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Please be aware that this old REACH registration data factsheet is no longer maintained; it remains frozen as of 19th May 2023.

The new ECHA CHEM database has been released by ECHA, and it now contains all REACH registration data. There are more details on the transition of ECHA's published data to ECHA CHEM here.

Diss Factsheets

Toxicological information

Specific investigations: other studies

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Administrative data

Link to relevant study record(s)

Reference
Endpoint:
biochemical or cellular interactions
Type of information:
experimental study
Adequacy of study:
key study
Reliability:
2 (reliable with restrictions)
Principles of method if other than guideline:
The PubChem BioAssay database was searched for chemogenomic, medicinal chemistry and functional genomics biological activities
Type of method:
in vivo
Specific details on test material used for the study:
PubChem CID: 84733
Substance SID: 144211799
Details on results:
150 bioassays were retrieved from the PubChem BioAssay data base. DMDO was inactive in 136 bioassays and inconclusive in 14 bioassays.

The list of all the assays performed is displayed in the enclosed excel file.

Executive summary:

The PubChem BioAssay database was searched for chemogenomic, medicinal chemistry and functional genomics biological activities. 150 bioassays were retrieved. DMDO was inactive in 136 bioassays and inconclusive in 14 bioassays. DMDO had no agonist and antagonist activities on the androgen receptor (AR), estrogen receptor alpha (ER-alpha), peroxisome proliferator-activated receptor gamma (PPARg) and delta (PPARd), glucocorticoid receptor (GR) and the farnesoid-X-receptor (FXR) signaling pathways.

Description of key information

Using a high-throughput robotic screening system (US EPA, 2017), DMDO was assessed for its potential to disrupt biological pathways (nuclear factor, erythroid 2-like 2, androgen receptor, aryl hydrocarbon receptor, cytochrome P450, family 19, subfamily A, polypeptide 1, ATPase family, AAA domain containing 5, estrogen receptor 1, activating transcription factor 6, nuclear receptor subfamily 1, group H, member 4, nuclear receptor subfamily 3, group C, member 1 (glucocorticoid receptor), heat shock transcription factor 1, nuclear factor of kappa light polypeptide gene enhancer in B-cells 1, peroxisome proliferator-activated receptor delta, thyroid hormone receptor, beta, cytochrome P450, family 24, subfamily A, polypeptide 1, and tumor protein p53) that may result in toxicity. 113 assays were performed. Cytotoxicity was assessed in 20 assays, no cytotoxicity was observed up to 100µM. DMDO induced a positive response in only 2 assays, which were flagged as "Noisy data" and deemed not reliable. Therefore, there is no evidence that DMDO could interfere with the expression of the screened genes.

The PubChem BioAssay database was searched for chemogenomic, medicinal chemistry and functional genomics biological activities (NCBI, 2017). 150 bioassays were retrieved. DMDO was inactive in 136 bioassays and inconclusive in 16 bioassays. DMDO had no agonist and antagonist activities on the androgen receptor (AR), estrogen receptor alpha (ER-alpha), peroxisome proliferator-activated receptor gamma (PPARg) and delta (PPARd), glucocorticoid receptor (GR) and the farnesoid-X-receptor (FXR) signaling pathways.

Additional information