| 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:27 | Cholestatic Liver Injury induced by Inhibition of the Bile Salt Export Pump (ABCB11) | Gastrointestinal system disease | Under Development | Humans | 0.12 | KE:288 | Activation of specific nuclear receptors, Transcriptional change |
| 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:167 | Early-life estrogen receptor activity leading to endometrial carcinoma in the mouse. | Reproductive system disease; Cancer | - | Mouse, Homo sapiens | 0.14 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:465 | Alcohol dehydrogenase leading to reproductive dysfunction | Unclassified | - | 0.12 | KE:748 | Increased, Estrogen receptor (ER) activity | |
| 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:504 | SULT1E1 inhibition leading to uterine adenocarcinoma via increased estrogen availability at target organ level | Unclassified | - | Mammals | 0.33 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:561 | Aromatase induction leading to estrogen receptor alpha activation via increased estradiol | Unclassified | - | Vertebrates | 0.2 | KE:1065 | Activation, estrogen receptor alpha |
| 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:232 | NFE2/Nrf2 repression to steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.25 | KE:1417 | NFE2/Nrf2 repression | |
| KE:1419 | Reduced, FXR activity | ||||||
| AOP:445 | Estrogen Receptor Alpha Agonism leads to Impaired Reproduction | Reproductive system disease | - | 0.12 | KE:1065 | Activation, estrogen receptor alpha | |
| AOP:503 | Activation of uterine estrogen receptor-alfa leading to endometrial adenocarcinoma, via epigenetic modulation | Reproductive system disease; Cancer | Under Review | Human, Mouse | 0.17 | KE:1065 | Activation, estrogen receptor alpha |
| AOP:507 | Nrf2 inhibition leading to vascular disrupting effects via inflammation pathway | Cardiovascular system disease | - | Mouse, Zebrafish, Human | 0.17 | KE:1417 | NFE2/Nrf2 repression |
| AOP:508 | Nrf2 inhibition leading to vascular disrupting effects through activating HIF1α, Semaphorin 6A, and Dll4-Notch pathway | Cardiovascular system disease | - | Mouse, Zebrafish, Human | 0.14 | KE:1417 | NFE2/Nrf2 repression |
| AOP:509 | Nrf2 inhibition leading to vascular disrupting effects through activating apoptosis signal pathway and mitochondrial dysfunction | Cardiovascular system disease | - | 0.14 | KE:1417 | NFE2/Nrf2 repression | |
| 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.