| 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:131 | Aryl hydrocarbon receptor activation leading to uroporphyria | Inherited metabolic disorder | WPHA/WNT Endorsed | Mouse, Rat, Human, Japanese quail, Chicken, Herring gull, Common Starling | 0.17 | KE:850 | Induction, CYP1A2/CYP1A5 |
| 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:209 | Perturbation of cholesterol and glutathione homeostasis leading to hepatotoxicity: Integrated multi-OMICS approach for building AOP | Gastrointestinal system disease | - | 0.12 | KE:1289 | Perturbation of cholesterol | |
| AOP:305 | 5α-reductase inhibition leading to short anogenital distance (AGD) in male (mammalian) offspring | Unclassified | Under Development | Rat, Human, Mouse | 0.2 | KE:1614 | Decrease, androgen receptor activation |
| AOP:306 | Androgen receptor (AR) antagonism leading to short anogenital distance (AGD) in male (mammalian) offspring | Unclassified | Under Development | Rat, Human, Mouse | 0.25 | KE:1614 | Decrease, androgen receptor activation |
| AOP:344 | Androgen receptor (AR) antagonism leading to nipple retention (NR) in male (mammalian) offspring | Unclassified | Under Development | 0.25 | KE:1614 | Decrease, androgen receptor activation | |
| AOP:345 | Androgen receptor (AR) antagonism leading to decreased fertility in females | Endocrine system disease; Reproductive system disease; Reproductive system disease | Under Development | Mammals | 0.17 | KE:1614 | Decrease, androgen receptor activation |
| AOP:372 | Androgen receptor antagonism leading to testicular cancer | Endocrine system disease; Reproductive system disease; Cancer | - | 0.2 | KE:1614 | Decrease, androgen receptor activation | |
| 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:459 | AhR activation in the thyroid leading to Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Cognitive disorder | - | Human, Mouse, Rat | 0.11 | KE:850 | Induction, CYP1A2/CYP1A5 |
| AOP:477 | Androgen receptor (AR) antagonism leading to hypospadias in male (mammalian) offspring | Physical disorder | - | 0.33 | KE:1614 | Decrease, androgen receptor activation |
| 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:463 | The AOP framwork on silica nanopariticles induced hepatoxicity | Gastrointestinal system disease | - | 0.09 | KE:2034 | liver dysfunction | |
| 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: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:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:60 | NR1I2 (Pregnane X Receptor, PXR) activation leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.08 | KE:245 | Activation, PXR/SXR | |
| AOP:111 | Decrease in androgen receptor activity leading to Leydig cell tumors (in rat) | Cancer; Reproductive system disease | - | Rattus norvegicus | 0.2 | KE:1614 | Decrease, androgen receptor activation |
| 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 | 0.25 | KE:1609 | Inhibition, Cytochrome P450 enzyme (CYP17A1) activity |
| KE:1614 | Decrease, androgen receptor activation | ||||||
| AOP:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| 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: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: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:517 | Pregnane X Receptor (PXR) activation leads to liver steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | Vertebrates | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.23 | KE:2217 | Binding of antagonist to glucocorticoid hormone receptor | |
| KE:2115 | Altered, cholesterol metabolism | ||||||
| KE:2220 | Antagonism, Glucocorticoid hormone receptor | ||||||
| AOP:545 | Activation, Pregnane-X receptor, NR1l2 leads to increased plasma low-density lipoprotein (LDL) cholesterol via increased cholesterol synthesis | Unclassified | - | Mammals | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
| AOP:548 | Activation, Pregnane-X receptor, NR1l2 leads to increased plasma low-density lipoprotein (LDL) cholesterol via increased PCSK9 protein expression | Unclassified | - | Mammals | 0.2 | KE:239 | Activation, Pregnane-X receptor, NR1l2 |
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.