| 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:289 | Decrease, Translocator protein (TSPO) |
| 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: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:443 | DNA damage and mutations leading to Metastatic Breast Cancer | Thoracic disease; Cancer | Under Development | Human and other cells in culture, Human, Mice, Rat, Canine heartworm nematode, Yeast | 0.1 | KE:112 | Antagonism, Estrogen receptor |
| AOP:449 | Ceramide synthase inhibition leading to neural tube defects | Neural tube defect | - | 0.14 | KE:1502 | Histone deacetylase inhibition | |
| 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: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: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: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 | 0.4 | KE:885 | Increase, Cancer |
| KE:233 | Decreased, PPAR-gamma activation | ||||||
| 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: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:30 | Estrogen receptor antagonism leading to reproductive dysfunction | Unclassified | Under Review | Zebra danio, Fathead minnow, Medaka | 0.17 | KE:112 | Antagonism, Estrogen receptor |
| AOP:36 | Peroxisomal Fatty Acid Beta-Oxidation Inhibition Leading to Steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.12 | KE:233 | Decreased, PPAR-gamma activation | |
| AOP:167 | Early-life estrogen receptor activity leading to endometrial carcinoma in the mouse. | Reproductive system disease; Cancer | - | Mouse, Homo sapiens | 0.29 | KE:1065 | Activation, estrogen receptor alpha |
| KE:1064 | prepubertal increase, Estrogen receptor (ER) activity | ||||||
| AOP:212 | Histone deacetylase inhibition leading to testicular atrophy | Reproductive system disease | WPHA/WNT Endorsed | Rat, Human, Mouse | 0.17 | KE:1502 | Histone deacetylase inhibition |
| AOP:232 | NFE2/Nrf2 repression to steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.12 | KE:1417 | NFE2/Nrf2 repression | |
| AOP:274 | Histone deacetylase inhibition leads to impeded craniofacial development | Musculoskeletal system disease | - | 0.25 | KE:1502 | Histone deacetylase inhibition | |
| AOP:275 | Histone deacetylase inhibition leads to neural tube defects | Neural tube defect | - | 0.2 | KE:1502 | Histone deacetylase inhibition | |
| AOP:314 | Binding to estrogen receptor (ER)-α in immune cells leading to exacerbation of systemic lupus erythematosus (SLE) | Immune system disease; Musculoskeletal system disease | Under Development | Homo sapiens | 0.2 | KE:1710 | Binding to estrogen receptor (ER)-α in immune cells |
| 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 | 0.22 | KE:1046 | Suppression, Estrogen receptor (ER) activity |
| KE:1973 | Increased, estrogens | ||||||
| AOP:445 | Estrogen Receptor Alpha Agonism leads to Impaired Reproduction | Reproductive system disease | - | 0.12 | KE:1065 | Activation, estrogen receptor alpha | |
| AOP:493 | ERa inactivation alters AT expansion and functions and leads to insulin resistance and metabolically unhealthy obesity | Acquired metabolic disease | - | Mus musculus, Homo sapiens | 0.1 | KE:2126 | Estrogen receptor alpha inactivation |
| AOP:497 | ERa inactivation alters mitochondrial functions and insulin signalling in skeletal muscle and leads to insulin resistance and metabolic syndrome | Inherited metabolic disorder; Disease of metabolism | - | 0.12 | KE:2126 | Estrogen receptor alpha inactivation | |
| 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.