| 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:8 | Upregulation of Thyroid Hormone Catabolism via Activation of Hepatic Nuclear Receptors, and Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Nervous system disease | Under Development | Rat | 0.11 | KE:295 | Induction, Upregulation of glucuronyltransferase activity |
| AOP:64 | Glucocorticoid Receptor (GR) Mediated Adult Leydig Cell Dysfunction Leading to Decreased Male Fertility | Reproductive system disease | - | Rattus norvegicus | 0.29 | KE:520 | Decreased sperm quantity or quality in the adult, Decreased fertility |
| KE:496 | Increased apoptosis, decreased fetal/adult Leydig Cells | ||||||
| AOP:194 | Hepatic nuclear receptor activation leading to altered amphibian metamorphosis | Unclassified | - | African clawed frog | 0.17 | KE:295 | Induction, Upregulation of glucuronyltransferase activity |
| AOP:420 | Aryl hydrocarbon receptor activation leading to lung cancer through sustained NRF2 toxicity pathway | Cancer | - | 0.25 | KE:1917 | Altered gene expression, NRF2 dependent antioxidant pathway | |
| 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:458 | AhR activation in the liver leading to Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Cognitive disorder | - | Rat, Mouse, Monkey, Human | 0.12 | KE:295 | Induction, Upregulation of glucuronyltransferase activity |
| AOP:504 | SULT1E1 inhibition leading to uterine adenocarcinoma via increased estrogen availability at target organ level | Unclassified | - | Mammals | 0.33 | KE:2251 | Estradiol availability, increased |
| AOP:561 | Aromatase induction leading to estrogen receptor alpha activation via increased estradiol | Unclassified | - | Vertebrates | 0.4 | KE:2294 | Plasma estradiol, increased |
| KE:2251 | Estradiol availability, increased |
| 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:21 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via increased COX-2 | Unclassified | WPHA/WNT Endorsed | Zebrafish, Medaka, Gallus gallus | 0.2 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:91 | Sodium channel inhibition leading to reduced survival | Unclassified | - | Medaka, Gammarus pulex, Hydra | 0.17 | KE:592 | Reduced, survival |
| AOP:95 | Ether-a-go-go (ERG) voltage-gated potassium channel inhibition leading to reduced survival | Unclassified | - | 0.17 | KE:592 | Reduced, survival | |
| AOP:99 | Histamine (H2) receptor antagonism leading to reduced survival | Unclassified | - | Zebrafish | 0.14 | KE:636 | Decreased, survival |
| AOP:139 | Alkylation of DNA leading to cancer 1 | Cancer | - | Homo sapiens, Mus musculus | 0.25 | KE:885 | Increase, Cancer |
| AOP:150 | Aryl hydrocarbon receptor activation leading to early life stage mortality, via reduced VEGF | Unclassified | WPHA/WNT Endorsed | Chicken, Zebrafish, Mouse, Rattus norvegicus | 0.14 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:212 | Histone deacetylase inhibition leading to testicular atrophy | Reproductive system disease | WPHA/WNT Endorsed | Rat, Human, Mouse | 0.17 | KE:1506 | Testicular atrophy |
| AOP:242 | Inhibition of lysyl oxidase leading to enhanced chronic fish toxicity | Unclassified | - | Fish | 0.12 | KE:636 | Decreased, survival |
| AOP:321 | Reduced environmental pH leading to thinner shells in Mytilus edulis | Unclassified | - | 0.18 | KE:592 | Reduced, survival | |
| KE:361 | Decline, Population | ||||||
| AOP:322 | Alkylation of DNA leading to reduced sperm count | Reproductive system disease | - | 0.2 | KE:1757 | Reduce, Sperm count | |
| AOP:323 | PPARalpha Agonism Leading to Decreased Viable Offspring via Decreased 11-Ketotestosterone | Unclassified | - | Teleost fish | 0.17 | KE:2147 | Decreased, Viable Offspring |
| AOP:455 | Aryl hydrocarbon receptor activation leading to early life stage mortality via sox9 repression induced impeded craniofacial development | Musculoskeletal system disease | Under Review | Zebrafish, Mouse, Human, Sebastiscus marmoratus, Salmo salar, Chicken | 0.17 | KE:947 | Increase, Early Life Stage Mortality |
| AOP:456 | Aryl hydrocarbon receptor activation leading to early life stage mortality via sox9 repression induced cardiovascular toxicity | Unclassified | Under Review | Zebrafish, Mouse, Human, Chicken | 0.17 | KE:947 | Increase, Early Life Stage Mortality |
| 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:521 | Essential element imbalance leads to reproductive failure via oxidative stress | Unclassified | - | Murinae gen. sp. | 0.29 | KE:2206 | Increased, histomorphological alteration of testis |
| KE:2147 | Decreased, Viable Offspring | ||||||
| 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:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| AOP:447 | Kidney failure induced by inhibition of mitochondrial electron transfer chain through apoptosis, inflammation and oxidative stress pathways | Urinary system disease | - | 0.08 | KE:1917 | Altered gene expression, NRF2 dependent antioxidant pathway |
| 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:201 | Juvenile hormone receptor agonism leading to male offspring induction associated population decline | Unclassified | - | Daphnia magna, Daphnia pulex | 1.0 | KE:1210 | Alteration, Food-web structures |
| KE:1205 | Activation, Juvenile hormone receptor | ||||||
| KE:361 | Decline, Population | ||||||
| KE:1208 | Increased, Male offspring | ||||||
| KE:1209 | Induction, Male reproductive tract | ||||||
| KE:1206 | Induction, Doublesex1 gene |
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.