| 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:112 | Increased dopaminergic activity leading to endometrial adenocarcinomas (in Wistar rat) | Reproductive system disease; Cancer | - | Rattus norvegicus | 0.17 | KE:111 | Agonism, Estrogen receptor |
| AOP:414 | Aryl hydrocarbon receptor activation leading to lung fibrosis through TGF-β dependent fibrosis toxicity pathway | Musculoskeletal system disease; Respiratory system disease | - | 0.2 | KE:1920 | Altered gene expression, TGF-β dependent fibrosis pathway | |
| AOP:440 | Hypothalamus estrogen receptors activity suppression leading to ovarian cancer via ovarian epithelial cell hyperplasia | Benign neoplasm; Endocrine system disease; Reproductive system disease; Reproductive system disease; Cancer; Endocrine system disease | Under Development | Human, Rat, Mice | 0.11 | KE:1973 | Increased, estrogens |
| AOP:465 | Alcohol dehydrogenase leading to reproductive dysfunction | Unclassified | - | 0.12 | KE:748 | Increased, Estrogen receptor (ER) activity |
| 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:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| AOP:536 | Estrogen receptor agonism leading to reduced survival and population growth due to renal failure | Unclassified | - | 0.17 | KE:111 | Agonism, Estrogen receptor | |
| AOP:537 | Estrogen receptor agonism leads to reduced fecundity via increased vitellogenin in the liver | Unclassified | - | 0.2 | KE:111 | Agonism, Estrogen receptor |
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.