| 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:96 | Axonal sodium channel modulation leading to acute mortality | Unclassified | - | Insects, Fish | 0.17 | KE:602 | Increased, Ataxia, paralysis, or hyperactivity |
| AOP:113 | Glutamate-gated chloride channel activation leading to acute mortality | Unclassified | - | Bombus impatiens, Chaetanaphothrips orchidii, Radopholus similis, Daphnia magna, Orius insidiosus, Hymenoptera, Helicoverpa zea, Lepidoptera, Liriomyza trifolii, Orius isidiosus, Acyrthosiphon kondoi | 0.17 | KE:764 | N/A, Ataxia, paralysis, or hyperactivity |
| AOP:124 | HMG-CoA reductase inhibition leading to decreased fertility | Reproductive system disease | - | Rattus rattus | 0.17 | KE:807 | Decreased, cholesterol |
| 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:267 | Uncoupling of oxidative phosphorylation leading to growth inhibition via glucose depletion | Unclassified | Under Development | 0.2 | KE:2071 | Decrease, Glucose pool | |
| 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 | 0.12 | KE:1614 | Decrease, androgen receptor activation |
| 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:323 | PPARalpha Agonism Leading to Decreased Viable Offspring via Decreased 11-Ketotestosterone | Unclassified | - | Teleost fish | 0.17 | KE:807 | Decreased, cholesterol |
| AOP:414 | Aryl hydrocarbon receptor activation leading to lung fibrosis through TGF-β dependent fibrosis toxicity pathway | Musculoskeletal system disease; Respiratory system disease | - | 0.2 | KE:1920 | Altered gene expression, TGF-β dependent fibrosis pathway | |
| AOP:431 | Increased tumor necrosis factor (TNF) leading to increased risk of gestational diabetes mellitus (GDM) | Inherited metabolic disorder | - | Human | 0.2 | KE:1952 | Abnormal, Glucose homeostasis |
| AOP:525 | Reduced oligodendrocyte differentiation during neurodevelopment leading to impaired learning and memory | Developmental disorder of mental health | - | 0.08 | KE:2115 | Altered, cholesterol metabolism | |
| AOP:569 | Decreased DNA methylation of FAM50B/PTCHD3 leading to IQ loss of children via PI3K-Akt pathway | Developmental disorder of mental health | - | 0.17 | KE:2195 | Increase, CNS Neural cell death |
| 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:6 | Antagonist binding to PPARα leading to body-weight loss | Symptom | WPHA/WNT Endorsed | Mus musculus, Homo sapiens, Pimephales promelas, Colinus virginianus, Rattus norvegicus | 0.12 | KE:864 | Decreased, Body Weight |
| AOP:270 | Elevated ATP demand for detoxification and repair mechanisms leading to impaired locomotor activity | Unclassified | - | 0.12 | KE:10016 | Impaired locomotor activity |
| 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:16 | Acetylcholinesterase inhibition leading to acute mortality | Unclassified | Under Development | 0.29 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| KE:10 | Acetylcholine accumulation in synapses | ||||||
| AOP:19 | Androgen receptor antagonism leading to adverse effects in the male foetus (mammals) | Reproductive system disease | - | 0.2 | KE:26 | Antagonism, Androgen receptor | |
| AOP:27 | Cholestatic Liver Injury induced by Inhibition of the Bile Salt Export Pump (ABCB11) | Gastrointestinal system disease | Under Development | Humans | 0.12 | KE:41 | Inhibition, Bile Salt Export Pump (ABCB11) |
| 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:281 | Acetylcholinesterase Inhibition Leading to Neurodegeneration | Nervous system disease | - | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| KE:10 | Acetylcholine accumulation in synapses | ||||||
| AOP:306 | Androgen receptor (AR) antagonism leading to short anogenital distance (AGD) in male (mammalian) offspring | Unclassified | Under Development | Rat, Human, Mouse | 0.5 | KE:1614 | Decrease, androgen receptor activation |
| KE:26 | Antagonism, Androgen receptor | ||||||
| AOP:312 | Acetylcholinesterase Inhibition leading to Acute Mortality via Impaired Coordination & Movement | Unclassified | - | 0.33 | KE:12 | Acetylcholinesterase (AchE) Inhibition | |
| KE:10 | Acetylcholine accumulation in synapses | ||||||
| AOP:344 | Androgen receptor (AR) antagonism leading to nipple retention (NR) in male (mammalian) offspring | Unclassified | Under Development | 0.5 | KE:1614 | Decrease, androgen receptor activation | |
| KE:26 | Antagonism, Androgen receptor | ||||||
| AOP:345 | Androgen receptor (AR) antagonism leading to decreased fertility in females | Endocrine system disease; Reproductive system disease; Reproductive system disease | Under Development | Mammals | 0.33 | KE:1614 | Decrease, androgen receptor activation |
| KE:26 | Antagonism, Androgen receptor | ||||||
| AOP:372 | Androgen receptor antagonism leading to testicular cancer | Endocrine system disease; Reproductive system disease; Cancer | - | 0.4 | KE:1614 | Decrease, androgen receptor activation | |
| KE:26 | Antagonism, Androgen receptor | ||||||
| AOP:392 | Decreased fibrinolysis and activated bradykinin system leading to hyperinflammation | Unclassified | Under Development | Humans | 0.2 | KE:1866 | Fibrinolysis, decreased |
| AOP:405 | Organo-Phosphate Chemicals induced inhibition of AChE leading to impaired cognitive function | Cognitive disorder | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.4 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| KE:10 | Acetylcholine accumulation in synapses | ||||||
| AOP:450 | Inhibition of AChE and activation of CYP2E1 leading to sensory axonal peripheral neuropathy and mortality | Nervous system disease | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.14 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
| AOP:477 | Androgen receptor (AR) antagonism leading to hypospadias in male (mammalian) offspring | Physical disorder | - | 0.67 | KE:1614 | Decrease, androgen receptor activation | |
| KE:26 | Antagonism, Androgen receptor | ||||||
| AOP:559 | Inhibition of acetylcholinesterase (AChE) leading to arrhythmias | Symptom | - | Human and other cells in culture, Rattus norvegicus, Dogs, Sus scrofa, Zebrafish, Insecta sp. BOLD:AAN5199 | 0.2 | KE:12 | Acetylcholinesterase (AchE) Inhibition |
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.