Acetonylacetone
| Predicted ADME Properties | |||||
|---|---|---|---|---|---|
| Type | Property | Tool | Interpretation | Probability/Value | |
| Absorption | Caco-2 permeability | admetSAR | High | 65.84 % | |
| pkCSM | High | 1.406 cm/s | |||
| Human Intestinal Absorption | admetSAR | High | 82.93 % | ||
| pkCSM | High | 100 % | |||
| SwissADME | High | - | |||
| Human Oral Bioavailability | admetSAR | High Bioavailability | 76.08 % | ||
| Log Kp (Skin permeation) | pkCSM | High | -2.632 logkp (cm/h) | ||
| SwissADME | - | -7.19 logkp (cm/s) | |||
| Distribution | P-glycoprotein substrate | admetSAR | Low | 5.91 % | |
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No Prediction | - | |||
| P-glycoprotein inhibitor | admetSAR | Low | 3.76 % | ||
| vNN | No Prediction | - | |||
| P-glycoprotein inhibitor I | pkCSM | No | - | ||
| P-glycoprotein inhibitor II | pkCSM | No | - | ||
| Blood Brain Barrier | admetSAR | High | 87.42 % | ||
| pkCSM | Moderate | -0.187 logBB | |||
| SwissADME | Yes | - | |||
| vNN | No Prediction | - | |||
| CNS permeability | pkCSM | Moderate | -2.517 logPS | ||
| Fraction unbound in human | pkCSM | - | 0.689 | ||
| Plasma protein binding | admetSAR | 2.58 % | Weak | ||
| Steady state volume of distribution (VDss) | pkCSM | Low | -0.202 log(L/kg) | ||
| Metabolism | CYP1A2 inhibitor | admetSAR | Low | 9.26 % | |
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No | - | |||
| CYP2C19 inhibitor | admetSAR | Low | 9.07 % | ||
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No | - | |||
| CYP2C9 inhibitor | admetSAR | Low | 5.75 % | ||
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No | - | |||
| CYP2C9 substrate | admetSAR | Low | 6.16 % | ||
| CYP2D6 inhibitor | admetSAR | Low | 2.99 % | ||
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No | - | |||
| CYP2D6 substrate | admetSAR | Low | 7.89 % | ||
| pkCSM | No | - | |||
| CYP3A4 inhibitor | admetSAR | Low | 1.73 % | ||
| pkCSM | No | - | |||
| SwissADME | No | - | |||
| vNN | No | - | |||
| CYP3A4 substrate | admetSAR | Low | 2.3 % | ||
| pkCSM | No | - | |||
| Human Liver Microsomal (HLM) stability assay | vNN | No Prediction | - | ||
| OATP2B1 inhibitor | admetSAR | Low | 9.77 % | ||
| OATP1B1 inhibitor | admetSAR | High | 98.17 % | ||
| OATP1B3 inhibitor | admetSAR | High | 99.03 % | ||
| MATE1 inhibitor | admetSAR | Low | 7.78 % | ||
| BSEP inhibitor | admetSAR | Low | 5.85 % | ||
| UGT catalysis | admetSAR | High | 74.03 % | ||
| Excretion | Renal OCT2 inhibitor | admetSAR | Low | 13.74 % | |
| Renal OCT2 substrate | pkCSM | No | - | ||
| Total clearance | pkCSM | - | 0.761 ml/min/kg | ||
| Predicted Toxicity properties | ||||
|---|---|---|---|---|
| Property | Tool | Interpretation | Probability/Value | |
| Acute oral toxicity | admetSAR | - | -3.47136354446411 log(mg/kg) | |
| ProTox | - | 1600 mg/kg | ||
| Acute oral toxicity class | admetSAR | Low | 13.52 % | |
| ProTox | 4 | - | ||
| Biodegradation | admetSAR | High | 80.47 % | |
| Toxtree | Class 2 (persistent chemical) | - | ||
| Carcinogens | admetSAR | Low | 41.29 % | |
| Toxtree | No | - | ||
| Cramer's rule | Toxtree | High (Class III) | - | |
| Cytotoxicity | vNN | NoPrediction | - | |
| Genotoxic carcinogenity | Toxtree | No | - | |
| Hepatotoxicity | admetSAR | High | 62.02 % | |
| pkCSM | No | - | ||
| vNN | NoPrediction | - | ||
| Human Ether-a-go-go-Related Gene Inhibitor | admetSAR | Low | 12.82 % | |
| vNN | No | - | ||
| Human Ether-a-go-go-Related Gene Inhibitor I | pkCSM | No | - | |
| Human Ether-a-go-go-Related Gene Inhibitor II | pkCSM | No | - | |
| Mitochondrial Membrane Potential (MMP) | vNN | No | - | |
| Maximum Recommended Tolerated Dose (MRTD) | pkCSM | High | 1.036 log(mg/kg/day) | |
| vNN | - | NoPrediction | ||
| Non-Genotoxic carcinogenicity | Toxtree | No | - | |
| Oral rat acute toxicity | pkCSM | - | 1.894 log(mg/kg_bw/day) (LD50) | |
| pkCSM | - | 2.4 log(mg/kg_bw/day) (LOAEL) | ||
| Micronucleus | admetSAR | Low | 5.47 % | |
| Skin sensitisation | pkCSM | Yes | - | |
DISCLAIMER
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.