| AOP Identifier | AOP Title | AO Classification | OECD Status | Taxonomic applicability | Coverage Score ⓘ The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints. | KE Identifier | KE Name |
|---|---|---|---|---|---|---|---|
| AOP:60 | NR1I2 (Pregnane X Receptor, PXR) activation leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.08 | KE:474 | Down Regulation, HMGCS2 | |
| AOP:108 | Inhibition of pyruvate dehydrogenase kinase leading to hepatocellular adenomas and carcinomas (in mouse and rat) | Cancer; Gastrointestinal system disease | - | Mus musculus, Rattus norvegicus | 0.17 | KE:726 | Increased, Induction of pyruvate dehydrogenase (PDH) |
| AOP:122 | Prolyl hydroxylase inhibition leading to reproductive dysfunction via increased HIF1 heterodimer formation | Unclassified | - | Pimephales promelas | 0.1 | KE:799 | Increased, HIF-1 heterodimer |
| AOP:207 | NADPH oxidase and P38 MAPK activation leading to reproductive failure in Caenorhabditis elegans | Reproductive system disease | - | Caenorhabditis elegans | 0.12 | KE:1280 | Activation, HIF-1 |
| AOP:439 | Activation of the AhR leading to metastatic breast cancer | Thoracic disease; Cancer | Under Development | Humans, Mice | 0.11 | KE:1971 | Increased, tumor growth |
| AOP:510 | Demethylation of PPAR promotor leading to vascular disrupting effects | Cardiovascular system disease | - | Human, Mouse, Zebrafish | 0.1 | KE:2165 | Activation of PPAR |
| AOP Identifier | AOP Title | AO Classification | OECD Status | Taxonomic applicability | Coverage Score ⓘ The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints. | KE Identifier | KE Name |
|---|---|---|---|---|---|---|---|
| AOP:139 | Alkylation of DNA leading to cancer 1 | Cancer | - | Homo sapiens, Mus musculus | 0.25 | KE:885 | Increase, Cancer |
| AOP:474 | Succinate dehydrogenase inactivation leads to cancer by promoting EMT | Cancer | Under Development | Human and other cells in culture | 0.2 | KE:885 | Increase, Cancer |
| AOP:505 | Reactive Oxygen Species (ROS) formation leads to cancer via inflammation pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:885 | Increase, Cancer |
| AOP:513 | Reactive Oxygen (ROS) formation leads to cancer via Peroxisome proliferation-activated receptor (PPAR) pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:885 | Increase, Cancer |
| AOP:534 | Succinate dehydrogenase (SDH) inhibition leads to cancer through oxidative stress | Cancer | - | Vertebrates | 0.17 | KE:885 | Increase, Cancer |
| AOP:546 | Succinate dehydrogenase inactivation leads to cancer through hypoxic-like mechanisms | Cancer | - | Human and other cells in culture | 0.2 | KE:885 | Increase, Cancer |
| AOP Identifier | AOP Title | AO Classification | OECD Status | Taxonomic applicability | Coverage Score ⓘ The fraction of KEs within the AOP, that are mapped to the chemical-associated toxicological endpoints. | KE Identifier | KE Name |
|---|---|---|---|---|---|---|---|
| AOP:18 | PPARα activation in utero leading to impaired fertility in males | Reproductive system disease | Under Review | Human, Rat, Mouse | 0.12 | KE:227 | Activation, PPARα |
| AOP:37 | PPARα activation leading to hepatocellular adenomas and carcinomas in rodents | Cancer; Gastrointestinal system disease | Under Development | Mouse, Rat | 0.2 | KE:227 | Activation, PPARα |
| AOP:123 | Unknown MIE leading to reproductive dysfunction via increased HIF-1alpha transcription | Unclassified | - | Pimephales promelas | 0.27 | KE:801 | modulation, Unknown |
| KE:802 | Increased, HIF-1 alpha transcription | ||||||
| KE:799 | Increased, HIF-1 heterodimer | ||||||
| AOP:323 | PPARalpha Agonism Leading to Decreased Viable Offspring via Decreased 11-Ketotestosterone | Unclassified | - | Teleost fish | 0.17 | KE:227 | Activation, PPARα |
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.