| 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:96 | Axonal sodium channel modulation leading to acute mortality | Unclassified | - | Insects, Fish | 0.17 | KE:602 | Increased, Ataxia, paralysis, or hyperactivity |
| 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:113 | Glutamate-gated chloride channel activation leading to acute mortality | Unclassified | - | Bombus impatiens, Chaetanaphothrips orchidii, Radopholus similis, Daphnia magna, Orius insidiosus, Hymenoptera, Helicoverpa zea, Lepidoptera, Liriomyza trifolii, Orius isidiosus, Acyrthosiphon kondoi | 0.17 | KE:764 | N/A, Ataxia, paralysis, or hyperactivity |
| 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: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: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: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 | 0.2 | 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: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:16 | Acetylcholinesterase inhibition leading to acute mortality | Unclassified | Under Development | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:64 | Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male Fertility | Reproductive system disease | - | Rattus norvegicus | 0.14 | KE:494 | Glucocorticoid Receptor Agonist, Activation |
| AOP:281 | Acetylcholinesterase Inhibition Leading to Neurodegeneration | Nervous system disease | - | 0.1 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:288 | Inhibition of 17α-hydrolase/C 10,20-lyase (Cyp17A1) activity leads to birth reproductive defects (cryptorchidism) in male (mammals) | Endocrine system disease | - | Human, Rat | 0.12 | KE:1609 | Inhibition, Cytochrome P450 enzyme (CYP17A1) activity |
| AOP:312 | Acetylcholinesterase Inhibition leading to Acute Mortality via Impaired Coordination & Movement​ | Unclassified | - | 0.17 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| AOP:318 | Glucocorticoid Receptor activation leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.2 | KE:122 | Activation, Glucocorticoid Receptor | |
| AOP:334 | Glucocorticoid Receptor Agonism Leading to Impaired Fin Regeneration | Unclassified | - | Teleost fish | 0.17 | KE:122 | Activation, Glucocorticoid Receptor |
| AOP:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| AOP:405 | Organo-Phosphate Chemicals induced inhibition of AChE leading to impaired cognitive function | Cognitive disorder | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:445 | Estrogen Receptor Alpha Agonism leads to Impaired Reproduction | Reproductive system disease | - | 0.25 | KE:1065 | Activation, estrogen receptor alpha | |
| KE:1987 | Decreased, Androgen and Progestin | ||||||
| AOP:450 | Inhibition of AChE and activation of CYP2E1 leading to sensory axonal peripheral neuropathy and mortality | Nervous system disease | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| 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:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.15 | KE:2217 | Binding of antagonist to glucocorticoid hormone receptor | |
| KE:2220 | Antagonism, Glucocorticoid hormone receptor | ||||||
| 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 | |
| AOP:559 | Inhibition of acetylcholinesterase (AChE) leading to arrhythmias | Symptom | - | Human and other cells in culture, Rattus norvegicus, Dogs, Sus scrofa, Zebrafish, Insecta sp. BOLD:AAN5199 | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
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.