Compounds > 3',5'-dimethylacetaminophen
Page last updated: 2024-12-07

3',5'-dimethylacetaminophen

Description

3',5'-dimethylacetaminophen: structure given in first source [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID89896
CHEMBL ID278698
SCHEMBL ID2552398
MeSH IDM0125546

Synonyms (18)

Synonym
3',5'-dimethylacetaminophen
acetamide, n-(4-hydroxy-3,5-dimethylphenyl)-
3,5-dimethyl-4-hydroxyacetanilide
acetamide, n-(3,5-dimethyl-4-hydroxyphenyl)-
3',5'-acetoxylidide, 4'-hydroxy-
3,5-dimethylparacetamol
3,5-dimethylacetaminophen
brn 2723443
22900-79-4
CHEMBL278698
n-(4-hydroxy-3,5-dimethylphenyl)acetamide
3',5'-dimethyl-4'-hydroxyacetanilide
3',5'-dimethylparacetamol
FQCIYRLHNCRDKD-UHFFFAOYSA-N
SCHEMBL2552398
DTXSID00177443
3',5'-di-methyl-4'-hydroxyacetanilide
Z1509144456
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (30)

Assay IDTitleYearJournalArticle
AID191477Nephrotoxicity upon intragastric administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120613Nephrotoxicity upon intragastric administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191487Nephrotoxicity upon intravenous administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID123230Nephrotoxicity upon intraperitoneal administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120616Nephrotoxicity upon intraperitoneal administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120611Nephrotoxicity upon intragastric administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID123231Nephrotoxicity upon intraperitoneal administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191484Nephrotoxicity upon intraperitoneal administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120608Nephrotoxicity upon intragastric administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191491Nephrotoxicity upon intravenous administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191483Nephrotoxicity upon intraperitoneal administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120615Nephrotoxicity upon intraperitoneal administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191476Nephrotoxicity upon intragastric administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120619Nephrotoxicity upon intraperitoneal administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191480Nephrotoxicity upon intraperitoneal administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191493Nephrotoxicity upon intravenous administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191472Nephrotoxicity upon intragastric administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191481Nephrotoxicity upon intraperitoneal administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191479Nephrotoxicity upon intraperitoneal administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191475Nephrotoxicity upon intragastric administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120612Nephrotoxicity upon intragastric administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120617Nephrotoxicity upon intraperitoneal administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191473Nephrotoxicity upon intragastric administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120609Nephrotoxicity upon intragastric administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191485Nephrotoxicity upon intraperitoneal administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191489Nephrotoxicity upon intravenous administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 5 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191471Nephrotoxicity upon intragastric administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191492Nephrotoxicity upon intravenous administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID120607Nephrotoxicity upon intragastric administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 10 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
AID191488Nephrotoxicity upon intravenous administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 2 mM1980Journal of medicinal chemistry, Nov, Volume: 23, Issue:11
Studies on the mechanism of toxicity of acetaminophen. Synthesis and reactions of N-acetyl-2,6-dimethyl- and N-acetyl-3,5-dimethyl-p-benzoquinone imines.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (9)

TimeframeStudies, This Drug (%)All Drugs %
pre-19906 (66.67)18.7374
1990's3 (33.33)18.2507
2000's0 (0.00)29.6817
2010's0 (0.00)24.3611
2020's0 (0.00)2.80
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Market Indicators

Research Demand Index: 12.05

According to the monthly volume, diversity, and competition of internet searches for this compound, as well the volume and growth of publications, there is estimated to be weak demand-to-supply ratio for research on this compound.

MetricThis Compound (vs All)
Research Demand Index12.05 (24.57)
Research Supply Index2.30 (2.92)
Research Growth Index4.36 (4.65)
Search Engine Demand Index0.00 (26.88)
Search Engine Supply Index0.00 (0.95)

This Compound (12.05)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Reviews1 (11.11%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other8 (88.89%)84.16%
[information is prepared from research data collected from National Library of Medicine (NLM), extracted Dec-2023]
SubstanceRelationship StrengthStudiesTrialsClassesRoles
acetaminophen
Acetaminophen: Analgesic antipyretic derivative of acetanilide. It has weak anti-inflammatory properties and is used as a common analgesic, but may cause liver, blood cell, and kidney damage.. paracetamol : A member of the class of phenols that is 4-aminophenol in which one of the hydrogens attached to the amino group has been replaced by an acetyl group.		9.6890acetamides;
phenols		antipyretic;
cyclooxygenase 1 inhibitor;
cyclooxygenase 2 inhibitor;
cyclooxygenase 3 inhibitor;
environmental contaminant;
ferroptosis inducer;
geroprotector;
hepatotoxic agent;
human blood serum metabolite;
non-narcotic analgesic;
non-steroidal anti-inflammatory drug;
xenobiotic
carmustine
Carmustine: A cell-cycle phase nonspecific alkylating antineoplastic agent. It is used in the treatment of brain tumors and various other malignant neoplasms. (From Martindale, The Extra Pharmacopoeia, 30th ed, p462) This substance may reasonably be anticipated to be a carcinogen according to the Fourth Annual Report on Carcinogens (NTP 85-002, 1985). (From Merck Index, 11th ed). carmustine : A member of the class of N-nitrosoureas that is 1,3-bis(2-chloroethyl)urea in which one of the nitrogens is substituted by a nitroso group.		2.3720N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
dithiothreitol
1,4-dimercaptobutane-2,3-diol : A glycol that is butane-2,3-diol in which a hydrogen from each of the methyl groups is replaced by a thiol group.. 1,4-dithiothreitol : The threo-diastereomer of 1,4-dimercaptobutane-2,3-diol.		1.97101,4-dimercaptobutane-2,3-diol;
butanediols;
dithiol;
glycol;
thiol		chelator;
human metabolite;
reducing agent
n-acetyl-4-benzoquinoneimine
N-acetyl-4-benzoquinoneimine: reactive arylating intermediate from acetaminophen & N-hydroxyacetaminophen; structure given in first source		3.4720ketoimine;
quinone imine
2,6-dimethylacetaminophen
2,6-dimethylacetaminophen: structure given in first source; major urinary metabolite of lidocaine		8.0650
thromboxanes
thromboxane : A class of oxygenated oxane derivatives, originally derived from prostaglandin precursors in platelets, that stimulate aggregation of platelets and constriction of blood vessels.		1.9610
n-acetyl-3,5-dimethyl-4-benzoquinone imine
N-acetyl-3,5-dimethyl-4-benzoquinone imine: reduction with GSH gives 3,5-dimethylacetaminophen; structure given in first source; also formed by oxidation of 3,5-dimethylacetaminophen with horseradish peroxidase		2.3720
arachidonic acid
icosa-5,8,11,14-tetraenoic acid : Any icosatetraenoic acid with the double bonds at positions 5, 8, 11 and 14.. arachidonate : A long-chain fatty acid anion resulting from the removal of a proton from the carboxy group of arachidonic acid.		1.9610icosa-5,8,11,14-tetraenoic acid;
long-chain fatty acid;
omega-6 fatty acid		Daphnia galeata metabolite;
EC 3.1.1.1 (carboxylesterase) inhibitor;
human metabolite;
mouse metabolite
dactinomycin
Dactinomycin: A compound composed of a two CYCLIC PEPTIDES attached to a phenoxazine that is derived from STREPTOMYCES parvullus. It binds to DNA and inhibits RNA synthesis (transcription), with chain elongation more sensitive than initiation, termination, or release. As a result of impaired mRNA production, protein synthesis also declines after dactinomycin therapy. (From AMA Drug Evaluations Annual, 1993, p2015)		1.9810actinomycinmutagen
sodium dodecyl sulfate
Sodium Dodecyl Sulfate: An anionic surfactant, usually a mixture of sodium alkyl sulfates, mainly the lauryl; lowers surface tension of aqueous solutions; used as fat emulsifier, wetting agent, detergent in cosmetics, pharmaceuticals and toothpastes; also as research tool in protein biochemistry.. sodium dodecyl sulfate : An organic sodium salt that is the sodium salt of dodecyl hydrogen sulfate.		1.9910organic sodium saltdetergent;
protein denaturant
diethyl maleate
diethyl maleate : A maleate ester resulting from the formal condensation of both carboxy groups of maleic acid with ethanol. A colourless liquid at room temperature (m.p. -10degreeC) with boiling point 220degreeC at 1 atm., it is commonly used as a dienophile for Diels-Alder-type cycloaddition reactions in organic synthesis.		2.3720ethyl ester;
maleate ester		glutathione depleting agent
thromboxane b2
Thromboxane B2: A stable, physiologically active compound formed in vivo from the prostaglandin endoperoxides. It is important in the platelet-release reaction (release of ADP and serotonin).. thromboxane B2 : A member of the class of thromboxanes B that is (5Z,13E)-thromboxa-5,13-dien-1-oic acid substituted by hydroxy groups at positions 9, 11 and 15.		1.9610thromboxanes Bhuman metabolite;
mouse metabolite
mocetinostat
mocetinostat: undergoing phase II clinical trials for treatment of cancer. mocetinostat : A benzamide obtained by formal condensation of the carboxy group of 4-({[4-(pyridin-3-yl)pyrimidin-2-yl]amino}methyl)benzoic acid with one of the amino groups of benzene-1,2-diamine. It is an orally active and isotype-selective HDAC inhibitor which exhibits antitumour activity (IC50 = 0.15, 0.29, 1.66 and 0.59 muM for HDAC1, HDAC2, HDAC3 and HDAC11).		1.9910aminopyrimidine;
benzamides;
pyridines;
secondary amino compound;
secondary carboxamide;
substituted aniline		antineoplastic agent;
apoptosis inducer;
autophagy inducer;
cardioprotective agent;
EC 3.5.1.98 (histone deacetylase) inhibitor;
hepatotoxic agent
ConditionIndicatedRelationship StrengthStudiesTrials
Acute Liver Injury, Drug-Induced
[description not available]		03.5730
Kidney Diseases
Pathological processes of the KIDNEY or its component tissues.		01.9510
Chemical and Drug Induced Liver Injury
A spectrum of clinical liver diseases ranging from mild biochemical abnormalities to ACUTE LIVER FAILURE, caused by drugs, drug metabolites, herbal and dietary supplements and chemicals from the environment.		03.5730
Liver Dysfunction
[description not available]		01.9710
Liver Diseases
Pathological processes of the LIVER.		01.9710
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