| 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: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:107 | Constitutive androstane receptor activation leading to hepatocellular adenomas and carcinomas in the mouse and the rat | Cancer; Gastrointestinal system disease | Under Review | Rattus norvegicus, Mus musculus | 0.2 | KE:1214 | Altered gene expression specific to CAR activation, Hepatocytes |
| 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: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:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| 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: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.