| 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:190 | Type II iodothyronine deiodinase (DIO2) inhibition leading to altered amphibian metamorphosis | Unclassified | - | African clawed frog | 0.17 | KE:1829 | Altered, Thyroid hormone-dependent gene expression |
| AOP:191 | Type III iodotyrosine deiodinase (DIO3) inhibition leading to altered amphibian metamorphosis | Unclassified | - | African clawed frog | 0.5 | KE:1154 | Increased, Triiodothyronine (T3) in tissues |
| KE:1829 | Altered, Thyroid hormone-dependent gene expression | ||||||
| AOP:232 | NFE2/Nrf2 repression to steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.12 | KE:1419 | Reduced, FXR activity | |
| AOP:419 | Aryl hydrocarbon receptor activation leading to impaired lung function through P53 toxicity pathway | Respiratory system disease | - | 0.25 | KE:1923 | Altered gene expression, P53 dependent apoptosis pathway | |
| AOP:441 | Ionizing radiation-induced DNA damage leads to microcephaly via apoptosis and premature cell differentiation | Congenital nervous system abnormality; Nervous system disease | - | Homo sapiens, Mus musculus musculus, Rattus norvegicus | 0.14 | KE:1974 | Activation of Tumor Protein 53 |
| AOP:460 | Antagonism of Smoothened receptor leading to orofacial clefting | Unclassified | Under Development | Mouse | 0.11 | KE:2043 | Decrease, Sonic Hedgehog second messenger production |
| AOP:491 | Decrease, GLI1/2 target gene expression leads to orofacial clefting | Unclassified | Under Development | Mouse | 0.17 | KE:2043 | Decrease, Sonic Hedgehog second messenger production |
| AOP:513 | Reactive Oxygen (ROS) formation leads to cancer via Peroxisome proliferation-activated receptor (PPAR) pathway | Cancer | - | Human, Mouse, Rat | 0.2 | KE:233 | Decreased, PPAR-gamma activation |
| AOP:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.08 | KE:1656 | Antagonism, Thyroid Receptor |
| 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:36 | Peroxisomal Fatty Acid Beta-Oxidation Inhibition Leading to Steatosis | Gastrointestinal system disease; Inherited metabolic disorder | - | 0.12 | KE:233 | Decreased, PPAR-gamma activation | |
| AOP:206 | Peroxisome proliferator-activated receptors γ inactivation leading to lung fibrosis | Musculoskeletal system disease; Respiratory system disease | Under Development | Homo sapiens | 0.17 | KE:1270 | Inactivation of PPARγ |
| AOP:300 | Thyroid Receptor Antagonism and Subsequent Adverse Neurodevelopmental Outcomes in Mammals | Cognitive disorder | Under Development | Human, Mouse | 0.2 | KE:1656 | Antagonism, Thyroid Receptor |
| AOP:347 | Toll-like receptor 4 activation and peroxisome proliferator-activated receptor gamma inactivation leading to pulmonary fibrosis | Musculoskeletal system disease; Respiratory system disease | - | 0.11 | KE:1270 | Inactivation of PPARγ | |
| AOP:485 | Thyroid hormone antagonism leading to impaired oligodendrocyte maturation during development and subsequent decreased cognition | Cognitive disorder | - | Human | 0.14 | KE:1656 | Antagonism, Thyroid Receptor |
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.