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EC number: 210-871-0 | CAS number: 624-92-0
- Life Cycle description
- Uses advised against
- Endpoint summary
- Appearance / physical state / colour
- Melting point / freezing point
- Boiling point
- Density
- Particle size distribution (Granulometry)
- Vapour pressure
- Partition coefficient
- Water solubility
- Solubility in organic solvents / fat solubility
- Surface tension
- Flash point
- Auto flammability
- Flammability
- Explosiveness
- Oxidising properties
- Oxidation reduction potential
- Stability in organic solvents and identity of relevant degradation products
- Storage stability and reactivity towards container material
- Stability: thermal, sunlight, metals
- pH
- Dissociation constant
- Viscosity
- Additional physico-chemical information
- Additional physico-chemical properties of nanomaterials
- Nanomaterial agglomeration / aggregation
- Nanomaterial crystalline phase
- Nanomaterial crystallite and grain size
- Nanomaterial aspect ratio / shape
- Nanomaterial specific surface area
- Nanomaterial Zeta potential
- Nanomaterial surface chemistry
- Nanomaterial dustiness
- Nanomaterial porosity
- Nanomaterial pour density
- Nanomaterial photocatalytic activity
- Nanomaterial radical formation potential
- Nanomaterial catalytic activity
- Endpoint summary
- Stability
- Biodegradation
- Bioaccumulation
- Transport and distribution
- Environmental data
- Additional information on environmental fate and behaviour
- Ecotoxicological Summary
- Aquatic toxicity
- Endpoint summary
- Short-term toxicity to fish
- Long-term toxicity to fish
- Short-term toxicity to aquatic invertebrates
- Long-term toxicity to aquatic invertebrates
- Toxicity to aquatic algae and cyanobacteria
- Toxicity to aquatic plants other than algae
- Toxicity to microorganisms
- Endocrine disrupter testing in aquatic vertebrates – in vivo
- Toxicity to other aquatic organisms
- Sediment toxicity
- Terrestrial toxicity
- Biological effects monitoring
- Biotransformation and kinetics
- Additional ecotoxological information
- Toxicological Summary
- Toxicokinetics, metabolism and distribution
- Acute Toxicity
- Irritation / corrosion
- Sensitisation
- Repeated dose toxicity
- Genetic toxicity
- Carcinogenicity
- Toxicity to reproduction
- Specific investigations
- Exposure related observations in humans
- Toxic effects on livestock and pets
- Additional toxicological data
Specific investigations: other studies
Administrative data
Link to relevant study record(s)
- Endpoint:
- biochemical or cellular interactions
- Type of information:
- experimental study
- Adequacy of study:
- key study
- Reliability:
- 2 (reliable with restrictions)
- Rationale for reliability incl. deficiencies:
- other: data from iCSS CompTox Dashboard. Data Quality 100%. Data manually curated with highest confidence
- Principles of method if other than guideline:
- Using a high-throughput robotic screening system, DMDS was assessed for its potential to disrupt biological pathways (DNA binding, growth factor, nuclear receptor (non-steroidal and steroidal), cell cycle, cytochrome P450, hydrolase and cell morphology) that may result in toxicity.
- Type of method:
- in vitro
- Vehicle:
- DMSO
- Remarks:
- 0.001 to 100µM
- Details on study design:
- See enclosed excel file
- Details on results:
- 113 assays were performed, dimethyl disulphide did not induce a positive response. Therefore, there is no evidence that dimethyl disulphide could interfere with the expression of the screened genes.
- Executive summary:
Dimethyl disulphide was evaluated in 113 in vitro high-throughput screening (HTS) assays to evaluate the effects on a target genes like, DNA binding, nuclear receptor (non-steroidal and steroidal), cell cycle, cyp (cytochrome P450 19A1 and 24A1), hydrolase (ATPase) and cell morphology (organelle conformation). Dimethyl disulphide did not induce a positive response in any assay. Therefore, there is no evidence that dimethyl disulphide could interfere with the expression of the genes screened.
- 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: 12232
PubChem SID: 17389037 and 144208723 - Details on results:
- 299 bioassays with 311 bioactivity outcomes were retrieved from the PubChem BioAssay data base. Dimethyl disulphide was active in 2 bioassays: AID 1224879 (A CellTox Green Cytotoxicity Assay to monitor cytotoxicity in HepG2 cells - 40 hour) and AID 1224838 (qHTS assay to identify small molecule antagonists of the constitutive androstane receptor (CAR) signaling pathway). Positivity was also reported in a third assay - AID 1224893 (qHTS assay to identify small molecule antagonists of the constitutive androstane receptor (CAR) signaling pathway) : Summary - but it is in fact a summary of the 2 previous ones. An antagonist activity of CAR was observed with a very large inter-wells variability. Significant antagonist effects were observed at concentrations inducing a decrease of the cell viability. Therefore, the toxicological significance of this effect is questionable.
- Executive summary:
299 bioassays with 311 bioactivity outcomes were retrieved from the PubChem BioAssay data base. DMDS was inactive in 283 bioassays, inconclusive in 24 bioassays and positive in 2 bioassays. DMDS had no activity on cell viability assays, no agonist and antagonist activities on the peroxisome proliferator-activated receptor alpha (PPARa), delta (PPARd) and gamma (PPARg), androgen receptor (AR), estrogen receptor alpha (ER-alpha), thyroid receptor (TR) and glucocorticoid receptor (GR) signaling pathways. Positive results were obtained for antagonist activities on the constitutive androstane receptor (CAR) signaling pathway. An antagonist activity of CAR was observed with a very large inter-wells variability and significant antagonist effects were observed at concentrations inducing a decrease of the cell viability. Therefore, the toxicological significance of this effect is questionable.
Referenceopen allclose all
113 assays were performed, all results are displayed in the enclosed excel file.
Dimethyl disulphide did not induce a positive response (see attached figure and table).
Assay Name |
Hit Call |
Top |
Scaled Top |
AC50 |
log AC50 |
Intended Target Family |
TOX21_AR_BLA_Agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AR_BLA_Agonist_ch2 |
INACTIVE |
4.14 |
0.162 |
0.0190 |
-1.72 |
background measurement |
TOX21_AR_BLA_Agonist_ratio |
INACTIVE |
17.7 |
0.541 |
42.4 |
1.63 |
nuclear receptor |
TOX21_AR_BLA_Antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_AR_BLA_Antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_AR_LUC_MDAKB2_Agonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_AR_LUC_MDAKB2_Antagonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_Aromatase_Inhibition |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cyp |
TOX21_AutoFluor_HEK293_Cell_blue |
INACTIVE |
0.239 |
0.0120 |
28.3 |
1.45 |
background measurement |
TOX21_AutoFluor_HEK293_Cell_green |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEK293_Cell_red |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEK293_Media_blue |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEK293_Media_green |
INACTIVE |
0.171 |
0.00854 |
1.61 |
0.206 |
background measurement |
TOX21_AutoFluor_HEK293_Media_red |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Cell_blue |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Cell_green |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Cell_red |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Media_blue |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Media_green |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AutoFluor_HEPG2_Media_red |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ELG1_LUC_Agonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
hydrolase |
TOX21_ERa_BLA_Agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ERa_BLA_Agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ERa_BLA_Agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_ERa_BLA_Antagonist_ratio |
INACTIVE |
5.17 |
0.156 |
0.0158 |
-1.80 |
nuclear receptor |
TOX21_ERa_BLA_Antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_ERa_LUC_BG1_Agonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_ERa_LUC_BG1_Antagonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_GR_BLA_Agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_GR_BLA_Agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_GR_BLA_Agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_GR_BLA_Antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_GR_BLA_Antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_MMP_ratio_down |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell morphology |
TOX21_MMP_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_PPARg_BLA_Agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARg_BLA_Agonist_ch2 |
INACTIVE |
7.61 |
0.168 |
0.00434 |
-2.36 |
background measurement |
TOX21_PPARg_BLA_Agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_TR_LUC_GH3_Agonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_TR_LUC_GH3_Antagonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_AhR_LUC_Agonist |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_ARE_BLA_Agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ARE_BLA_Agonist_ch2 |
INACTIVE |
9.71 |
0.162 |
0.00163 |
-2.79 |
background measurement |
TOX21_ARE_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_HSE_BLA_agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_HSE_BLA_agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_HSE_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_p53_BLA_p1_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p1_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p1_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_FXR_BLA_agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_FXR_BLA_agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_FXR_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_FXR_BLA_antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_FXR_BLA_antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_PPARd_BLA_agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARd_BLA_agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARd_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_PPARd_BLA_antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_PPARd_BLA_antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_PPARg_BLA_antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
nuclear receptor |
TOX21_PPARg_BLA_antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_VDR_BLA_agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_VDR_BLA_agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_VDR_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cyp |
TOX21_VDR_BLA_antagonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cyp |
TOX21_VDR_BLA_antagonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_ARE_BLA_agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_HSE_BLA_agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_p53_BLA_p1_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_FXR_BLA_agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_ERa_BLA_Antagonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ERa_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_FXR_BLA_Antagonist_ch1 |
INACTIVE |
7.85 |
0.145 |
0.00339 |
-2.47 |
background measurement |
TOX21_FXR_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_GR_BLA_Antagonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_GR_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARd_BLA_Agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_PPARd_BLA_Antagonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARd_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARg_BLA_Antagonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_PPARg_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_VDR_BLA_Antagonist_ch1 |
INACTIVE |
124 |
0.280 |
6.25 |
0.796 |
background measurement |
TOX21_VDR_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AR_BLA_Antagonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_AR_BLA_Antagonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p2_ch1 |
INACTIVE |
46.7 |
0.341 |
0.00477 |
-2.32 |
background measurement |
TOX21_p53_BLA_p2_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p2_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_p53_BLA_p2_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_p53_BLA_p3_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p3_ch2 |
INACTIVE |
8.14 |
0.407 |
13.4 |
1.13 |
background measurement |
TOX21_p53_BLA_p3_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_p53_BLA_p3_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_p53_BLA_p4_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p4_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p4_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_p53_BLA_p4_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_p53_BLA_p5_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p5_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_p53_BLA_p5_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_p53_BLA_p5_viability |
INACTIVE |
25.7 |
0.373 |
1.65 |
0.218 |
cell cycle |
TOX21_VDR_BLA_Agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_ESRE_BLA_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ESRE_BLA_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_ESRE_BLA_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_ESRE_BLA_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_NFkB_BLA_agonist_ch1 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_NFkB_BLA_agonist_ch2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
background measurement |
TOX21_NFkB_BLA_agonist_ratio |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
dna binding |
TOX21_NFkB_BLA_agonist_viability |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell cycle |
TOX21_MMP_ratio_up |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
cell morphology |
TOX21_AR_LUC_MDAKB2_Antagonist2 |
INACTIVE |
0.00 |
0.00 |
1.00 |
0.00 |
- |
The list of all the assays performed is displayed in the enclosed excel file.
Detailled data for the positive assays and dose-response curves are diplayed below and in the attached file:
Data for SID 144208723 in AID 1224893, qHTS assay to identify small molecule antagonists of the constitutive androstane receptor (CAR) signaling pathway: Summary
Activity Summary |
active antagonist |
Antagonist Activity |
active antagonist |
Antagonist Potency (uM) [uM]* |
11.6555 |
Antagonist Efficacy (%) [%] |
-80.5488 |
Viability Activity |
inconclusive antagonist |
Viability Potency (uM) [uM] |
|
Viability Efficacy (%) [%] |
|
Sample Source |
SIGMA |
Data for SID 144208723 in AID 1224879, A CellTox Green Cytotoxicity Assay to monitor cytotoxicity in HepG2 cells - 40 hour
Phenotype-Replicate_1 |
Activator |
Potency-Replicate_1 [uM]* |
7.8566 |
Efficacy-Replicate_1 [%] |
36.8305 |
Analysis Comment-Replicate_1 |
|
Activity_Score-Replicate_1 |
41 |
Curve_Description-Replicate_1 |
Complete curve; partial efficacy |
Fit_LogAC50-Replicate_1 |
-5.1048 |
Fit_HillSlope-Replicate_1 |
2.7202 |
Fit_R2-Replicate_1 |
0.9106 |
Fit_InfiniteActivity-Replicate_1 [%] |
39.9203 |
Fit_ZeroActivity-Replicate_1 [%] |
3.0897 |
Fit_CurveClass-Replicate_1 |
1.2 |
Excluded_Points-Replicate_1 |
0 0 0 0 0 0 0 0 0 0 0 0 0 0 1 |
Max_Response-Replicate_1 [%] |
6.232 |
Activity at 0.00141 uM-Replicate_1 [%] |
4.5229 |
Activity at 0.00434 uM-Replicate_1 [%] |
-2.4082 |
Activity at 0.011 uM-Replicate_1 [%] |
11.0564 |
Activity at 0.025 uM-Replicate_1 [%] |
3.8875 |
Activity at 0.057 uM-Replicate_1 [%] |
5.674 |
Activity at 0.127 uM-Replicate_1 [%] |
-0.253 |
Activity at 0.290 uM-Replicate_1 [%] |
5.8506 |
Activity at 0.887 uM-Replicate_1 [%] |
2.8765 |
Activity at 2.716 uM-Replicate_1 [%] |
3.4419 |
Activity at 6.973 uM-Replicate_1 [%] |
18.8671 |
Activity at 15.76 uM-Replicate_1 [%] |
38.0003 |
Activity at 35.30 uM-Replicate_1 [%] |
36.5706 |
Data for SID 144208723 in AID 1224838, qHTS assay to identify small molecule antagonists of the constitutive androstane receptor (CAR) signaling pathway
Phenotype-Replicate_1 |
Inhibitor |
Potency-Replicate_1 [uM]* |
21.9549 |
Efficacy-Replicate_1 [%] |
83.1454 |
Analysis Comment-Replicate_1 |
|
Activity_Score-Replicate_1 |
41 |
Curve_Description-Replicate_1 |
Partial curve; high efficacy |
Fit_LogAC50-Replicate_1 |
-4.6585 |
Fit_HillSlope-Replicate_1 |
2.0437 |
Fit_R2-Replicate_1 |
0.9614 |
Fit_InfiniteActivity-Replicate_1 [%] |
-82.4946 |
Fit_ZeroActivity-Replicate_1 [%] |
0.6507 |
Fit_CurveClass-Replicate_1 |
-2.1 |
Excluded_Points-Replicate_1 |
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 |
Max_Response-Replicate_1 [%] |
-79.1617 |
Activity at 0.00170 uM-Replicate_1 [%] |
0.6152 |
Activity at 0.00522 uM-Replicate_1 [%] |
-11.2844 |
Activity at 0.013 uM-Replicate_1 [%] |
2.5092 |
Activity at 0.030 uM-Replicate_1 [%] |
-3.5479 |
Activity at 0.068 uM-Replicate_1 [%] |
3.7635 |
Activity at 0.153 uM-Replicate_1 [%] |
4.034 |
Activity at 0.349 uM-Replicate_1 [%] |
-0.753 |
Activity at 1.067 uM-Replicate_1 [%] |
3.3552 |
Activity at 3.264 uM-Replicate_1 [%] |
5.3866 |
Activity at 8.390 uM-Replicate_1 [%] |
-10.9793 |
Activity at 18.95 uM-Replicate_1 [%] |
-37.403 |
Activity at 42.46 uM-Replicate_1 [%] |
-61.6062 |
Activity at 92.41 uM-Replicate_1 [%] |
-79.1617 |
Compound QC-Replicate_1 |
QC'd by SIGMA |
Phenotype-Replicate_2 |
Inhibitor |
Potency-Replicate_2 [uM] |
6.1877 |
Efficacy-Replicate_2 [%] |
77.9523 |
Analysis Comment-Replicate_2 |
|
Activity_Score-Replicate_2 |
83 |
Curve_Description-Replicate_2 |
Complete curve; high efficacy |
Fit_LogAC50-Replicate_2 |
-5.2085 |
Fit_HillSlope-Replicate_2 |
2.8473 |
Fit_R2-Replicate_2 |
0.9937 |
Fit_InfiniteActivity-Replicate_2 [%] |
-74.2569 |
Fit_ZeroActivity-Replicate_2 [%] |
3.6953 |
Fit_CurveClass-Replicate_2 |
-1.1 |
Excluded_Points-Replicate_2 |
0 0 0 0 0 0 0 0 0 0 0 0 0 0 0 |
Max_Response-Replicate_2 [%] |
-76.6268 |
Activity at 0.00170 uM-Replicate_2 [%] |
3.0831 |
Activity at 0.00522 uM-Replicate_2 [%] |
6.6839 |
Activity at 0.013 uM-Replicate_2 [%] |
0.9494 |
Activity at 0.030 uM-Replicate_2 [%] |
9.4666 |
Activity at 0.068 uM-Replicate_2 [%] |
1.3654 |
Activity at 0.153 uM-Replicate_2 [%] |
1.3694 |
Activity at 0.349 uM-Replicate_2 [%] |
4.0819 |
Activity at 1.067 uM-Replicate_2 [%] |
1.2 |
Activity at 3.264 uM-Replicate_2 [%] |
-8.0592 |
Activity at 8.390 uM-Replicate_2 [%] |
-50.16 |
Activity at 18.95 uM-Replicate_2 [%] |
-67.9545 |
Activity at 42.46 uM-Replicate_2 [%] |
-74.6841 |
Description of key information
Dimethyl disulphide was evaluated in 113 in vitro high-throughput screening (HTS) assays (US EPA, 2017) to evaluate the effects on a target genes like, DNA binding, nuclear receptor (non-steroidal and steroidal), cell cycle, cyp (cytochrome P450 19A1 and 24A1), hydrolase (ATPase) and cell morphology (organelle conformation). Dimethyl disulphide did not induce a positive response in any assay. Therefore, there is no evidence that dimethyl disulphide could interfere with the expression of the genes screened.
299 bioassays with 311 bioactivity outcomes were retrieved from the PubChem BioAssay data base (NCBI, 2017). DMDS was inactive in 283 bioassays, inconclusive in 24 bioassays and positive in 2 bioassays. DMDS had no activity on cell viability assays, no agonist and antagonist activities on the peroxisome proliferator-activated receptor alpha (PPARa), delta (PPARd) and gamma (PPARg), androgen receptor (AR), estrogen receptor alpha (ER-alpha), thyroid receptor (TR) and glucocorticoid receptor (GR) signaling pathways. Positive results were obtained for antagonist activities on the constitutive androstane receptor (CAR) signaling pathway. An antagonist activity of CAR was observed with a very large inter-wells variability and significant antagonist effects were observed at concentrations inducing a decrease of the cell viability. Therefore, the toxicological significance of this effect is questionable.
Additional information
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