Tadalafil


Curated chemical-phenotype interactions from CTD
GO IDGO nameInteraction typeReference
GO:0000278 Mitotic cell cycle Increases phenotype PMID:16959227
GO:0001774 Microglial cell activation Increases phenotype PMID:31323263
GO:0002027 Regulation of heart rate Affects phenotype PMID:29233027
GO:0002158 Osteoclast proliferation Affects phenotype PMID:32513693
GO:0004035 Alkaline phosphatase activity Increases phenotype PMID:35608386
GO:0004340 Glucokinase activity Increases phenotype PMID:24911673
GO:0004346 Glucose-6-phosphatase activity Increases phenotype PMID:24911673
GO:0004457 Lactate dehydrogenase activity Increases phenotype PMID:35608386
GO:0004679 Amp-activated protein kinase activity Decreases phenotype PMID:34428446
GO:0004743 Pyruvate kinase activity Increases phenotype PMID:24911673
GO:0005980 Glycogen catabolic process Increases phenotype PMID:24911673
GO:0006006 Glucose metabolic process Affects phenotype PMID:35608386
GO:0006089 Lactate metabolic process Affects phenotype PMID:35608386
GO:0006749 Glutathione metabolic process Increases phenotype PMID:29233027; PMID:32621855
GO:0006809 Nitric oxide biosynthetic process Increases phenotype PMID:31323263
GO:0006915 Apoptotic process Affects phenotype PMID:18082193; PMID:20543097; PMID:21056623
GO:0006954 Inflammatory response Increases phenotype PMID:29233027
GO:0006979 Response to oxidative stress Increases phenotype PMID:20543097
GO:0007283 Spermatogenesis Decreases phenotype PMID:32621855
GO:0007612 Learning Decreases phenotype PMID:31323263
GO:0007613 Memory Decreases phenotype PMID:31323263
GO:0008184 Glycogen phosphorylase activity Decreases phenotype PMID:24911673
GO:0008283 Cell population proliferation Increases phenotype PMID:16959227; PMID:21056623
GO:0016042 Lipid catabolic process Affects phenotype PMID:29233027
GO:0019627 Urea metabolic process Affects phenotype PMID:35608386
GO:0030263 Apoptotic chromosome condensation Increases phenotype PMID:29233027
GO:0030282 Bone mineralization Increases phenotype PMID:32513693
GO:0032148 Activation of protein kinase b activity Decreases phenotype PMID:34428446
GO:0033687 Osteoblast proliferation Increases phenotype PMID:32513693
GO:0034440 Lipid oxidation Increases phenotype PMID:32621855
GO:0042310 Vasoconstriction Increases phenotype PMID:16368379
GO:0042311 Vasodilation Increases phenotype PMID:15464333; PMID:16368379
GO:0043065 Positive regulation of apoptotic process Increases phenotype PMID:32621855
GO:0045429 Positive regulation of nitric oxide biosynthetic process Increases phenotype PMID:32621855
GO:0046068 Cgmp metabolic process Increases phenotype PMID:34428446
GO:0046209 Nitric oxide metabolic process Affects phenotype PMID:29233027
GO:0046621 Negative regulation of organ growth Increases phenotype PMID:32621855
GO:0048143 Astrocyte activation Increases phenotype PMID:31323263
GO:0050729 Positive regulation of inflammatory response Increases phenotype PMID:32621855
GO:0050808 Synapse organization Decreases phenotype PMID:31323263
GO:0060048 Cardiac muscle contraction Decreases phenotype PMID:20543097
GO:0060348 Bone development Increases phenotype PMID:32513693
GO:0060612 Adipose tissue development Increases phenotype PMID:20471953
GO:0070265 Necrotic cell death Increases phenotype PMID:29233027
GO:0071902 Positive regulation of protein serine/threonine kinase activity Decreases phenotype PMID:34428446
GO:1901318 Negative regulation of flagellated sperm motility Increases phenotype PMID:32621855
GO:2000844 Negative regulation of testosterone secretion Increases phenotype PMID:32621855

DISCLAIMER

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.