| 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:48 | Binding of agonists to ionotropic glutamate receptors in adult brain causes excitotoxicity that mediates neuronal cell death, contributing to learning and memory impairment. | Developmental disorder of mental health | WPHA/WNT Endorsed | Human, Mouse, Rat | 0.11 | KE:352 | N/A, Neurodegeneration |
| 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:321 | Reduced environmental pH leading to thinner shells in Mytilus edulis | Unclassified | - | 0.09 | KE:10042 | Abnormal development | |
| AOP:374 | Binding of Sars-CoV-2 spike protein to ACE 2 receptors expressed on brain cells (neuronal and non-neuronal) leads to neuroinflammation resulting in encephalitis | Nervous system disease | Under Development | Human | 0.25 | KE:352 | N/A, Neurodegeneration |
| 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: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:352 | N/A, Neurodegeneration |
| AOP:497 | ERa inactivation alters mitochondrial functions and insulin signalling in skeletal muscle and leads to insulin resistance and metabolic syndrome | Inherited metabolic disorder; Disease of metabolism | - | 0.12 | KE:2144 | Impaired insulin signaling | |
| AOP:500 | Activation of MEK-ERK1/2 leads to deficits in learning and cognition via ROS and apoptosis | Developmental disorder of mental health | - | Rattus norvegicus, Mus musculus, Homo sapiens | 0.14 | KE:352 | N/A, Neurodegeneration |
| 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:12 | Chronic binding of antagonist to N-methyl-D-aspartate receptors (NMDARs) during brain development leads to neurodegeneration with impairment in learning and memory in aging | Nervous system disease; Developmental disorder of mental health | WPHA/WNT Endorsed | Monkey, Rat, Human, Mouse, Zebrafish | 0.12 | KE:352 | N/A, Neurodegeneration |
| AOP:260 | CYP2E1 activation and formation of protein adducts leading to neurodegeneration | Nervous system disease | - | Human | 0.14 | KE:1514 | Neurodegeneration |
| 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:270 | Elevated ATP demand for detoxification and repair mechanisms leading to impaired locomotor activity | Unclassified | - | 0.12 | KE:10016 | Impaired locomotor activity | |
| AOP:281 | Acetylcholinesterase Inhibition Leading to Neurodegeneration | Nervous system disease | - | 0.1 | KE:352 | N/A, Neurodegeneration |
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.