Compounds > 2,6-dimethylacetaminophen
Page last updated: 2024-12-07

2,6-dimethylacetaminophen

Description Research Excerpts Clinical Trials Roles Classes Pathways Study Profile Bioassays Related Drugs Related Conditions Protein Interactions Research Growth Market Indicators

Description

2,6-dimethylacetaminophen: structure given in first source; major urinary metabolite of lidocaine [Medical Subject Headings (MeSH), National Library of Medicine, extracted Dec-2023]

Cross-References

ID SourceID
PubMed CID80641
CHEMBL ID15679
SCHEMBL ID20857699
MeSH IDM0131939

Synonyms (31)

Synonym
2,6-dimethyl-4-hydroxyacetanilide
2',6'-acetoxylidide, 4'-hydroxy-
acetamide, n-(2,6-dimethyl-4-hydroxyphenyl)-
nsc 38035
brn 2804933
acetamide, n-(4-hydroxy-2,6-dimethylphenyl)-
2,6-dimethylacetaminophen
nsc38035
nsc-38035
6337-56-0
4-hydroxy-2,6-dimethylacetanilide
CHEMBL15679
2,6-dimethylparacetamol
FT-0669549
n-(4-hydroxy-2,6-dimethylphenyl)acetamide
AKOS001044941
1-13-00-00245 (beilstein handbook reference)
unii-r7r7ko00sw
r7r7ko00sw ,
4-acetamido-3,5-dimethylphenol
mfcd00748645
SY016115
DTXSID70212774
n-(4-hydroxy-2,6-dimethylphenyl)acet-amide
SCHEMBL20857699
AC6513
3,5-dimethyl-4-acetaminophenol
A868161
LS-07623
4?-hydroxy-2?,6?-acetoxylidide
Z56871774
[information is derived through text-mining from research data collected from National Library of Medicine (NLM), extracted Dec-2023]

Bioassays (40)

Assay IDTitleYearJournalArticle
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.
AID120610Nephrotoxicity upon intragastric administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 1 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.
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.
AID191482Nephrotoxicity upon intraperitoneal administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 1 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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
AID191474Nephrotoxicity upon intragastric administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 1 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.
AID120618Nephrotoxicity upon intraperitoneal administration was assessed in mice liver as centrilobular vacuolation or necrosis at a dose of 1 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.
AID191470Nephrotoxicity upon intragastric administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 1 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.
AID120614Nephrotoxicity upon intraperitoneal administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 1 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.
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.
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.
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.
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.
AID191478Nephrotoxicity upon intraperitoneal administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 1 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.
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.
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.
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.
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.
AID191490Nephrotoxicity upon intravenous administration was assessed in rat liver as centrilobular vacuolation or necrosis at a dose of 1 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.
AID120606Nephrotoxicity upon intragastric administration was assessed in mice kidney as proximal tublar necrosis deep in the cortex at a dose of 1 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.
AID191486Nephrotoxicity upon intravenous administration was assessed in rat kidney as proximal tublar necrosis deep in the cortex at a dose of 1 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.
[information is prepared from bioassay data collected from National Library of Medicine (NLM), extracted Dec-2023]

Research

Studies (10)

TimeframeStudies, This Drug (%)All Drugs %
pre-19906 (60.00)18.7374
1990's3 (30.00)18.2507
2000's0 (0.00)29.6817
2010's1 (10.00)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: 11.82

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 Index11.82 (24.57)
Research Supply Index2.40 (2.92)
Research Growth Index4.21 (4.65)
Search Engine Demand Index0.00 (26.88)
Search Engine Supply Index0.00 (0.95)

This Compound (11.82)

All Compounds (24.57)

Study Types

Publication TypeThis drug (%)All Drugs (%)
Trials0 (0.00%)5.53%
Reviews0 (0.00%)6.00%
Case Studies0 (0.00%)4.05%
Observational0 (0.00%)0.25%
Other10 (100.00%)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.		3.68100acetamides;
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
benzocaine
Benzocaine: A surface anesthetic that acts by preventing transmission of impulses along NERVE FIBERS and at NERVE ENDINGS.. dextran sulfate sodium : An organic sodium salt of dextran sulfate. It induces colitis in mice.. benzocaine : A benzoate ester having 4-aminobenzoic acid as the acid component and ethanol as the alcohol component. A surface anaesthetic, it is used to suppress the gag reflex, and as a lubricant and topical anaesthetic on the larynx, mouth, nasal cavity, respiratory tract, oesophagus, rectum, urinary tract, and vagina.		2.1510benzoate ester;
substituted aniline		allergen;
antipruritic drug;
sensitiser;
topical anaesthetic
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.		1.9710N-nitrosoureas;
organochlorine compound		alkylating agent;
antineoplastic agent
lidocaine
Lidocaine: A local anesthetic and cardiac depressant used as an antiarrhythmia agent. Its actions are more intense and its effects more prolonged than those of PROCAINE but its duration of action is shorter than that of BUPIVACAINE or PRILOCAINE.. lidocaine : The monocarboxylic acid amide resulting from the formal condensation of N,N-diethylglycine with 2,6-dimethylaniline.		2.4220benzenes;
monocarboxylic acid amide;
tertiary amino compound		anti-arrhythmia drug;
drug allergen;
environmental contaminant;
local anaesthetic;
xenobiotic
ethylmaleimide
Ethylmaleimide: A sulfhydryl reagent that is widely used in experimental biochemical studies.		1.9710maleimidesanticoronaviral agent;
EC 1.3.1.8 [acyl-CoA dehydrogenase (NADP(+))] inhibitor;
EC 2.1.1.122 [(S)-tetrahydroprotoberberine N-methyltransferase] inhibitor;
EC 2.7.1.1 (hexokinase) inhibitor
phenobarbital
Phenobarbital: A barbituric acid derivative that acts as a nonselective central nervous system depressant. It potentiates GAMMA-AMINOBUTYRIC ACID action on GABA-A RECEPTORS, and modulates chloride currents through receptor channels. It also inhibits glutamate induced depolarizations.. phenobarbital : A member of the class of barbiturates, the structure of which is that of barbituric acid substituted at C-5 by ethyl and phenyl groups.		6.9710barbituratesanticonvulsant;
drug allergen;
excitatory amino acid antagonist;
sedative
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
monoethylglycinexylidide
monoethylglycinexylidide: RN given refers to unlabeled parent cpd; metabolite of xylocaine; structure. monoethylglycinexylidide : Amino acid amide formed from 2,6-dimethylaniline and N-ethylglycine components; an active metabolite of lidocaine, formed by oxidative deethylation. Used as an indicator of hepatic function.		1.9710amino acid amidedrug metabolite
glycinexylidide
glycinexylidide: dealkylated metabolite of lidocaine; structure; RN given refers to parent cpd with dimethylphenyl moiety in positions 2,6. glycinexylidide : A amino acid amide with 2,6-dimethylaniline and glycine components; an active metabolite of lidocaine, formed by oxidative deethylation. Used as an indicator of hepatic function.		1.9710amino acid amidedrug metabolite
3',5'-dimethylacetaminophen
3',5'-dimethylacetaminophen: structure given in first source		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
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
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.		1.9710ethyl 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
glycolipids
[no description available]		1.9610
ConditionIndicatedRelationship StrengthStudiesTrials
Acute Liver Injury, Drug-Induced
[description not available]		01.9510
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.		01.9510
Methemoglobinemia
The presence of methemoglobin in the blood, resulting in cyanosis. A small amount of methemoglobin is present in the blood normally, but injury or toxic agents convert a larger proportion of hemoglobin into methemoglobin, which does not function reversibly as an oxygen carrier. Methemoglobinemia may be due to a defect in the enzyme NADH methemoglobin reductase (an autosomal recessive trait) or to an abnormality in hemoglobin M (an autosomal dominant trait). (Dorland, 27th ed)		02.1510
Adenocarcinoma, Basal Cell
[description not available]		01.9610
Cancer of Colon
[description not available]		01.9610
Adenocarcinoma
A malignant epithelial tumor with a glandular organization.		01.9610
Colonic Neoplasms
Tumors or cancer of the COLON.		01.9610