| 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:34 | LXR activation leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.08 | KE:89 | Synthesis, De Novo Fatty Acid (FA) | |
| AOP:39 | Covalent Binding, Protein, leading to Increase, Allergic Respiratory Hypersensitivity Response | Respiratory system disease | Under Development | Human, Mouse | 0.2 | KE:272 | Activation/Proliferation, T-cells |
| AOP:40 | Covalent Protein binding leading to Skin Sensitisation | Integumentary system disease | WPHA/WNT Endorsed | Mouse, Human | 0.2 | KE:272 | Activation/Proliferation, T-cells |
| AOP:41 | Sustained AhR Activation leading to Rodent Liver Tumours | Cancer; Gastrointestinal system disease | Under Review | Rattus sp. ABTC 42503, Mus sp. 2000082 | 0.2 | KE:139 | N/A, Hepatotoxicity, Hepatopathy, including a constellation of observable effects |
| AOP:54 | Inhibition of Na+/I- symporter (NIS) leads to learning and memory impairment | Developmental disorder of mental health | WPHA/WNT Endorsed | Homo sapiens, Rattus sp. | 0.1 | KE:425 | Decrease of Thyroidal iodide |
| AOP:58 | NR1I3 (CAR) suppression leading to hepatic steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | Human, Mouse, Rat | 0.06 | KE:458 | Increased, De Novo FA synthesis |
| AOP:134 | Sodium Iodide Symporter (NIS) Inhibition and Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Cognitive disorder | - | Rat, Homo sapiens | 0.11 | KE:425 | Decrease of Thyroidal iodide |
| AOP:176 | Sodium Iodide Symporter (NIS) Inhibition leading to altered amphibian metamorphosis | Unclassified | - | African clawed frog | 0.2 | KE:425 | Decrease of Thyroidal iodide |
| AOP:188 | Iodotyrosine deiodinase (IYD) inhibition leading to altered amphibian metamorphosis | Unclassified | - | African clawed frog | 0.2 | KE:425 | Decrease of Thyroidal iodide |
| AOP:220 | Cyp2E1 Activation Leading to Liver Cancer | Cancer; Gastrointestinal system disease | WPHA/WNT Endorsed | Rodents, Homo sapiens | 0.2 | KE:1393 | Hepatocytotoxicity |
| AOP:321 | Reduced environmental pH leading to thinner shells in Mytilus edulis | Unclassified | - | 0.09 | KE:10042 | Abnormal development | |
| AOP:518 | Liver X Receptor (LXR) activation leads to liver steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | Vertebrates | 0.2 | KE:89 | Synthesis, De Novo Fatty Acid (FA) |
| 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:269 | Elevated ATP demand for detoxification and repair mechanisms leading to impaired growth and development | Unclassified | - | 0.17 | KE:10013 | Impaired growth and development |
| 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:118 | Chronic cytotoxicity leading to hepatocellular adenomas and carcinomas (in mouse and rat) | Cancer; Gastrointestinal system disease | - | Mus musculus, Rattus norvegicus | 0.25 | KE:786 | Increase, Cytotoxicity (hepatocytes) |
| AOP:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
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.