Flutamide


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000731 Dna synthesis involved in dna repair Increases phenotype PMID:1347714
GO:0001568 Blood vessel development Decreases phenotype PMID:32662666
GO:0004784 Superoxide dismutase activity Decreases phenotype PMID:23135684
GO:0006629 Lipid metabolic process Affects phenotype PMID:35156134
GO:0006749 Glutathione metabolic process Increases phenotype PMID:25371773; PMID:26921665; PMID:8014883
GO:0006750 Glutathione biosynthetic process Decreases phenotype PMID:23135684; PMID:29407385; PMID:30426164
GO:0006754 Atp biosynthetic process Decreases phenotype PMID:29407385
GO:0006805 Xenobiotic metabolic process Increases phenotype PMID:29162470
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:23135684; PMID:31416231
GO:0006915 Apoptotic process Increases phenotype PMID:16293769; PMID:16301331; PMID:19635294; PMID:29606031
GO:0007204 Positive regulation of cytosolic calcium ion concentration Increases phenotype PMID:28762043
GO:0007283 Spermatogenesis Decreases phenotype PMID:14585929; PMID:32662666
GO:0007613 Memory Decreases phenotype PMID:24902786
GO:0007614 Short-term memory Decreases phenotype PMID:24902786
GO:0007616 Long-term memory Decreases phenotype PMID:24902786
GO:0008202 Steroid metabolic process Affects phenotype PMID:38176580
GO:0008219 Cell death Increases phenotype PMID:15190103
GO:0008283 Cell population proliferation Affects phenotype PMID:24189122; PMID:35598691
GO:0008284 Positive regulation of cell population proliferation Increases phenotype PMID:11118046; PMID:26485406
GO:0008285 Negative regulation of cell population proliferation Increases phenotype PMID:32739440
GO:0008610 Lipid biosynthetic process Affects phenotype PMID:30426164
GO:0008654 Phospholipid biosynthetic process Affects phenotype PMID:30426164
GO:0010918 Positive regulation of mitochondrial membrane potential Decreases phenotype PMID:25371773; PMID:26921665; PMID:28762043
GO:0010942 Positive regulation of cell death Increases phenotype PMID:23397584; PMID:25371773; PMID:25371773; PMID:8014883; PMID:28762043; PMID:8014883
GO:0014902 Myotube differentiation Affects phenotype PMID:36822333
GO:0016049 Cell growth Decreases phenotype PMID:29407385; PMID:30426164
GO:0030154 Cell differentiation Increases phenotype PMID:11466222; PMID:8912815
GO:0030521 Androgen receptor signaling pathway Increases phenotype PMID:19368227
GO:0030850 Prostate gland development Decreases phenotype PMID:1324152
GO:0032930 Positive regulation of superoxide anion generation Increases phenotype PMID:28762043
GO:0034109 Homotypic cell-cell adhesion Increases phenotype PMID:34049886
GO:0034440 Lipid oxidation Increases phenotype PMID:25371773
GO:0036211 Protein modification process Increases phenotype PMID:8014883; PMID:8386241
GO:0042554 Superoxide anion generation Affects phenotype PMID:30426164
GO:0042775 Mitochondrial atp synthesis coupled electron transport Decreases phenotype PMID:8014883
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:28762043
GO:0043433 Negative regulation of dna-binding transcription factor activity Increases phenotype PMID:26022396
GO:0044237 Cellular metabolic process Affects phenotype PMID:28176351
GO:0046622 Positive regulation of organ growth Decreases phenotype PMID:26485406
GO:0046660 Female sex differentiation Increases phenotype PMID:1324152; PMID:18340380
GO:0046661 Male sex differentiation Decreases phenotype PMID:1324152; PMID:18340380
GO:0048808 Male genitalia morphogenesis Decreases phenotype PMID:1324152; PMID:18340380; PMID:20002220
GO:0051881 Regulation of mitochondrial membrane potential Affects phenotype PMID:24189122; PMID:24189122; PMID:30426164; PMID:35156134
GO:0051965 Positive regulation of synapse assembly Increases phenotype PMID:29278848
GO:0055074 Calcium ion homeostasis Affects phenotype PMID:30426164
GO:0060081 Membrane hyperpolarization Affects phenotype PMID:35156134
GO:0060512 Prostate gland morphogenesis Decreases phenotype PMID:20002220
GO:0060736 Prostate gland growth Decreases phenotype PMID:26485406
GO:0060766 Negative regulation of androgen receptor signaling pathway Increases phenotype PMID:30247711
GO:0060999 Positive regulation of dendritic spine development Increases phenotype PMID:29278848
GO:0061068 Urethra development Affects phenotype PMID:32662666
GO:0061107 Seminal vesicle development Decreases phenotype PMID:1324152
GO:0061370 Testosterone biosynthetic process Decreases phenotype PMID:11118046
GO:0061682 Seminal vesicle morphogenesis Decreases phenotype PMID:20002220
GO:0061951 Establishment of protein localization to plasma membrane Increases phenotype PMID:30591588
GO:0070509 Calcium ion import Increases phenotype PMID:30707916
GO:0070994 Detection of oxidative stress Increases phenotype PMID:24486436
GO:0072593 Reactive oxygen species metabolic process Increases phenotype PMID:24189122; PMID:35156134
GO:1900272 Negative regulation of long-term synaptic potentiation Increases phenotype PMID:29278848
GO:1903409 Reactive oxygen species biosynthetic process Increases phenotype PMID:24136188; PMID:30426164
GO:1903428 Positive regulation of reactive oxygen species biosynthetic process Increases phenotype PMID:26921665; PMID:28762043
GO:1905867 Epididymis development Decreases phenotype PMID:1324152
GO:1990375 Baculum development Decreases phenotype PMID:32662666
GO:2000256 Positive regulation of male germ cell proliferation Increases phenotype PMID:17679765
GO:2000553 Positive regulation of t-helper 2 cell cytokine production Increases phenotype PMID:21735453
GO:2000825 Positive regulation of androgen receptor activity Increases phenotype PMID:31393563
GO:2000845 Positive regulation of testosterone secretion Increases phenotype PMID:26485406
GO:2001025 Positive regulation of response to drug Increases phenotype PMID:21735453
GO:2001171 Positive regulation of atp biosynthetic process Decreases phenotype PMID:26921665

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We have built a comprehensive resource which compiles potential endocrine disrupting chemicals (EDCs) based on the observed adverse effects or endocrine-mediated endpoints in published experiments on humans or rodents to support basic research. We are not responsible for any errors or omissions in the published research articles or supporting literature on potential EDCs compiled in this resource. Users are advised to exercise their own judgement on the weight of evidence for potential EDCs compiled in this resource. Importantly, our sole goal to build this resource on potential EDCs is to enable future basic research towards better understanding of the systems-level perturbations upon chemical exposure rather than influencing regulatory advice on chemical use.