L; >=50 and <100 Giga/L; >=700 Giga/L~White blood cells (WBC): <3.0 Giga/L (Non-Black [NB]) or <2.0 Giga/L (Black [B]); >=16.0 Giga/L~Neutrophils: <1.5 Giga/L (NB) or <1.0 Giga/L (B); <1.0 Giga/L~Lymphocytes: <0.5 Giga/L; >=0.5 Giga/L and 4.0 Giga/L~Monocytes: >0.7 Giga/L~Basophils: >0.1 Giga/L~Eosinophils: >0.5 Giga/L or >upper limit of normal (ULN) (if ULN >=0.5 Giga/L)" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
Hemoglobin <=115 g/L (M) or <=95 g/L (F)Hemoglobin >=185 g/L (M) or >=165 g/L (F)Hemoglobin DFB >=20 g/LHematocrit <=0.37 v/v (M) or <=0.32 v/v (F)Hematocrit >0.55 v/v (M) or >=0.5 v/v (F)RBC >=6 Tera/LPlatelets <50 Giga/LPlatelets >=50 and <100 Giga/LPlatelets >=700 Giga/LWBC <3.0 Giga/L (NB) or <2.0 Giga/L (B)WBC >=16.0 Giga/LNeutrophils <1.5 Giga/L (NB) or <1.0 Giga/L (B)Neutrophils <1.0 Giga/LLymphocytes <0.5 Giga/LLymphocytes >=0.5 Giga/L and Lymphocytes >4.0 Giga/LMonocytes >0.7 Giga/LBasophils >0.1 Giga/LEosinophils >0.5 Giga/L or >ULN (ULN >=0.5 Giga/L)
Sarilumab 150 mg q2w1002000107082030302
Sarilumab 150 mg q2w + DMARDs0000000106085030110
Sarilumab 200 mg q2w30260000090134180252
Sarilumab 200 mg q2w + DMARDs10030001090113041000

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Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Metabolic Parameters

"Criteria for potentially clinically significant abnormalities:~Glucose: <=3.9 mmol/L and =11.1 mmol/L (unfasted [unfas]) or >=7 mmol/L (fasted [fas])~Hemoglobin A1c (HbA1c): >8%~Total cholesterol: >=6.2 mmol/L; >=7.74 mmol/L~LDL cholesterol: >=4.1 mmol/L; >=4.9 mmol/L~Triglycerides: >=4.6 mmol/L; >=5.6 mmol/L" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
Glucose <=3.9 mmol/L and Glucose >=11.1 mmol/L (unfas) or >=7 mmol/L (fas)HbA1c >8%Total Cholesterol >=6.2 mmol/LTotal Cholesterol >=7.74 mmol/LLDL Cholesterol >=4.1 mmol/LLDL Cholesterol >=4.9 mmol/LTriglycerides >=4.6 mmol/LTriglycerides >=5.6 mmol/L
Sarilumab 150 mg q2w1001216200
Sarilumab 150 mg q2w + DMARDs000611000
Sarilumab 200 mg q2w1211323111
Sarilumab 200 mg q2w + DMARDs010713100

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Number of Participants With Potentially Clinically Significant Electrocardiogram (ECG) Abnormalities

"Criteria for potentially clinically significant ECG abnormalities:~PR Interval: >200 milliseconds (ms); >200 ms and IFB >=25%; >220 ms; >220 ms and IFB >=25%; >240 ms; >240 ms and IFB >=25%~QRS Interval: >110 ms; >110 ms and IFB >=25%; >120 ms; >120 ms and IFB >=25%~QT Interval: >500 ms~QTc Bazett (QTc B): >450 ms; >480 ms; >500 ms; IFB >30 and <=60 ms, IFB >60 ms~QTc Fridericia (QTc F): >450 ms; >480 ms; >500 ms; IFB >30 and <=60 ms; IFB >60 ms" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
PR >200 msPR >200 ms and IFB >=25%PR >220 msPR >220 ms and IFB >=25%PR >240 msPR >240 ms and IFB >=25%QRS >110 msQRS >110 ms and IFB >=25%QRS >120 msQRS >120 ms and IFB >=25%QT >500 msQTc B >450 msQTc B >480 msQTc B >500 msQTc B IFB >30 and <=60 msQTc B IFB >60 msQTc F >450 msQTc F >480 msQTc F >500 msQTc F IFB >30 and <=60 msQTc F IFB >60 ms
Sarilumab 150 mg q2w000000000006002020000
Sarilumab 150 mg q2w + DMARDs000000000002000020000
Sarilumab 200 mg q2w1010001000110101061000
Sarilumab 200 mg q2w + DMARDs000000202001101010000

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Number of Participants With Potentially Clinically Significant Laboratory Abnormalities: Electrolytes

"Criteria for potentially clinically significant abnormalities:~Sodium: <=129 mmol/L; >=160 mmol/L~Potassium: <3 mmol/L; >=5.5 mmol/L~Chloride: <80 mmol/L; >115 mmol/L" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
Sodium <=129 mmol/LSodium >=160 mmol/LPotassium <3 mmol/LPotassium >=5.5 mmol/LChloride <80 mmol/LChloride >115 mmol/L
Sarilumab 150 mg q2w000000
Sarilumab 150 mg q2w + DMARDs000000
Sarilumab 200 mg q2w000000
Sarilumab 200 mg q2w + DMARDs000000

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Change From Baseline in Health Assessment Questionnaire-Disability Index (HAQ-DI) Score at Week 52

HAQ-DI assessed the degree of difficulty participants experienced in 8 daily living activity domains during a week: dressing/grooming, arising, eating, walking, hygiene, reach, grip, and other activities. Each activity category consisted of 2-3 items. Each items's difficulty was scored from 0-3 (0=no difficulty, 1=some difficulty, 2=much difficulty, 3=unable to do). Overall HAQ-DI score was computed as the sum of domain scores divided by the number of domains answered, providing a score from 0-3. Low scores denoted improvement of disability/lower degree of domain difficulty. (NCT02373202)
Timeframe: Baseline, Week 52

Interventionunits on a scale (Mean)
Sarilumab 150 mg q2w + DMARDs-0.52
Sarilumab 200 mg q2w + DMARDs-0.34
Sarilumab 150 mg q2w-0.48
Sarilumab 200 mg q2w-0.38

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Change From Baseline at Week 52 in Disease Activity Score for 28 Joints Based on C-Reactive Protein (DAS28-CRP)

DAS28-CRP is a composite score that contains 4 variables: TJC (based on 28 joints), SJC (based on 28 joints), participant's assessment of general health on VAS (range 0 [very well] to 100 mm [extremely bad]) and CRP (mg/L). DAS28-CRP total score ranges from 2-10 with a lower score indicating less disease activity. A DAS28-CRP above 5.1 indicates high disease activity, whereas below 3.2 indicates low disease activity and below 2.6 as disease remission. (NCT02373202)
Timeframe: Baseline, Week 52

Interventionunits on a scale (Mean)
Sarilumab 150 mg q2w + DMARDs-2.90
Sarilumab 200 mg q2w + DMARDs-2.47
Sarilumab 150 mg q2w-2.62
Sarilumab 200 mg q2w-2.64

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Number of Participants With Potentially Clinically Significant Vital Signs Abnormalities

"Criteria for potentially clinically significant vital sign abnormalities:~Systolic blood pressure (SBP) supine: <=95 mmHg and decrease from baseline (DFB) >=20 mmHg; >=160 mmHg and increase from baseline (IFB) >=20 mmHg~Diastolic blood pressure (DBP) supine: <=45 mmHg and DFB >=10 mmHg; >=110 mmHg and IFB ≥10 mmHg~SBP (Orthostatic): <=-20 mmHg~DBP (Orthostatic): <=-10 mmHg~Heart rate (HR) supine: <=50 beats per minute (bpm) and DFB >=20 bpm; >=120 bpm and IFB >=20 bpm~Weight: >=5% DFB; >=5% IFB" (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
SBP (supine) <=95 mmHg and DFB >=20 mmHgSBP (supine) >=160 mmHg and IFB >=20 mmHgDBP (supine) <=45 mmHg and DFB >=10 mmHgDBP (supine) >=110 mmHg and IFB >=10 mmHgSBP (orthostatic) <=-20 mmHgDBP (orthostatic) <=-10 mmHgHR (supine) <=50 bpm and DFB >= 20 bpmHR (supine) >=120 bpm and IFB >=20 bpmWeight >=5% DFBWeight >=5% IFB
Sarilumab 150 mg q2w01005510212
Sarilumab 150 mg q2w + DMARDs0100830013
Sarilumab 200 mg q2w01009101007
Sarilumab 200 mg q2w + DMARDs0100530012

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Number of Participants With Treatment-Emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

Adverse event (AE) was defined as any untoward medical occurrence in a participant who received IMP and did not necessary have to had a causal relationship with treatment. All AEs that occurred from the first dose of the IMP administration up to 6 weeks after last dose of treatment (up to Week 58) were considered as TEAEs. SAEs were AEs resulting in any of the following outcomes or deemed significant for any other reason: death; initial or prolonged inpatient hospitalization; life-threatening experience (immediate risk of dying); persistent or significant disability/incapacity; congenital anomaly or a medically important event. TEAEs included both SAEs and non-SAEs. (NCT02373202)
Timeframe: Baseline up to Week 58

,,,
Interventionparticipants (Number)
Any TEAESAE
Sarilumab 150 mg q2w251
Sarilumab 150 mg q2w + DMARDs140
Sarilumab 200 mg q2w282
Sarilumab 200 mg q2w + DMARDs133

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Percentage of Participants Achieving American College of Rheumatology (ACR) 20, 50 and 70 Responses at Week 52

ACR response is a composite rating scale that includes 7 variables: tender joints count (TJC [68 joints]); swollen joints count (SJC [66 joints]); levels of an acute phase reactant (high sensitivity C-reactive protein [hs-CRP level]); participant's assessment of pain (measured on 0 [no pain]-100 mm [worst pain] visual analog scale [VAS]); participant's global assessment of disease activity (measured on 0 [no arthritis activity]-100 mm [maximal arthritis activity] VAS); physician's global assessment of disease activity (measured on 0 [no arthritis activity]-100 mm [maximal arthritis activity] VAS); participant's assessment of physical function (measured by Health Assessment Question-Disability Index [HAQ-DI], with scoring range of 0 [better health] - 3 [worst health]). ACR20/50/70 response is defined as at least 20/50/70% improvement in both TJC and SJC, and at least 20/50/70% improvement in at least 3 of the 5 other assessments, respectively. (NCT02373202)
Timeframe: Week 52

,,,
Interventionpercentage of participants (Number)
ACR20ACR50ACR70
Sarilumab 150 mg q2w76.756.726.7
Sarilumab 150 mg q2w + DMARDs73.360.053.3
Sarilumab 200 mg q2w74.254.825.8
Sarilumab 200 mg q2w + DMARDs40.033.326.7

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Change From Baseline in the Average TBR of the Bilateral Carotids

"The outcome was the change in the target to background ratio (TBR) of the average of the left and right carotids as measured by FDG-PET/CT scans conducted at baseline and after 24 weeks of randomized treatment allocation (MDS meanmaxTBR). The baseline values of the left and right carotids were averaged and then the follow-up values of the left and right carotids were averaged resulting in one value at each time point. Higher values indicate greater vascular inflammation.~FDG uptake measurement: PET-CT images were batch-analyzed by an investigator blinded to the patients' clinical information. FDG uptake was evaluated within the wall of the ascending aorta and bilateral carotid arteries (as maximum and mean standardized FDG uptake value [SUVmax and SUVmean, respectively]) approximately every 5 mm on axial images. Subsequently, the target-to-background ratio (TBR) was reported (ratio of the average arterial to blood axial slice SUVmax) to correct for the blood compartment contribution. (NCT02374021)
Timeframe: 0, 6 months

InterventionRatio (Mean)
Triple Therapy (MTX+SSZ+HCQ)-0.10
TNF Inhibitor (Etanercept or Adalimumab)-0.06

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Change From Baseline in the Average TBR of the Aorta

"The outcome was the change in the target to background ratio (TBR) of the aorta as measured by FDG-PET/CT scans conducted at baseline and after 24 weeks of randomized treatment allocation (MDS meanmaxTBR). Higher values indicate greater vascular inflammation.~FDG uptake measurement: PET-CT images were batch-analyzed by an investigator blinded to the patients' clinical information. FDG uptake was evaluated within the wall of the ascending aorta and bilateral carotid arteries (as maximum and mean standardized FDG uptake value [SUVmax and SUVmean, respectively]) approximately every 5 mm on axial images. Subsequently, the target-to-background ratio (TBR) was reported (ratio of the average arterial to blood axial slice SUVmax) to correct for the blood compartment contribution." (NCT02374021)
Timeframe: 0, 6 months

InterventionRatio (Mean)
Triple Therapy (MTX+SSZ+HCQ)-0.06
TNF Inhibitor (Etanercept or Adalimumab)-0.02

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Change From Baseline in the Average TBR of the Index Vessel

"The outcome was the change in the target to background ratio (TBR) in the index vessel as measured by FDG-PET/CT scans conducted at baseline and after 24 weeks of randomized treatment allocation (MDS meanmaxTBR). Higher values indicate greater vascular inflammation.~FDG uptake measurement: PET-CT images were batch-analyzed by an investigator blinded to the patients' clinical information. FDG uptake was evaluated within the wall of the ascending aorta and bilateral carotid arteries (as maximum and mean standardized FDG uptake value [SUVmax and SUVmean, respectively]) approximately every 5 mm on axial images. Subsequently, the target-to-background ratio (TBR) was reported (ratio of the average arterial to blood axial slice SUVmax) to correct for the blood compartment contribution." (NCT02374021)
Timeframe: 0, 6 months

InterventionRatio (Mean)
Triple Therapy (MTX+SSZ+HCQ)-0.07
TNF Inhibitor (Etanercept or Adalimumab)-0.09

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Change From Baseline in the MDS of the Aorta

"The outcome was the change in the mean of the maximum of the target to background ratio (TBR) in the most diseased segment (MDS) of the aorta as measured by FDG-PET/CT scans conducted at baseline and after 24 weeks of randomized treatment allocation (MDS meanmaxTBR). Higher values indicate greater vascular inflammation.~FDG uptake measurement: PET-CT images were batch-analyzed by an investigator blinded to the patients' clinical information. FDG uptake was evaluated within the wall of the ascending aorta and bilateral carotid arteries (as maximum and mean standardized FDG uptake value [SUVmax and SUVmean, respectively]) approximately every 5 mm on axial images. Subsequently, the target-to-background ratio (TBR) was reported (ratio of the average arterial to blood axial slice SUVmax) to correct for the blood compartment contribution." (NCT02374021)
Timeframe: 0, 6 months

InterventionRatio (Mean)
Triple Therapy (MTX+SSZ+HCQ)-0.17
TNF Inhibitor (Etanercept or Adalimumab)-0.17

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Change From Baseline in Vascular Inflammation as Measured by FDG-PET/CT at 6 Months

"The primary outcome was the change in the mean of the maximum of the target to background ratio (TBR) in the most diseased segment (MDS) of of the index vessel as measured by FDG-PET/CT scans conducted at baseline and after 24 weeks of randomized treatment allocation (MDS meanmaxTBR). The index vessel is the vessel (either aorta, left carotid, or right carotid) with the highest meanmaxTBR at baseline. Higher values indicate greater vascular inflammation.~FDG uptake measurement: PET-CT images were batch-analyzed by an investigator blinded to the patients' clinical information. FDG uptake was evaluated within the wall of the ascending aorta and bilateral carotid arteries (as maximum and mean standardized FDG uptake value [SUVmax and SUVmean, respectively]) approximately every 5 mm on axial images. Subsequently, the target-to-background ratio (TBR) was reported (ratio of the average arterial to blood axial slice SUVmax) to correct for the blood compartment contribution." (NCT02374021)
Timeframe: 0, 6 months

Interventionratio (Mean)
Triple Therapy (MTX+SSZ+HCQ)-0.19
TNF Inhibitor (Etanercept or Adalimumab)-0.24

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Indian Health Assessment Questionnaire (iHAQ)

Indian version of Health assessment Questionnaire (iHAQ) Comprises of 12 questions relating to functional activity iHAQ score ranges from 0 to 3 (minimum 0, maximum 3) Higher scores indicate more disability (NCT02930343)
Timeframe: 12 weeks

Interventionscore on a scale (Median)
Group 1- MTX+LEF+HCQ0.7
Group 2- MTX+SSZ+HCQ0.5

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Number of Patients Achieving Good EULAR Response at the End of 12 Weeks

"EULAR response criteria for Rheumatoid arthritis includes- estimation of DAS 28 ESR, that includes-~Tender joint count 28~Swollen joint count 28~ESR~Patient global assessment of health" (NCT02930343)
Timeframe: 12 weeks

Interventionparticipants (Number)
Group 1- MTX+LEF+HCQ40
Group 2- MTX+SSZ+HCQ37

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Number of Participants With Adverse Drug Reactions

Infections, transaminitis, nausea, vomiting, derranged renal function tests etc (NCT02930343)
Timeframe: 24 weeks

,
InterventionParticipants (Count of Participants)
Total number of any adverse eventsSerious adverse eventsAny gastrointestinal adverse reactionNauseaDiarrheaSwitch to parenteral MethotrexateRaised liver enzymes > 2 times upper limit normalHerpes labialisupper respiratory tract infectionurinary tract infectionHypertensionhairfallCytopenia
Group 1- MTX+LEF+HCQ150114151051120
Group 2- MTX+SSZ+HCQ2101661141250020

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Disease Activity as Per Ultrasound-7 (US-7) Score

Ultrasound 7 score (US-7) Calculates ultrasound score in 7 joints using greyscale and power doppler to evaluate for disease activity (synovitis, tenosynovitis) and damage (erosions) Score minimum value= 0 Maximum value = 108 Higher score indicates worse disease (NCT02930343)
Timeframe: 12 weeks

Interventionunits on a scale (Median)
Group 1- MTX+LEF+HCQ3.5
Group 2- MTX+SSZ+HCQ4

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Change From Baseline in Multidimensional Assessment of Thymic States Scale Total Score at Weeks 4, 12 and 24

MAThyS was a multi-dimensional self-administered questionnaire comprised of five dimensions (emotional reactivity, cognition speed, psychomotor function, motivation and sensory perception) divided into 20 items relating to individual states as perceived by participants for the preceding week (at each specified Week). Each item was measured on a VAS (in cm) ranging from 0 (inhibition of the state evaluated by the item) to 10 (excitation for the evaluated state). Total MAThyS score was sum of the 20 items and that might vary from score range 0 to 200 with lower scores indicated general inhibition and higher scores indicated general excitation. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventioncm (Mean)
Week 4Week 12Week 24
Sarilumab-0.22.9-1.1

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Change From Baseline in Number of Swelling Joints at Weeks 4, 12, and 24

Number of joints with swelling are reported. Joints which were assessed included 28 joints (which included shoulders, elbows, wrists, knees and 2 joints in each finger and thumb). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionjoints (Mean)
Week 4Week 12Week 24
Sarilumab-3.9-4.1-4.7

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Change From Baseline in Number of Tender Joints at Weeks 4, 12, and 24

Number of joints with tenderness are reported. Joints which were assessed included 28 joints (which included shoulders, elbows, wrists, knees and 2 joints in each finger and thumb). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionjoints (Mean)
Week 4Week 12Week 24
Sarilumab-2.5-3.7-4.8

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Change From Baseline in Patient Global Assessment of Disease Activity Score by Visual Analog Scale at Weeks 4, 12, and 24

PtGA of disease activity was measured using a 100 mm horizontal VAS ranged from 0=no pain to 100=maximum pain imaginable, where higher score indicated more disease activity. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionmm (Mean)
Week 4Week 12Week 24
Sarilumab-17.2-24.3-26.7

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Change From Baseline in Rheumatoid Arthritis Impact of Disease Total Score at Weeks 4 and 12

RAID was a participant reported outcome measure used to evaluate the impact of RA on participant's quality of life which comprised 7 domains: • pain, • function, • fatigue, • physical and psychological wellbeing, • sleep disturbance, and • coping. Each domain was a single question scored on a 0 to 10 continuous NRS. The values for each of these domains were weighed by participant assessment of relative importance and combined in a single value. Total RAID score range was 0 (not affected, very good) to 10 (most affected), where higher value indicated worse status. (NCT03449758)
Timeframe: Baseline, Weeks 4 and 12

Interventionscore on a scale (Mean)
Week 4Week 12
Sarilumab-1.2-1.8

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Change From Baseline in Disease Activity Score-28 for Rheumatoid Arthritis With Erythrocyte Sedimentation Rate at Weeks 4, 12, and 24

DAS28-ESR was a composite score that included 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); participant's global assessment of health activity using 100 mm VAS: range 0 (no pain) to 100 (maximum pain imaginable); marker of inflammation assessed by ESR in mm/h. DAS28-ESR total score ranged from 0-10, higher score indicated more disease activity. The DAS28-ESR score provided a number indicating the current disease activity of the RA. A DAS28-ESR score above 5.1 indicated high disease activity, DAS28-ESR score <= 3.2 indicated LDA, > 3.2 to <=5.1 implied moderate disease activity and DAS28-ESR score below 2.6 indicated disease remission. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
Week 4Week 12Week 24
Sarilumab-1.8-2.3-2.7

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Change From Baseline in Rheumatoid Arthritis Impact of Disease Total Score at Week 24

RAID was a participant reported outcome measure used to evaluate the impact of RA on participant's quality of life which comprised 7 domains: • pain, • function, • fatigue, • physical and psychological well-being, • sleep disturbance, and • coping. Each domain was a single question scored on a 0 to 10 continuous NRS. The values for each of these domains were weighed by participant assessment of relative importance and combined in a single value. Total RAID score range was 0 (not affected, very good) to 10 (most affected), where higher value indicated worse status. (NCT03449758)
Timeframe: Baseline, Week 24

Interventionscore on a scale (Mean)
Sarilumab-2.4

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Change From Baseline in Clinical Disease Activity Index Total Score at Weeks 4, 12, and 24

CDAI was a composite index constructed to measure clinical remission in RA that does not include a laboratory test, and is a numerical summation of 4 components: SJC (28 joints), TJC (28 joints), participant's global disease activity (in cm), and physician's global assessment of disease (in cm). CDAI total score ranges from 0 to 76 with a lower score indicating less disease activity. A CDAI score of <=2.8 represents clinical remission and a score of <=10.0 represents LDA. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
Week 4Week 12Week 24
Sarilumab-9.8-12.2-14.6

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Change From Baseline in Duration of Morning Stiffness at Weeks 4, 12, and 24

Duration of morning stiffness was defined as the time elapsed (in minutes) between the time of usual awakening (even if not in the morning) and the time the participant was able to resume normal activities without stiffness. At each specified time point, duration of morning stiffness was reported by the participant during the visit. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionminutes (Mean)
Week 4Week 12Week 24
Sarilumab-39.9-47.9-52.8

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Stanford Health Assessment Questionnaire Disability Index (HAQ-DI) Total Score at Baseline, Weeks 4, 12 and 24

HAQ-DI was a participant-oriented questionnaire developed specifically to assess the extent of a RA participant's functional ability. It consisted of at least 2 or 3 questions per category, participant reported assessment of ability to perform tasks in 8 categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week (at each specified visit) rated on a 4-point scale where 0 = no difficulty; 1 = some difficulty; 2 = much difficulty; 3 = unable to do. Overall score was computed as the sum of category scores and divided by the number of categories answered, and ranged from 0 to 3, where 0 = no disability and 3 = completely disabled, higher score indicated more disability. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab1.31.10.80.8

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Rheumatoid Arthritis Impact of Disease Total Score at Baseline, Weeks 4, 12 and 24

RAID was a participant reported outcome measure used to evaluate the impact of RA on participant's quality of life which comprised 7 domains: • pain, • function, • fatigue, • physical and psychological well-being, • sleep disturbances, and • coping. Each domain was a single question scored on a 0 to 10 continuous NRS. The values for each of these domains were weighed by participant assessment of relative importance and combined in a single value. Total RAID score range was 0 (not affected, very good) to 10 (most affected), where higher value indicated worse status. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
Week 4Week 12Week 24
Sarilumab4.63.93.3

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Erythrocyte Sedimentation Rate (ESR) at Baseline, Weeks 4, 12, and 24

ESR was a laboratory test to provide non-specific measure of inflammation in the body. The test assessed the rate at which red blood cells fell in a test tube and was measured in millimeter per hour (mm/h). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionmm/h (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab28.810.59.28.4

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Number of Tender Joints at Baseline, Weeks 4, 12, and 24

Number of joints with tenderness are reported. Joints which were assessed included 28 joints (which included shoulders, elbows, wrists, knees and 2 joints in each finger and thumb). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionjoints (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab7.34.73.52.5

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Number of Swollen Joints at Baseline, Weeks 4, 12, and 24

Number of joints with swelling are reported. Joints which were assessed included 28 joints (which included shoulders, elbows, wrists, knees and 2 joints in each finger and thumb). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionjoints (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab6.32.51.91.6

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Number of Participants With Treatment-emergent Adverse Events (TEAEs) and Serious Adverse Events (SAEs)

An adverse event (AE) was defined as any untoward medical occurrence in a participant who received study drug and did not necessarily had a causal relationship with the study treatment. SAE: Any untoward medical occurrence that resulted in any of the following outcomes: death, life-threatening, required initial or prolonged in-patient hospitalization, persistent or significant disability/incapacity, congenital anomaly/birth defect, or considered as medically important event. TEAEs were defined as AEs that occurred in the time from the first injection of study drug up to 39.7 weeks. (NCT03449758)
Timeframe: Baseline up to end of study (up to 39.7 weeks)

InterventionParticipants (Count of Participants)
SAETEAEAE leading to death
Sarilumab10760

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Number of Participants Achieving Low Disease Activity (DAS28 ESR Score <=3.2) and Remission (DAS28 ESR Score <2.6) at Weeks 12, and 24

DAS28-ESR was a composite score that included 4 variables: TJC (based on 28 joints); SJC (based on 28 joints); participant's global assessment of health activity using 100 mm VAS: range 0 (no pain) to 100 (maximum pain imaginable) marker of inflammation assessed by ESR in mm/h. DAS28-ESR total score ranged from 0-10, higher score indicated more disease activity. The DAS28-ESR score provided a number indicating the current disease activity of the RA. A DAS28-ESR score above 5.1 indicated high disease activity, DAS28-ESR score <= 3.2 indicated LDA, > 3.2 to <=5.1 implied moderate disease activity and DAS28-ESR score below 2.6 indicated disease remission. (NCT03449758)
Timeframe: Weeks 12 and 24

InterventionParticipants (Count of Participants)
LDA: Week 12LDA: Week 24Remission: Week 12Remission: Week 24
Sarilumab1244045

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Number of Participants Achieving Clinical Disease Activity Index: Low Disease Activity (CDAI Score <=10.0) and Remission (CDAI Score <=2.8) Weeks 12, and 24

CDAI was a composite index constructed to measure clinical remission in RA that does not included a laboratory test, and is a numerical summation of 4 components: SJC (28 joints), TJC (28 joints), participant's global disease activity (in cm), and physician's global assessment (in cm). Total score ranged from 0 to 76 with a lower score indicated less disease activity. A CDAI score of <=2.8 represents clinical remission and a score of <=10.0 represents LDA. (NCT03449758)
Timeframe: Weeks 12 and 24

InterventionParticipants (Count of Participants)
LDA: Week 12LDA: Week 24Remission: Week 12Remission: Week 24
Sarilumab29291820

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Change From Baseline in Erythrocyte Sedimentation Rate at Weeks 4, 12, and 24

ESR was a laboratory test to provide non-specific measure of inflammation in the body. The test assessed the rate at which red blood cells fell in a test tube and was measured in mm/h. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionmm/h (Mean)
Week 4Week 12Week 24
Sarilumab-18.1-19.5-22.0

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Change From Baseline in Hospital Anxiety and Depression Scale: Anxiety (HADS-A) and Depression (HADS-D) Subscale Scores at Weeks 4, 12 and 24

HADS questionnaire measures the presence and severity of anxiety and depression in both hospital and community settings. The questionnaire comprised of 14 items divided into 2 subscales: 7 items for anxiety subscale (HADS-A) and 7 items for depression subscale (HADS-D). Each item was scored on a 0 to 3 rating scale. The anxiety and depression subscales each ranged from 0 to 21 (0-7: normal, 8-10: borderline abnormal and 11-21: abnormal), where higher scores indicated greater severity of anxiety/depression. The subscales were independent for each result of depression and anxiety. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
HADS-A: Week 4HADS-A: Week 12HADS-A: Week 24HADS-D: Week 4HADS-D: Week 12HADS-D: Week 24
Sarilumab-1.0-2.1-1.9-0.4-1.2-1.7

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Change From Baseline in International Physical Activity Questionnaire Total Score at Weeks 4, 12 and 24

IPAQ was a 27-item self-reported questionnaire designed to measure physical activity of participant. The score was reported in MET minutes per week. MET minutes represented the amount of energy expended to carry out physical activity. For IPAQ total score, the minimum value is zero and there is no maximum. Higher scores mean better levels of physical activity. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

InterventionMET minutes per week (Mean)
Week 4Week 12Week 24
Sarilumab175.6533.4382.0

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Change From Baseline in Functional Assessment of Chronic Illness Therapy - Fatigue Total Scores at Weeks 4, 12 and 24

FACIT-F was a 13-item questionnaire that assess fatigue in participants under chronic illness therapy. Participants scored each item on a 5-point Likert scale ranged from 0 to 4 (0 = not at all; 1 = a little bit; 2 = somewhat; 3 = quite a bit; 4 = very much). The scores of each item were reversed during score calculations, so that higher score values indicated more favorable conditions. Total score was the sum of score from each item and resulted in a score range from 0 to 52, with higher score indicated better participant health status (lower level of fatigue). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
Week 4Week 12Week 24
Sarilumab-4.8-6.4-7.6

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Multidimensional Assessment of Thymic States (MAThyS) Scale Total Score at Baseline, Weeks 4, 12 and 24

MAThyS was a multi-dimensional self-administered questionnaire comprised of five dimensions (emotional reactivity, cognition speed, psychomotor function, motivation and sensory perception) divided into 20 items relating to individual states as perceived by participants for the preceding week (at each specified Week). Each item was measured on a visual analog scale (VAS; in centimeters [cm]) ranged from 0 (inhibition of the state evaluated by the item) to 10 (excitation for the evaluated state). Total MAThyS score was sum of the 20 items and that might vary from score range 0 to 200 with lower scores indicated general inhibition and higher scores indicated general excitation. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventioncm (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab88.489.694.890.9

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International Physical Activity Questionnaire (IPAQ) Total Score at Baseline, Weeks 4, 12 and 24

IPAQ was a 27-item self-reported questionnaire designed to measure physical activity of participant. The score was reported in metabolic equivalent (MET)-minutes per week. MET minutes represented the amount of energy expended to carry out physical activity. For IPAQ total score, the minimum value is zero and there is no maximum. Higher scores mean better levels of physical activity. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

InterventionMET minutes per week (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab1759.91881.12061.02089.5

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Hospital Anxiety and Depression Scale (HADS): Anxiety (HADS-A) and Depression (HADS-D) Subscale Scores at Baseline, Weeks 4, 12, and 24

HADS questionnaire measures the presence and severity of anxiety and depression in both hospital and community settings. The questionnaire comprised of 14 items divided into 2 subscales: 7 items for anxiety subscale (HADS-A) and 7 items for depression subscale (HADS-D). Each item was scored on a 0 to 3 rating scale. The anxiety and depression subscales each ranged from 0 to 21 (0-7: normal, 8-10: borderline abnormal and 11-21: abnormal), where higher scores indicated greater severity of anxiety/depression. The subscales were independent for each result of depression and anxiety. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
HADS-A: BaselineHADS-A: Week 4HADS-A: Week 12HADS-A: Week 24HADS-D: BaselineHADS-D: Week 4HADS-D: Week 12HADS-D: Week 24
Sarilumab8.17.26.16.67.06.65.75.5

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Functional Assessment of Chronic Illness Therapy - Fatigue (FACIT-F) Total Scores at Baseline, Weeks 4, 12 and 24

FACIT-F was a 13-item questionnaire that assess fatigue in participants under chronic illness therapy. Participants scored each item on a 5-point Likert scale ranged from 0 to 4 (0 = not at all; 1 = a little bit; 2 = somewhat; 3 = quite a bit; 4 = very much). The scores of each item were reversed during score calculations, so that higher score values indicated more favorable conditions. Total score was the sum of score from each item and resulted in a score range from 0 to 52, with higher score indicated better participant health status (lower level of fatigue). (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab25.521.018.817.9

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Duration of Morning Stiffness at Baseline, Weeks 4, 12, and 24

Duration of morning stiffness was defined as the time elapsed (in minutes) between the time of usual awakening (even if not in the morning) and the time the participant was able to resume normal activities without stiffness. At each specified time point, duration of morning stiffness was reported by the participant during the visit. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionminutes (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab72.334.728.921.3

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Disease Activity Score-28 for Rheumatoid Arthritis With Erythrocyte Sedimentation Rate (DAS28-ESR) at Baseline, Weeks 4, 12, and 24

DAS28-ESR was a composite score that included 4 variables: tender joint count (TJC) (based on 28 joints); swollen joint count (SJC) (based on 28 joints); participant's global assessment of health activity using 100 mm VAS: range 0 (no pain) to 100 (maximum pain imaginable); marker of inflammation assessed by ESR in mm/h. DAS28-ESR total score ranged from 0-10, higher score indicated more disease activity. The DAS28-ESR score provided a number indicating the current disease activity of the RA. A DAS28-ESR score above 5.1 indicated high disease activity, DAS28-ESR score less than or equal to (<=) 3.2 indicated low disease activity (LDA), greater than (>) 3.2 to <=5.1 implied moderate disease activity and DAS28-ESR score below 2.6 indicated disease remission. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab5.03.12.62.3

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Clinical Disease Activity Index (CDAI) Total Score at Baseline, Weeks 4, 12, and 24

CDAI was a composite index constructed to measure clinical remission in RA that does not include a laboratory test, and is a numerical summation of 4 components: SJC (28 joints), TJC (28 joints), participant's global disease activity (in cm), and physician's global assessment of disease (in cm). CDAI total score ranges from 0 to 76 with a lower score indicating less disease activity. A CDAI score of <=2.8 represents clinical remission and a score of <=10.0 represents LDA. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab22.512.69.98.1

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Change From Baseline in Stanford Health Assessment Questionnaire Disability Index Total Score at Weeks 4, 12 and 24

HAQ-DI was a participant-oriented questionnaire developed specifically to assess the extent of a RA participant's functional ability. It consisted of at least 2 or 3 questions per category, participant reported assessment of ability to perform tasks in 8 categories of daily living activities: dress/groom; arise; eat; walk; reach; grip; hygiene; and common activities over past week (at each specified visit) rated on a 4-point scale where 0 = no difficulty; 1 = some difficulty; 2 = much difficulty; 3 = unable to do. Overall score was computed as the sum of category scores and divided by the number of categories answered, and ranged from 0 to 3, where 0 = no disability and 3 = completely disabled, higher score indicated more disability. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionscore on a scale (Mean)
Week 4Week 12Week 24
Sarilumab-0.2-0.4-0.5

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Patient Global Assessment (PtGA) of Disease Activity Score by Visual Analog Scale (VAS) at Baseline, Weeks 4, 12 and 24

PtGA of disease activity was measured using a 100 millimeters (mm) horizontal VAS ranged from 0=no pain to 100=maximum pain imaginable, where higher score indicated more disease activity. (NCT03449758)
Timeframe: Baseline, Weeks 4, 12 and 24

Interventionmm (Mean)
BaselineWeek 4Week 12Week 24
Sarilumab61.144.136.634.6

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Number of Participants Who Are Eligible, Consent, and Complete the 48 Weeks Study

To establish acceptability of this treatment approach assessing proportion of patients who are eligible, consent and complete the 48 week study. We will examine how many patients in the MONITOR cohort are eligible per year. All eligible patients in the MONITOR cohort will be approached and invited to join the study. We will then review how many patients complete the 48 week study period attending all visits from baseline to 48 weeks (0, 12, 24, 36 and 48). (NCT03797872)
Timeframe: 48 weeks

InterventionParticipants (Count of Participants)
Standard Care0

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