2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans
In 2000, the Expert Group of the World Health Organization considered developmental toxicity as the most pertinent risk of dioxins to human beings. Because people are usually exposed simultaneously to several dioxin-like chemicals, a more detailed account is given at dioxins and dioxin-like compounds.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Developmental effects
In Vietnam and the United States, teratogenic or birth defects were observed in children of persons who were exposed to Agent Orange or 2,4,5-T that contained TCDD as an impurity out of the production process. However there has been some uncertainty on the causal link between Agent Orange/dioxin exposure. In 2006 a meta-analysis indicated large amount of heterogeneity between studies and emphasized a lack of consensus on the issue. Still-births, cleft palate, and neural tube defects, with spina bifida were the most statistically significant defects. Later some tooth defects and borderline neurodevelopmental effects have been reported. After Seveso accident tooth development defects, changed sex ratio and decreased sperm quality have been noted. Various developmental effects have been clearly shown after high mixed exposures to dioxins and dioxin-like compounds, the most dramatic in Yusho and Yu-chen catastrophes, in Japan and Taiwan, respectively.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Cancer
It is largely agreed that TCDD is not mutagenic or genotoxic. Its main action is cancer promotion; it promotes the carcinogenicity initiated by other compounds. Very high doses may, in addition, cause cancer indirectly; one of the proposed mechanisms is oxidative stress and the subsequent oxygen damage to DNA. There are other explanations such as endocrine disruption or altered signal transduction. The endocrine disrupting activities seem to be dependent on life stage, being anti-estrogenic when estrogen is present (or in high concentration) in the body, and estrogenic in the absence of estrogen.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Cancer
TCDD was classified by the International Agency for Research on Cancer as a carcinogen for humans (group 1). In the occupational cohort studies available for the classification, the risk was weak and borderline detectable, even at very high exposures. Therefore, the classification was, in essence, based on animal experiments and mechanistic considerations. This was criticized as a deviation from IARC's 1997 classification rules. The main problem with IARC classification is that it only assesses qualitative hazard, i.e. carcinogenicity at any dose, and not the quantitative risk at different doses.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Cancer
According to a 2006 Molecular Nutrition & Food Research article, there were debates on whether TCDD was carcinogenic only at high doses which also cause toxic damage of tissues. A 2011 review concluded that, after 1997, further studies did not support an association between TCDD exposure and cancer risk. One of the problems is that in all occupational studies the subjects have been exposed to a large number of chemicals, not only TCDD. By 2011, it was reported that studies that include the update of Vietnam veteran studies from Operation Ranch Hand, had concluded that after 30 years the results did not provide evidence of disease. On the other hand, the latest studies on Seveso population support TCDD carcinogenicity at high doses.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Cancer
In 2004, an article in the International Journal of Cancer provided some direct epidemiological evidence that TCDD or other dioxins are not causing soft-tissue sarcoma at low doses, although this cancer has been considered typical for dioxins. There was in fact a trend of cancer to decrease. This is called a J-shape dose-response, low doses decrease the risk, and only higher doses increase the risk, according to a 2005 article in the journal Dose-Response.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Safety recommendations
The Joint FAO/WHO Expert Committee on Food Additives (JECFA) derived in 2001 a provisional tolerable monthly intake (PTMI) of 70 pg TEQ/kg body weight. The United States Environmental Protection Agency (EPA) established an oral reference dose (RfD) of 0.7 pg/kg b.w. per day for TCDD (see discussion on the differences in). According to the Aspen Institute, in 2011, "The general environmental limit in most countries is 1,000 ppt TEq in soils and 100 ppt in sediment. Most industrialized countries have dioxin concentrations in soils of less than 12 ppt.


2,3,7,8-Tetrachlorodibenzodioxin, Toxicity in humans, Safety recommendations
The U.S. Agency for Toxic Substance and Disease Registry has determined that levels higher than 1,000 ppt TEq in soil require intervention, including research, surveillance, health studies, community and physician education, and exposure investigation. The EPA is considering reducing these limits to 72 ppt TEq. This change would significantly increase the potential volume of contaminated soil requiring treatment."


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology
By far most information on toxicity of dioxin-like chemicals is based on animal studies utilizing TCDD. Almost all organs are affected by high doses of TCDD. In short-term toxicity studies in animals, the typical effects are anorexia and wasting, and even after a huge dose animals die only 1 to 6 weeks after the TCDD administration. Seemingly similar species have varying sensitivities to acute effects: lethal dose for a guinea pig is about 1 μg/kg, but to a hamster it is more than 1,000 μg/kg. A similar difference can be seen even between two different rat strains.


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology
Various hyperplastic (overgrowth) or atrophic (wasting away) responses are seen in different organs, thymus atrophy is very typical in several animal species. TCDD also affects the balance of several hormones. In some species, but not in all, severe liver toxicity is seen. Taking into account the low doses of dioxins in the present human population, only two types of toxic effects have been considered to cause a relevant risk to humans: developmental effects and cancer.


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology, Developmental effects
Developmental effects occur at very low doses in animals. They include frank teratogenicity such as cleft palate and hydronephrosis. Development of some organs may be even more sensitive: very low doses perturb the development of sexual organs in rodents, and the development of teeth in rats. The latter is important in that tooth deformities were also seen after the Seveso accident and possibly after a long breast-feeding of babies in the 1970s and 1980s when the dioxin concentrations in Europe were about ten times higher than at present.


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology, Cancer
Cancers can be induced in animals at many sites. At sufficiently high doses TCDD has caused cancer in all animals tested. The most sensitive is liver cancer in female rats, and this has long been a basis for risk assessment. Dose-response of TCDD in causing cancer does not seem to be linear, and there is a threshold below which it seems to cause no cancer.


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology, Cancer
TCDD is not mutagenic or genotoxic, in other words, it is not able to initiate cancer, and the cancer risk is based on promotion of cancer initiated by other compounds or on indirect effects such as disturbing defense mechanisms of the body e.g. by preventing apoptosis or programmed death of altered cells. Carcinogenicity is associated with tissue damage, and it is often viewed now as secondary to tissue damage.


2,3,7,8-Tetrachlorodibenzodioxin, Animal toxicology, Cancer
TCDD may in some conditions potentiate the carcinogenic effects of other compounds. An example is benzo(a)pyrene that is metabolized in two steps, oxidation and conjugation. Oxidation produces epoxide carcinogens that are rapidly detoxified by conjugation, but some molecules may escape to the nucleus of the cell and bind to DNA causing a mutation, resulting in cancer initiation. When TCDD increases the activity of oxidative enzymes more than conjugation enzymes, the epoxide intermediates may increase, increasing the possibility of cancer initiation. Thus a beneficial activation of detoxifying enzymes may lead to deleterious side effects.


2,3,7,8-Tetrachlorodibenzodioxin, Sources
TCDD has never been produced commercially except as a pure chemical for scientific research. It is, however, formed as a synthesis side product when producing certain chlorophenols or chlorophenoxy acid herbicides. It may also be formed along with other polychlorinated dibenzodioxins and dibenzofuranes in any burning of hydrocarbons where chlorine is present, especially if certain metal catalysts such as copper are also present. Usually a mixture of dioxin-like compounds is produced, therefore a more thorough treatise is under dioxins and dioxin-like compounds.


2,3,7,8-Tetrachlorodibenzodioxin, Sources
The greatest production occurs from waste incineration, metal production, and fossil-fuel and wood combustion. Dioxin production can usually be reduced by increasing the combustion temperature. Total U.S. emissions of PCCD/Fs were reduced from ca. 14 kg TEq in 1987 to 1.4 kg TEq in 2000.


2,3,7,8-Tetrachlorodibenzodioxin, Cases of exposure
There have been numerous incidents where people have been exposed to high doses of TCDD.


2,3-(S)-Hexahydroxydiphenoyl-D-glucose
2,3-(S)-Hexahydroxydiphenoyl-d-glucose is an hydrolyzable tannin that can be found in Eucalyptus delegatensis, the Alpine ash (Myrtaceae), in Terminalia catappa, the Bengal almond, and Combretum glutinosum (both Combretaceae).


2,3-Bis(acetylmercaptomethyl)quinoxaline
2,3-Bis(acetylmercaptomethyl)quinoxaline ia an antiviral agent which can inhibits poliovirus RNA synthesis in vitro and in vivo and inhibits human herpesvirus 1 multiplication in vitro. It does not interfere with attachment, penetration or DNA synthesis, but interrupts a late stage in virus assembly and/or maturation.


2,3-Bisphosphoglyceric acid
2,3-Bisphosphoglyceric acid (conjugate base 2,3-bisphosphoglycerate) (2,3-BPG), also known as 2,3-diphosphoglyceric acid (conjugate base 2,3-diphosphoglycerate) (2,3-DPG), is a three-carbon isomer of the glycolytic intermediate 1,3-bisphosphoglyceric acid (1,3-BPG).


2,3-Bisphosphoglyceric acid
2,3-BPG is present in human red blood cells (RBC; erythrocyte) at approximately 5 mmol/L. It binds with greater affinity to deoxygenated hemoglobin (e.g., when the red blood cell is near respiring tissue) than it does to oxygenated hemoglobin (e.g., in the lungs) due to conformational differences: 2,3-BPG (with an estimated size of about 9 Å) fits in the deoxygenated hemoglobin conformation (with an 11-Angstrom pocket), but not as well in the oxygenated conformation (5 Angstroms). It interacts with deoxygenated hemoglobin beta subunits and decreases the affinity for oxygen and allosterically promotes the release of the remaining oxygen molecules bound to the hemoglobin. Therefore, it enhances the ability of RBCs to release oxygen near tissues that need it most. 2,3-BPG is thus an allosteric effector.


2,3-Bisphosphoglyceric acid
Its function was discovered in 1967 by Reinhold Benesch and Ruth Benesch.


2,3-Bisphosphoglyceric acid, Metabolism
2,3-BPG is formed from 1,3-BPG by the enzyme BPG mutase. It can then be broken down by 2,3-BPG phosphatase to form 3-phosphoglycerate. Its synthesis and breakdown are, therefore, a way around a step of glycolysis, with the net expense of one ATP per molecule of 2,3-BPG generated as the high-energy carboxylic acid-phosphate mixed anhydride bond is cleaved by bisphosphoglycerate mutase.


2,3-Bisphosphoglyceric acid, Metabolism
The normal glycolytic pathway generates 1,3-BPG, which may be dephosphorylated by phosphoglycerate kinase (PGK), generating ATP, or it may be shunted into the Luebering-Rapoport pathway, where bisphosphoglycerate mutase catalyzes the transfer of a phosphoryl group from C1 to C2 of 1,3-BPG, giving 2,3-BPG. 2,3-BPG, the most concentrated organophosphate in the erythrocyte, forms 3-PG by the action of bisphosphoglycerate phosphatase. The concentration of 2,3-BPG varies proportionately to the [H+].


2,3-Bisphosphoglyceric acid, Metabolism
There is a delicate balance between the need to generate ATP to support energy requirements for cell metabolism and the need to maintain appropriate oxygenation/deoxygenation status of hemoglobin. This balance is maintained by isomerisation of 1,3-BPG to 2,3-BPG, which enhances the deoxygenation of hemoglobin.


2,3-Bisphosphoglyceric acid, Effects of binding
When 2,3-BPG binds to deoxyhemoglobin, it acts to stabilize the low oxygen affinity state (T state) of the oxygen carrier. It fits neatly into the cavity of the deoxy- conformation, exploiting the molecular symmetry and positive polarity by forming salt bridges with lysine and histidine residues in the ß subunits of hemoglobin. The R state, with oxygen bound to a heme group, has a different conformation and does not allow this interaction.


2,3-Bisphosphoglyceric acid, Effects of binding
By itself, hemoglobin has sigmoid-like kinetics. In selectively binding to deoxyhemoglobin, 2,3-BPG stabilizes the T state conformation, making it harder for oxygen to bind hemoglobin and more likely to be released to adjacent tissues. 2,3-BPG is part of a feedback loop that can help prevent tissue hypoxia in conditions where it is most likely to occur.


2,3-Bisphosphoglyceric acid, Effects of binding
Conditions of low tissue oxygen concentration such as high altitude (2,3-BPG levels are higher in those acclimated to high altitudes), airway obstruction, or congestive heart failure will tend to cause RBCs to generate more 2,3-BPG, because changes in pH and oxygen modulate the enzymes that make and degrade it. The accumulation of 2,3-BPG decreases the affinity of hemoglobin for oxygen. Ultimately, this mechanism increases oxygen release from RBCs under circumstances where it is needed most.


2,3-Bisphosphoglyceric acid, Effects of binding
This release is potentiated by the Bohr effect, in which hemoglobin's binding affinity for oxygen is also reduced by a lower pH and high concentration of carbon dioxide. In tissues with high energetic demands, oxygen is rapidly consumed, which increases the concentration of H+ and carbon dioxide. Through the Bohr effect, hemoglobin is induced to release more oxygen to supply cells that need it. In contrast, 2,3-BPG has no effect on the related compound myoglobin. (reference required)


2,3-Bisphosphoglyceric acid, Effects of binding
In pregnant women, there is a 30% increase in intracellular 2,3-BPG. This lowers the maternal hemoglobin affinity for oxygen, and therefore allows more oxygen to be offloaded to the fetus in the maternal uterine arteries. The fetus has a low sensitivity to 2,3-BPG, so its hemoglobin has a higher affinity for oxygen. Therefore, although the pO2 in the uterine arteries is low, the fetal umbilical artery (which carries deoxygenated blood) can still get oxygenated from them.


2,3-Bisphosphoglyceric acid, Fetal hemoglobin
Fetal hemoglobin (HbF) exhibits a low affinity for 2,3-BPG, resulting in a higher binding affinity for oxygen. This increased oxygen-binding affinity relative to that of adult hemoglobin (HbA) is due to HbF's having two α/γ dimers as opposed to the two α/β dimers of HbA. The positive histidine residues of HbA β-subunits that are essential for forming the 2,3-BPG binding pocket are replaced by serine residues in HbF γ-subunits. Like that, histidine nº143 gets lost, so 2,3-BPG has difficulties in linking to the fetal hemoglobin, and it looks like the pure hemoglobin. That’s the way O2 flows from the mother to the fetus. As we can see in the following image, fetal hemoglobin has more affinity to oxygen than adult hemoglobin. Moreover, myoglobin has the highest affinity to oxygen.


2,3-Bisphosphoglyceric acid, Fetal hemoglobin
Differences between myoglobin (Mb), fetal hemoglobin (Hb F), adult hemoglobin (Hb A)


2,3-Bisphosphoglyceric acid, Diseases related to 2,3-BPG
A 2004 study checked the effects of thyroid hormone on 2,3-BPG levels. The result was that the hyperthyroidism modulates in vivo 2,3-BPG content in erythrocytes by changes in the expression of phosphoglycerate mutase (PGM) and 2,3-BPG synthase. This result shows that the increase in the 2,3-BPG content of erythrocytes observed in hyperthyroidism doesn’t depend on any variation in the rate of circulating hemoglobin, but seems to be a direct consequence of the stimulating effect of thyroid hormones on erythrocyte glycolytic activity.


2,3-Bisphosphoglyceric acid, Diseases related to 2,3-BPG
Red cells increase their intracellular 2,3-BPG concentration as much as five times within one to two hours in patients with chronic anemia, when the oxygen carrying capacity of the blood is diminished. This results in a rightward shift of the oxygen dissociation curve and more oxygen being released to the tissues.


2,3-Bisphosphoglyceric acid, Diseases related to 2,3-BPG
Recently, scientists have found similarities between low amounts of 2,3-BPG with the occurrence of high altitude pulmonary edema at high altitudes.


2,3-Bisphosphoglyceric acid, Hemodialysis
In a 1998 study, erythrocyte 2,3-BPG concentration was analyzed during the hemodialysis process. The 2,3-BPG concentration was expressed relative to the hemoglobin tetramer (Hb4) concentration as the 2,3-BPG/Hb4 ratio. Physiologically, an increase in 2,3-BPG levels would be expected to counteract the hypoxia that is frequently observed in this process. Nevertheless, the results show a 2,3-BPG/Hb4 ratio decreased. This is due to the procedure itself: mechanical stress on the erythrocytes is believed to cause the 2,3-BPG escape, which is then removed by hemodialysis. The concentrations of calcium, phosphate, creatinine, urea and albumin did not correlate significantly with the total change in 2,3-BPG/Hb4 ratio. However, the ratio sampled just before dialysis correlated significantly and positively with the total weekly dosage of erythropoietin (main hormone in erythrocyte formation) given to the patients.


2,3-Butanediol
2,3-Butanediol is the organic compound with the formula (CH3CHOH)2. It is classified as a vic-diol (glycol). It exists as three stereoisomers, a chiral pair and the meso isomer. All are colorless liquids. Applications include precursors to various plastics and pesticides.


2,3-Butanediol, Isomerism
Of the three stereoisomers, two are enantiomers (levo- and dextro-2,3-butanediol) and one is a meso compound. The enantiomeric pair have (2R, 3R) and (2S, 3S) configurations at carbons 2 and 3, while the meso compound has configuration (2R, 3S) or, equivalently, (2S, 3R).


2,3-Butanediol, Industrial production and uses
The isomer distribution depends on the stereochemistry of the epoxide.


2,3-Butanediol, Industrial production and uses
The meso isomer is used to combine with naphthalene-1,5-diisocyanate. The resulting polyurethane is called "Vulkollan".


2,3-Butanediol, Biological production
The (2R,3R)-stereoisomer of 2,3-butanediol is produced by a variety of microorganisms in a process known as butanediol fermentation. It is found naturally in cocoa butter, in the roots of Ruta graveolens, sweet corn, and in rotten mussels. It is used in the resolution of carbonyl compounds in gas chromatography.


2,3-Butanediol, Biological production
During World War II research was done towards producing 2,3-butanediol by fermentation in order to produce 1,3-butadiene, the monomer of the polybutadiene used in a leading type of synthetic rubber. It can be derived from the fermentation of sugarcane molasses.


2,3-Butanediol, Biological production
Fermentative production of 2,3-butanediol from carbohydrates involves a network of biochemical reactions that can be manipulated to maximize production.


2,3-Diaminopropionic acid
2,3-Diaminopropionic acid (2,3-diaminopropionate, Dpr) is a non-proteinogenic amino acid found in certain secondary metabolites, including zwittermicin A and tuberactinomycin.


2,3-Diaminopropionic acid, Biosynthesis
2,3-Diaminopropionate is formed by the pyridoxal phosphate (PLP) mediated amination of serine.


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone
2,3-Dichloro-5,6-dicyano-1,4-benzoquinone (or DDQ) is the chemical reagent with formula C6Cl2(CN)2O2. This oxidant is useful for the dehydrogenation of alcohols, phenols, and steroid ketones in organic chemistry. DDQ decomposes in water, but is stable in aqueous mineral acid.


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone, Preparation
Synthesis of DDQ involves cyanation of chloranil. Thiele and Günther first reported a 6-step preparation in 1906. The substance did not receive interest until its potential as a dehydrogenation agent was discovered. A single-step chlorination from 2,3-dicyanohydroquinone was reported in 1965.


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone, Reactions
The reagent removes pairs of H atoms from organic molecules. The stoichiometry of its action is illustrated by the conversion of tetralin to naphthalene:


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone, Reactions
The resulting hydroquinone is poorly soluble in typical reaction solvents (dioxane, benzene, alkanes), which facilitates workup.


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone, Reactions
Solutions of DDQ in benzene are red, due to the formation of a charge-transfer complex.


2,3-Dichloro-5,6-dicyano-1,4-benzoquinone, Safety
DDQ reacts with water to release highly toxic hydrogen cyanide (HCN). A low-temperature and weakly acidic environment increases the stability of DDQ.


2,3-Dichlorobutadiene
2,3-Dichlorobutadiene is the organic compound with the formula H2C=C(Cl)C(Cl)=CH2. This colorless liquid is prone to polymerization, moreso than 2-chlorobutadiene (chloroprene). It is used to produce specialized neoprene rubbers. It can be prepared by the copper-catalyzed isomerization of dichlorobutynes. Alternatively dehydrochlorination of 2,3,4-trichloro-1-butene:


2,3-Dichlorophenylpiperazine
2,3-Dichlorophenylpiperazine (2,3-DCPP or DCPP) is a chemical compound from the phenylpiperazine family. It is both a precursor in the synthesis of aripiprazole and one of its metabolites. It is unclear whether 2,3-DCPP is pharmacologically active as a serotonin receptor agonist similar to its close analogue 3-chlorophenylpiperazine (mCPP), though it has been shown to act as a partial agonist of the dopamine D2 and D3 receptors.


2,3-Dichlorophenylpiperazine, Legality
2,3-DCPP has been made illegal in Japan and Hungary after having been identified in seized designer drug samples.


2,3-Dichlorophenylpiperazine, Positional Isomer
The positional isomer 3,4-dichlorophenylpiperazine (3,4-DCPP) is also known, and acts as both a serotonin releaser via the serotonin transporter, and a β1-adrenergic receptor blocker, though with relatively low affinity at both targets.


2,3-Dichlorophenylpiperazine, Triple Substituted
The 3,4,5-Trichlorophenylpiperazine [67305-64-0] ("3 stripes") is also a highly regarded arrangement & has been awarded the Beecham patent of . Such 3,4,5-Trisunstituted aromatic entities is already known from clenbuterol. Leading to    (Ex 6 is a concrete example of this) i.e. 1-(4-Amino-3,5-dichlorophenyl)-4-(4-phthalimido-1- butyl)piperazine.


2,3-Dihydrofuran
2,3-Dihydrofuran is a heterocyclic compound. It is one of the simplest enol ethers and a position isomer of 2,5-dihydrofuran. It is a colorless volatile liquid.


2,3-Dihydrothiophene
2,3-Dihydrothiophene is a heterocyclic compound and an organosulfur compound with the formula SC4H6. It is isomeric with the more symmetrical 2,5-dihydrothiophene. Both isomers of dihydrothiophene are colorless liquids with a thioether-like odor. In terms of their reactivity, both isomers exhibit characteristics of alkenes and thioethers, undergoing addition reactions at carbon and oxidation at sulfur. In contrast, thiophene engages in neither reaction.


2,3-Dihydrothiophene, Dihydrothiophenes in nature
Dihydrothiophenes contribute to the aroma of the white truffle. The major component is 3-methyl-4,5-dihydrothiophene (alternative name:4-methyl-2,3-dihydrothiophene), produced by bacterial colonies in the truffle's fruiting bodies.


2,3-Dihydroxy-3-methylpentanoic acid
2,3-Dihydroxy-3-methylpentanoic acid is an intermediate in the metabolism of isoleucine.


2,3-Dihydroxy-3-methylpentanoic acid
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2,3-Dihydroxybenzoic acid
2,3-Dihydroxybenzoic acid is a natural phenol found in Phyllanthus acidus and in the aquatic fern Salvinia molesta. It is also abundant in the fruits of Flacourtia inermis. It is a dihydroxybenzoic acid, a type of organic compound. The colorless solid occurs naturally, being formed via the shikimate pathway. It is incorporated into various siderophores, which are molecules that strongly complex iron ions for absorption into bacteria. 2,3-DHB consists of a catechol group, which upon deprotonation binds iron centers very strongly, and the carboxylic acid group by which the ring attaches to various scaffolds through amide bonds. A famous high affinity siderophore is enterochelin, which contains three dihydroxybenzoyl substituents linked to the depsipeptide of serine.


2,3-Dihydroxybenzoic acid
It is a potentially useful iron-chelating drug and has antimicrobial properties.


2,3-Dihydroxybenzoic acid
2,3-Dihydroxybenzoic acid is also a product of human aspirin metabolism.


2,3-Dihydroxycinnamic acid
2,3-Dihydroxycinnamic acid is a hydroxycinnamic acid. It is an isomer of caffeic acid.


2,3-Dimercapto-1-propanesulfonic acid
2,3-Dimercapto-1-propanesulfonic acid (abbreviated DMPS) and its sodium salt (known as Unithiol) are chelating agents that form complexes with various heavy metals. They are related to dimercaprol, which is another chelating agent.


2,3-Dimercapto-1-propanesulfonic acid
The synthesis of DMPS was first reported in 1956 by V. E. Petrunkin. The effects of DMPS on heavy metal poisoning, including with polonium-210, were investigated in the following years. DMPS was found to have some protective effect, prolonging the survival time.


2,3-Dimercapto-1-propanesulfonic acid
A study was undertaken of DMPS use by workers involved in the production of a calomel skin bleaching lotion and in direct contact with mercurous chloride and that already showed elevated urine mercury levels. The sodium salt of DMPS was found to be effective in lowering the body burden of mercury and in decreasing the urinary mercury concentration to normal levels.


2,3-Dimercapto-1-propanesulfonic acid
DMPS administrated to a mercury poisoned animal model failed to remove the mercury from tissues and reduce the inorganic mercury burden in the brain.


2,3-Dimercapto-1-propanesulfonic acid
A 2008 study reported a case of Stevens–Johnson syndrome (SJS), a potentially serious disease, in a child undergoing chelation therapy with DMPS; the SJS resolved gradually after the chelation therapy was stopped.


2,3-Dimercapto-1-propanesulfonic acid
A 2020 study found DMPS to provide some benefits taken orally in mitigating effects from hemotoxic snakebites (using venom from saw-scaled vipers Viperidae Echis) in mouse models when given soon after exposure, suggesting its potential for repurposing as a prehospital treatment. [ Albulescu, L.; Hale, M.S. ;Ainsworth, S.; Alsolaiss, J.; Crittenden, E.; Calvete, J.J.; Evans, C.; Wilkinson, M.C. ; Harrison, R.A.; Kool, J.; Casewell, N.R. (2020). "Preclinical validation of a repurposed metal chelator as an early-intervention therapeutic for hemotoxic snakebite". Science Translational Medicine, Vol 12, Issue 542, 8314 DOI: 10.1126/scitranslmed.aay8314]


2,3-Dimethylbutane
2,3-Dimethylbutane is an isomer of hexane. It has the chemical formula (CH3)2CHCH(CH3)2. It is a colorless liquid which boils at 57.9 °C.


2,3-Dimethylpentane
2,3-Dimethylpentane is an organic compound of carbon and hydrogen with formula C7H16, more precisely CH3–CH(CH3)–CH(CH3)–CH2–CH3: a molecule of pentane with methyl groups –CH3 replacing hydrogen atoms on carbon atoms 2 and 3. It is an alkane ("paraffin" in older nomenclature), a fully saturated hydrocarbon; specifically, one of the isomers of heptane.


2,3-Dimethylpentane
Like typical alkanes, it is a colorless flammable compound; under common ambient conditions, it is a  mobile liquid, less dense than water.


2,3-Dimethylpentane
2,3-Dimethylpentane is notable for being one of the two simplest alkanes with optical (enantiomeric) isomerism. The optical center is the middle carbon of the pentane backbone, which is connected to one hydrogen atom, one methyl group, one ethyl group –C2H5, and one isopropyl group –CH(CH3)2. The two enantiomers are denoted (3R)-2,3-dimethylpentane and (3S)-2,3-dimethylpentane. (The other simplest chiral alkane is its structural isomer 3-methylhexane.)


2,3-Dimethylpentane, Properties
Most properties listed in the literature refer to the racemic compound (an equimolar mixture of the two optical isomers).


2,3-Dimethylpentane, Properties
The boiling point of 89.7 °C is 0.3 °C higher than the value of 89.4 °C predicted by Wiener's formula, based on the structure of the molecule and the boiling point of n-heptane.


2,3-Dimethylpentane, Properties
The speed of sound at 3 MHz is 1149.5 m/s at 20 °C and 889.5 m/s at 80 °C.


2,3-Dimethylpentane, Properties
The racemic mixture has a glass transition temperature of about 123 K (−150 °C), but reportedly it does not crystallize—a fact that has been claimed to be a characteristic of high-purity optically active alkanes.


2,3-Dimethylpentane, Preparation
2,3-Dimethylpentane is practically absent in the synthetic fuel produced from hydrogen and carbon monoxide by the Fischer–Tropsch process.


2,3-Dimethylpentane, Preparation
The pure compound can be prepared by reacting the Grignard reagent sec-butyl magnesium bromide C4H9–MgBr with acetone to form 2,3-dimethyl-2-pentanol, then dehydrating this alcohol to form 2,3-dimethyl-2-pentene, and hydrogenating this product.


2,3-Dimethylpentane, Preparation
The isomer is present at about 2.4% by weight in the hydrocarbon mixture obtained by the condensation of methanol at 200 °C with a zinc iodide catalyst (the main component of the mixture being the isomer 2,2,3-trimethylbutane, obtained at almost 50% yield).


2,3-Dinitrophenol
2,3-Dinitrophenol (2,3-DNP) is an organic compound with the formula HOC6H3(NO2)2.


2,3-Diphenylpropylamine
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2,3-Epoxybutane
2,3-Epoxybutane is an organic compound with the formula CH3CH(O)CHCH3. It is an epoxide. The compound exists as three stereoisomers, a pair of enantiomers and the meso isomer. All are colorless liquids.


2,3-Epoxybutane, Preparation and reactions
A common reaction is its hydration to 2,3-butanediol. Many such ring-opening reactions have been reported.


2,3-Methylenedioxyamphetamine
2,3-Methylenedioxyamphetamine (2,3-MDA) or ORTHO-MDA is an amphetamine derivative which is mentioned in PIHKAL as a fairly potent and long-lasting stimulant drug, but with little or none of the entactogenic effects associated with its better-known structural isomer MDA.


2,3-Methylenedioxymethamphetamine
2,3-Methylenedioxymethamphetamine (2,3-MDMA) is a positional isomer of the recreational drug 3,4-MDMA (commonly known as Ecstasy or Molly).


2,3-Oxidosqualene
(S)-2,3-Oxidosqualene ((S)-2,3-epoxysqualene) is an intermediate in the synthesis of the cell membrane sterol precursors lanosterol and cycloartenol, as well as saponins. It is formed when squalene is oxidized by the enzyme squalene monooxygenase. 2,3-Oxidosqualene is the substrate of various oxidosqualene cyclases, including lanosterol synthase, which produces lanosterol, a precursor to cholesterol.


2,3-Wittig rearrangement
The [2,3]-Wittig rearrangement is the transformation of an allylic ether into a homoallylic alcohol via a concerted, pericyclic process. Because the reaction is concerted, it exhibits a high degree of stereocontrol, and can be employed early in a synthetic route to establish stereochemistry. The Wittig rearrangement requires strongly basic conditions, however, as a carbanion intermediate is essential. [ 1,2]-Wittig rearrangement is a competitive process.


2,3-Wittig rearrangement, Introduction
[2,3]-Sigmatropic rearrangements occur for a variety of groups X and Y (see below). When X is a carbanion and Y an alkoxide, the rearrangement is called the [2,3]-Wittig rearrangement and the products are pent-1-en-5-ols. The [1,2]-Wittig rearrangement, which produces isomeric pent-5-en-1-ols, is a competitive process that takes place at high temperatures. Because of the high atom economy and stereoselectivity of the [2,3]-rearrangement, it has gained considerable synthetic utility. The carbanion is generated by direct lithiation of moderately acidic substrates, tin transmetallation, or reductive lithiation of O,S-acetals. Stereoselective methods employing chiral starting materials have been used to effect either asymmetric induction or simple diastereoselection


2,3-Wittig rearrangement, Mechanism and stereochemistry, Prevailing mechanism
After carbanion formation, the [2,3]-Wittig rearrangement is rapid and selective at low temperatures. However, if the reaction mixture is allowed to reach temperatures above −60 °C, [1,2]-rearrangement becomes competitive.


2,3-Wittig rearrangement, Mechanism and stereochemistry, Prevailing mechanism
The postulated transition state possesses a five-membered, envelope-like structure. The group attached to the carbanion (G) can occupy either a pseudoequatorial or pseudoaxial position, although the former is usually preferred. Large substituents on the other side of the ether oxygen prefer to occupy the exo position (RE) to avoid A1,3 strain. These restrictions lead to a preference for the syn product from (Z) isomers and anti products from (E) isomers; however, some exceptions to this rule are known.


2,3-Wittig rearrangement, Mechanism and stereochemistry, Stereoselective variants
Stereoselective variants of the [2,3]-Wittig rearrangement have employed three strategies: diastereoselection based on an existing, established stereocenter, placement of a chiral auxiliary on the starting material whose configuration is unaffected by the reaction, and the use of a chiral base. The relative diastereoselection strategy works well only for a limited number of G groups, but usually results in high yields because no chiral auxiliary group needs to be removed or modified. The stereocenter opposite the carbanion usually must be tertiary (rather than quaternary) in order to enforce the placement of the largest substituent in the RE position.


2,3-Wittig rearrangement, Mechanism and stereochemistry, Stereoselective variants
The asymmetric induction approach relies on stereocenters already set in the starting material that are unaffected by the reaction (chiral auxiliaries). The most success has been achieved by placing these stereocenters either in the G group or in a substituent attached to the end of the double bond. Diastereomeric ratios in excess of 90:10 are common for these reactions; however, removal of the chiral auxiliary is sometimes difficult.


2,3-Wittig rearrangement, Mechanism and stereochemistry, Stereoselective variants
The use of chiral bases has afforded enantioenriched rearrangement products in a few cases, although this method does not appear to be general. Enantioselectivity in these reactions is often low, suggesting that the association between the conjugate acid of the base and the rearranging carbanion is likely weak.


2,3-Wittig rearrangement, Scope and limitations
A variety of allylic ethers undergo the Wittig rearrangement—the fundamental requirement is the ability to generate the appropriate carbanion in the substrate. This demands either acidic hydrogens, a reducible functional group, or a carbon-metal bond. Historically, alkenyl, alkynyl, and phenyl groups have been used to acidify the α position. Free terminal alkynes are tolerated, although yields are higher when silyl-protected alkynes are used.


2,3-Wittig rearrangement, Scope and limitations
When an alkene is used as the anion-stabilizing group G, issues of selectivity arise concerning the site of the carbanion. Anion-stabilizing groups such as (trimethyl)silyl or methylthio provide essentially complete site selectivity.


2,3-Wittig rearrangement, Scope and limitations
Carbonyl groups may also be used as the anion-stabilizing group; carbonyl groups are particularly useful for asymmetric rearrangements that employ chiral auxiliaries.


2,3-Wittig rearrangement, Scope and limitations
A highly enantioselective method employing chromium carbonyl complexes involves the use of the acidified phenyl ring as an anion-stabilizing group.


2,3-Wittig rearrangement, Scope and limitations
That the substrate must contain acidic hydrogens adjacent to the ether oxygen was a significant limitation of the original reaction. Thus, the development of transmetallation methods that allowed the selective generation of carbanions from carbon-tin bonds represented a profound methodological advance. The scope of the groups that could be attached to the anionic center expanded dramatically as a result.


2,3-Wittig rearrangement, Synthetic applications
The products of the [2,3]-Wittig rearrangement of bis(allylic) ethers are 1,5-dien-3-ols. These substrates may undergo the oxy-Cope rearrangement upon deprotonation, affording δ,ε-unsaturated carbonyls. This tandem sigmatropic strategy has been employed in the synthesis of some natural products, including brevicomine and oxocrinol.


2,3-Wittig rearrangement, Variations
One variation of the 2,3-Wittig rearrangement is the Wittig-Still rearrangement


2,3-Wittig rearrangement, Experimental conditions and procedure, Typical conditions
Rearrangements must be carried out at temperatures below −60 °C to avoid competitive [1,2]-rearrangement. Typically, simple treatment of the substrate with n-butyllithium is sufficient to cause rearrangement. Reactions involving butyllithium should be carried out under nitrogen or argon with strict exclusion of water.


2,3-Xylidine
2,3-Xylidine is the organic compound with the formula C6H3(CH3)2NH2. it is one of several isomeric xylidines. It is a colorless viscous liquid. The compound is used in the production of the drug mefenamic acid and the herbicide xylachlor.


2,3-bisphosphoglycerate 3-phosphatase
2,3-bisphosphoglycerate 3-phosphatase (EC , MIPP1, 2,3-BPG 3-phosphatase) is an enzyme with systematic name 2,3-bisphospho-D-glycerate 3-phosphohydrolase. This enzyme catalyses the following chemical reaction


2,3-diaminopropionate N-oxalyltransferase
In enzymology, a 2,3-diaminopropionate N-oxalyltransferase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-diaminopropionate N-oxalyltransferase
Thus, the two substrates of this enzyme are oxalyl-CoA and L-2,3-diaminopropanoate, whereas its two products are CoA and N3-oxalyl-L-2,3-diaminopropanoate.


2,3-diaminopropionate N-oxalyltransferase
This enzyme belongs to the family of transferases, specifically those acyltransferases transferring groups other than aminoacyl groups. The systematic name of this enzyme class is oxalyl-CoA:L-2,3-diaminopropanoate N3-oxalyltransferase. Other names in common use include oxalyldiaminopropionate synthase, ODAP synthase, oxalyl-CoA:L-alpha,beta-diaminopropionic acid oxalyltransferase, oxalyldiaminopropionic synthase, and oxalyl-CoA:L-2,3-diaminopropanoate 3-N-oxalyltransferase.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase
In enzymology, a 2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase
Thus, the two substrates of this enzyme are 2,3-dihydro-2,3-dihydroxybenzoate and NAD+, whereas its 3 products are 2,3-dihydroxybenzoate, NADH, and H+.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is 2,3-dihydro-2,3-dihydroxybenzoate:NAD+ oxidoreductase. This enzyme is also called 2,3-diDHB dehydrogenase. This enzyme participates in biosynthesis of siderophore group nonribosomal.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Structure
2,3-diDHB dehydrogenase is a tetramer protein with dimension 65x69x43 Å. It has a crystallographic 222 symmetry, which exhibited for other members of short-chain oxireductase (SCOR) family of enzymes. The length of each monomer is 248 residues and the weight of the protein is 24647 Da. Each monomer consists of 7 beta-pleated sheets and 6 alpha helices.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Structure
Although the structure of the binding protein is not clearly defined, it was proposed that the binding pocket is made out of Leu83, Met85, Arg138, Gly140, Met141, Ser176, Met181, Gln182 and Leu185. It was also speculated that Arg138 is a likely subunit that interacts with the carboxyl group of 2,3-diDHB. Since there was a strong indication of oxidation at C3 position, Ser176 and Gln182 interact with the C2-hydroxyl group in order for the stereo-selective reaction to occur.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Reaction mechanism
In times of limited iron number in the environment, the EntA reaction is irreversible physiologically. The exact mechanism for the reaction is unknown; however, the proposed reaction scheme for the reaction is as following:


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Rate of reaction
The rate of the conversion reaction is determined by several factors. The regiochemical position of the carboxyl group and the 3-hydroxyl group plays one role in the reaction, in which the rate of reaction of 1,3-cis-substituted substrate gives about 40-fold higher kcat/Km value than the 1,3-trans-substituted substrate.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Roles in bacteria, E. coli
2,3-diDHB dehydrogenase catalyzes the NAD+-dependent oxidation of 2,3-dihydro-2,3-dihydroxybenzoate to produce an aromatic compound 2,3-dihydroxybenzoic acid (2,3-DHB or simply DHB). In times of iron deficiency, iron uptake is controlled by three genes: ent, fep, and fes for synthesis, export, and uptake of ferric Enterobactin and its hydrolytic cleavage to release Fe3+ into the cell. This production of this compound is controlled by eight genes: entA-entF, entH, and entS. In E. coli, all of these genes are controlled by the Fur repressor, such that the genes are turned on when the concentration of iron in the environment is low. From these six genes, EntA, EntB, and EntC are responsible for the synthesis of DHB from chorismic acid and the gene EntA encodes the information of 2,3-diDHB dehydrogenase. Without entA, entB, and entC, the bacteria show almost an absolute requirement of DHB in order to survive.


2,3-dihydro-2,3-dihydroxybenzoate dehydrogenase, Roles in bacteria, A. tumefaciens
Production of siderophores also exhibited in some plant-infecting bacteria, such as Agrobacterium tumefaciens. The enzyme is controlled by gene cluster agb and the production of 2,3-diDHB dehydrogenase is controlled by the gene agbA. The enzyme AgbA is homologous to the EntA enzyme in E. coli, the same enzyme that produces 2,3-diDHB dehydrogenase.


2,3-dihydroxy-2,3-dihydro-p-cumate dehydrogenase
In enzymology, a 2,3-dihydroxy-2,3-dihydro-p-cumate dehydrogenase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydroxy-2,3-dihydro-p-cumate dehydrogenase
Thus, the two substrates of this enzyme are cis-5,6-dihydroxy-4-isopropylcyclohexa-1,3-dienecarboxylate and NAD+, whereas its 3 products are 2,3-dihydroxy-p-cumate, NADH, and H+.


2,3-dihydroxy-2,3-dihydro-p-cumate dehydrogenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on the CH-CH group of donor with NAD+ or NADP+ as acceptor. The systematic name of this enzyme class is cis-2,3-dihydroxy-2,3-dihydro-p-cumate:NAD+ oxidoreductase. This enzyme participates in biphenyl degradation.


2,3-dihydroxybenzoate 2,3-dioxygenase
In enzymology, a 2,3-dihydroxybenzoate 2,3-dioxygenase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydroxybenzoate 2,3-dioxygenase
Thus, the two substrates of this enzyme are 2,3-dihydroxybenzoate and O2, whereas its product is 2-carboxy-cis,cis-muconate.


2,3-dihydroxybenzoate 2,3-dioxygenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on single donors with O2 as oxidant and incorporation of two atoms of oxygen into the substrate (oxygenases). The oxygen incorporated need not be derived from O2. The systematic name of this enzyme class is 2,3-dihydroxybenzoate:oxygen 2,3-oxidoreductase (decyclizing). This enzyme is also called 2,3-dihydroxybenzoate 2,3-oxygenase.


2,3-dihydroxybenzoate 3,4-dioxygenase
In enzymology, a 2,3-dihydroxybenzoate 3,4-dioxygenase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydroxybenzoate 3,4-dioxygenase
Thus, the two substrates of this enzyme are 2,3-dihydroxybenzoate and O2, whereas its product is 3-carboxy-2-hydroxymuconate semialdehyde.


2,3-dihydroxybenzoate 3,4-dioxygenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on single donors with O2 as oxidant and incorporation of two atoms of oxygen into the substrate (oxygenases). The oxygen incorporated need not be derived from O2. The systematic name of this enzyme class is 2,3-dihydroxybenzoate:oxygen 3,4-oxidoreductase (decyclizing). Other names in common use include o-pyrocatechuate oxygenase, 2,3-dihydroxybenzoate 1,2-dioxygenase, 2,3-dihydroxybenzoic oxygenase, and 2,3-dihydroxybenzoate oxygenase. This enzyme participates in benzoate degradation via hydroxylation.


2,3-dihydroxybenzoate—serine ligase
In enzymology, a 2,3-dihydroxybenzoate—serine ligase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydroxybenzoate—serine ligase
The 3 substrates of this enzyme are ATP, 2,3-dihydroxybenzoate, and L-serine, whereas its two products are products of ATP breakdown and N-(2,3-dihydroxybenzoyl)-L-serine.


2,3-dihydroxybenzoate—serine ligase
This enzyme belongs to the family of ligases, specifically those forming carbon-nitrogen bonds as acid-D-amino-acid ligases (peptide synthases). The systematic name of this enzyme class is 2,3-dihydroxybenzoate:L-serine ligase. Other names in common use include N-(2,3-dihydroxybenzoyl)-serine synthetase, and 2,3-dihydroxybenzoylserine synthetase.


2,3-dihydroxyindole 2,3-dioxygenase
In enzymology, a 2,3-dihydroxyindole 2,3-dioxygenase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dihydroxyindole 2,3-dioxygenase
Thus, the two substrates of this enzyme are 2,3-dihydroxyindole and O2, whereas its two products are anthranilate and CO2.


2,3-dihydroxyindole 2,3-dioxygenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on single donors with O2 as oxidant and incorporation of two atoms of oxygen into the substrate (oxygenases). The oxygen incorporated need not be derived from O2. The systematic name of this enzyme class is 2,3-dihydroxyindole:oxygen 2,3-oxidoreductase (decyclizing). This enzyme participates in tryptophan metabolism.


2,3-diketo-5-methylthiopentyl-1-phosphate enolase
2,3-diketo-5-methylthiopentyl-1-phosphate enolase (EC , DK-MTP-1-P enolase, MtnW, YkrW, RuBisCO-like protein, RLP) is an enzyme with systematic name 2,3-diketo-5-methylthiopentyl-1-phosphate keto-enol-isomerase. This enzyme catalyses the following chemical reaction


2,3-diketo-5-methylthiopentyl-1-phosphate enolase
The enzyme participates in the methionine salvage pathway in Bacillus subtilis.


2,3-dimethylmalate lyase
In enzymology, a 2,3-dimethylmalate lyase (EC ) is an enzyme that catalyzes the chemical reaction


2,3-dimethylmalate lyase
Hence, this enzyme has one substrate, (2R,3S)-2,3-dimethylmalate, and two products, propanoate and pyruvate.


2,3-dimethylmalate lyase
This enzyme belongs to the family of lyases, specifically the oxo-acid-lyases, which cleave carbon-carbon bonds. The systematic name of this enzyme class is (2R,3S)-2,3-dimethylmalate pyruvate-lyase (propanoate-forming). Other names in common use include 2,3-dimethylmalate pyruvate-lyase, and (2R,3S)-2,3-dimethylmalate pyruvate-lyase. This enzyme participates in c5-branched dibasic acid metabolism.


2,3-sigmatropic rearrangement
2,3-Sigmatropic rearrangements are a type of sigmatropic rearrangements and can be classified into two types. Rearrangements of allylic sulfoxides, amine oxides, selenoxides are neutral. Rearrangements of carbanions of allyl ethers are anionic. The general scheme for this kind of rearrangement is:


2,3-sigmatropic rearrangement
Atom Y may be sulfur, selenium, or nitrogen. If Y is nitrogen, the reaction is referred to as the Sommelet–Hauser rearrangement if a quaternary ammonium salt is involved or the aza-Wittig reaction if an alpha-metalated tertiary amine is involved; if Y is oxygen, then it is called a 2,3-Wittig rearrangement (not to be confused with the well-known Wittig reaction, which involves a phosphonium ylide). If Y is sulfur, the product can be treated with a thiophile to generate an allylic alcohol in what is known as the Mislow–Evans rearrangement.


2,3-sigmatropic rearrangement
A [2,3]-rearrangement may result in carbon-carbon bond formation. It can also be used as a ring-expansion reaction.


2,3-sigmatropic rearrangement, Stereoselectivity
2,3-sigmatropic rearrangements can offer high stereoselectivity. At the newly formed double bond there is a strong preference for formation of the E-alkene or trans isomer product. The stereochemistry of the newly formed C-C bond is harder to predict. It can be inferred from the five-membered ring transition state. Generally, the E-alkene will favor the formation of anti product, while Z-alkene will favor formation of syn product.


2,3-sigmatropic rearrangement, Stereoselectivity
Diastereoselectivity can be high for Z-alkene with alkynyl, alkenyl, or aryl anion-stabilizing group. Diastereoselectivity is usually lower with E-alkenes. Hydrocarbon groups will prefer exo orientation in the envelope-like transition state. Anion-stabilizing group will prefer the endo orientation in transition state.


2,4 Dienoyl-CoA reductase
2,4 Dienoyl-CoA reductase also known as DECR1 is an enzyme which in humans is encoded by the DECR1 gene which resides on chromosome 8. This enzyme catalyzes the following reactions


2,4 Dienoyl-CoA reductase
DECR1 participates in the beta oxidation and metabolism of polyunsaturated fatty enoyl-CoA esters. Specifically, it catalyzes the reduction of 2,4 dienoyl-CoA thioesters of varying length by NADPH cofactor to 3-trans-enoyl-CoA of equivalent length. Unlike the breakdown of saturated fat, cis and trans polyunsaturated fatty acid degradation requires three additional enzymes to generate a product compatible with the standard beta oxidation pathway. DECR is the second such enzyme (the others being enoyl CoA isomerase and dienoyl CoA isomerase) and is the rate limiting step in this auxiliary flow. DECR is capable of reducing both 2-trans,4-cis-dienoyl-CoA and 2-trans,4-trans-dienoyl-CoA thioesters with equal efficiency. At this time, there is no clear explanation for this of lack of stereo-specificity.


2,4 Dienoyl-CoA reductase, Structure
Eukaryotic DECR exists in both the mitochondria (mDECR) and the peroxisome (pDECR, coded by gene DECR2). The enzymes from each organelle are homologous and part of the short-chain dehydrogenase/reductase SDR super-family. mDECR is 124 kDa consisting of 335 amino acids before post-translational modification. The secondary structure shares many of the motifs of SDR, including a Rossmann fold for strong NADPH binding. The protein exists as a homotetramer in physiological environment, but has been shown to also form monomers and dimers in solution.


2,4 Dienoyl-CoA reductase, Structure
Crystallization of mDECR shows the enzyme provides a network of hydrogen bonds from key residues in the active site to NADPH and the 2,4-dienoyl-CoA which positions the hydride at 3.4 Å to the Cδ, compared with 4.0 Å to the Cβ (not shown). The enolate intermediate discussed earlier is stabilized by residues additional hydrogen bonds to Tyr166 and Asn148. Lys214 and Ser210 (conserved residues in all SDR enzymes) are thought to increase the pKa of Tyr166 and stabilize the transition state.


2,4 Dienoyl-CoA reductase, Structure
Additionally, at one end of the active site there is a flexible loop that provides sufficient room for long carbon chains. This likely gives the enzyme flexibility to process fatty acid chains of various lengths. Substrate length for mDECR catalysis is thought to be limited at 20 carbons, at which this very long chain fatty acid is first partially oxidized by pDECR in the peroxisome.


2,4 Dienoyl-CoA reductase, Enzyme mechanism, Eukaryotic DECR
2,4 Dienoyl-CoA thioester reduction by NADPH to 3-Enoyl CoA occurs by a two-step sequential mechanism via an enolate intermediate. DECR binds NADPH and the fatty acid thioester and positions them for specific hydride transfer to the Cδ on the hydrocarbon chain. The electrons from the Cγ-Cδ double bond move over to the Cβ-Cγ position, and those from the Cα-Cβ form an enolate. In the final step, a proton is abstracted from the water to the Cα and the thioester is reformed, resulting in a single Cβ-Cγ trans double bond.


2,4 Dienoyl-CoA reductase, Enzyme mechanism, Eukaryotic DECR
Since the final proton comes from water, the pH has a significant effect on the catalytic rate with the enzyme demonstrating maximal activity at ~6.0. A decrease in activity at pH < 6.0 can be explained by de-protonation of titratable residues that affect protein folding or substrate binding. Mutant proteins with modifications at key acidic amino acids (E154, E227, E276, D300, D117) show order of magnitude increases in Km and/or decreases in Vmax.


2,4 Dienoyl-CoA reductase, Enzyme mechanism, Prokaryotic DECR
2,4 Dienoyl-CoA Reductase from Escherichia coli shares very similar kinetic properties to that of eukaryotes, but differs significantly in both structure and mechanism. In addition to NADPH, E. Coli DECR requires a set of FAD, FMN and iron–sulfur cluster molecules to complete the electron transfer. A further distinction is E. Coli DECR produces the final 2-trans-enoyl-CoA without the need for Enoyl CoA Isomerase. The active site contains accurately positioned Tyr166 that donates a proton to the Cγ after hydride attack at the Cδ, completing the reduction in a single concerted step. Surprisingly, mutation of the Tyr166 does not eliminate enzyme activity but instead changes the product to 3-trans-enoyl-CoA. The current explanation is that Glu164, an acidic residue in the active site, acts as a proton donor to Cα when Tyr166 is not present.


2,4 Dienoyl-CoA reductase, Function
DECR is one of three auxiliary enzymes involved in a rate-limiting step of unsaturated fatty acid oxidation in mitochondria. In particular, this enzyme contributes to breaking the double bonds at all even-numbered positions, and some double bonds at odd-numbered position. The structure of the ternary complex of pDCR (peroxisomal 2,4-dienoyl CoA reductases) with NADP and its substrate provides essential and unique insights into the mechanism of catalysis. Unlike other members belonging to the SDR family, catalysis by pDCR does not involve a tyrosine-serine pair.


2,4 Dienoyl-CoA reductase, Function
Instead, a catalytically critical aspartate, together with an invariant lysine, polarizes a water molecule to donate a proton for the formation of the product. Although pDCR can use 2,4-hexadienoyl CoA as a substrate, the affinities for short chain fatty acids are lower. Analysis of the hinge movement of DCRs from the mitochondrion and peroxisomes sheds light on the reason behind the unique ability of the peroxisome to shorten very long chain fatty acids.


2,4 Dienoyl-CoA reductase, Clinical significance
Mutations in the DECR1 gene may result in 2,4 Dienoyl-CoA reductase deficiency, a rare but lethal disorder.


2,4 Dienoyl-CoA reductase, Clinical significance
Due to its role in fatty acid oxidation, DECR may serve as a therapeutic target for treating non-insulin dependent diabetes mellitus (NIDDM), which features hyperglycemia due to increased fatty acid oxidation.


2,4 Dienoyl-CoA reductase, Clinical significance
In knockout mice studies, DECR1−/− subjects accumulate significant concentrations of mono and polyunsaturated fatty acids in the liver during fasting (such as oleic acid, palmitoleic acid, linoleic acid, and linolenic acid). Mutant subjects were also found to have poor tolerance to cold, decrease in diurnal activity, and an overall reduction in adaptation to metabolic stressors.


2,4 Dienoyl-CoA reductase deficiency
2,4 Dienoyl-CoA reductase deficiency is an inborn error of metabolism resulting in defective fatty acid oxidation caused by a deficiency of the enzyme 2,4 Dienoyl-CoA reductase. Lysine degradation is also affected in this disorder leading to hyperlysinemia. The disorder is inherited in an autosomal recessive manner, meaning an individual must inherit mutations in NADK2, located at 5p13.2 from both of their parents. NADK2 encodes the mitochondrial NAD kinase. A defect in this enzyme leads to deficient mitochondrial nicotinamide adenine dinucleotide phosphate levels. 2,4 Dienoyl-CoA reductase, but also lysine degradation are performed by NADP-dependent oxidoreductases explaining how NADK2 deficiency can lead to multiple enzyme defects.


2,4 Dienoyl-CoA reductase deficiency
2,4-Dienoyl-CoA reductase deficiency was initially described in 1990 based on a single case of a black female who presented with persistent hypotonia. Laboratory investigations revealed elevated lysine, low levels of carnitine and an abnormal acylcarnitine profile in urine and blood. The abnormal acylcarnitine species was eventually identified as 2-trans,4-cis-decadienoylcarnitine, an intermediate of linoleic acid metabolism. The index case died of respiratory failure at four months of age. Postmortem enzyme analysis on liver and muscle samples revealed decreased 2,4-dienoyl-CoA reductase activity when compared to normal controls. A second case with failure to thrive, developmental delay, lactic acidosis and severe encephalopathy was reported in 2014.


2,4 Dienoyl-CoA reductase deficiency
2,4-Dienoyl-CoA reductase deficiency was included as a secondary condition in the American College of Medical Genetics Recommended Uniform Panel for newborn screening. Its status as a secondary condition means there was not enough evidence of benefit to include it as a primary target, but it may be detected during the screening process or as part of a differential diagnosis when detecting conditions included as primary target. Despite its inclusion in newborn screening programs in several states for a number of years, no cases have been identified via neonatal screening.


2,4'-dihydroxyacetophenone dioxygenase
In enzymology, a 2,4'-dihydroxyacetophenone dioxygenase (EC ) is an enzyme that catalyzes the chemical reaction


2,4'-dihydroxyacetophenone dioxygenase
Thus, the two substrates of this enzyme are 2,4'-dihydroxyacetophenone and O2, whereas its two products are 4-hydroxybenzoate and formate.


2,4'-dihydroxyacetophenone dioxygenase
This enzyme belongs to the family of oxidoreductases, specifically those acting on single donors with O2 as oxidant and incorporation of two atoms of oxygen into the substrate (oxygenases). The oxygen incorporated need not be derived from O2. The systematic name of this enzyme class is 2,4'-dihydroxyacetophenone oxidoreductase (C-C-bond-cleaving). This enzyme is also called (4- hydroxybenzoyl)methanol oxygenase. This enzyme participates in bisphenol a degradation.


2,4,5-Trichlorophenol
2,4,5-Trichlorophenol is an organochloride with the molecular formula C6H3Cl3O1. 2,4,5-Trichlorophenol has been used as a  fungicide and herbicide.


2,4,5-Trichlorophenoxyacetic acid
2,4,5-Trichlorophenoxyacetic acid (also known as 2,4,5-T), a synthetic auxin, is a chlorophenoxy acetic acid herbicide used to defoliate broad-leafed plants. It was developed in the late 1940s and was widely used in the agricultural industry until being phased out, starting in the late 1970s due to toxicity concerns. Agent Orange, a defoliant used by the British in the Malayan Emergency and the U.S. in the Vietnam War, was equal parts 2,4,5-T and 2,4-D (2,4-dichlorophenoxyacetic acid). 2,4,5-T itself is toxic with a NOAEL of 3 mg/kg/day and a LOAEL of 10 mg/kg/day.


2,4,5-Trichlorophenoxyacetic acid
Additionally, the manufacturing process for 2,4,5-T contaminates this chemical with trace amounts of  2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). TCDD is a carcinogenic persistent organic pollutant with long-term effects on the environment. With proper temperature control during production of 2,4,5-T, TCDD levels can be held to about .005 ppm. Before the TCDD risk was well understood, early production facilities lacked proper temperature controls and individual batches tested later were found to have as much as 60 ppm of TCDD.


2,4,5-Trichlorophenoxyacetic acid
In 1970, the United States Department of Agriculture halted the use of 2,4,5-T on all food crops except rice, and in 1985, the EPA terminated all remaining uses in the U.S. of this herbicide. In Canada, the use and sale of 2,4,5-T was prohibited after 1985. The international trade of 2,4,5-T is restricted by the Rotterdam Convention. 2,4,5-T has since largely been replaced by dicamba and triclopyr.


2,4,5-Trichlorophenoxyacetic acid
Human health effects from 2,4,5-T at low environmental doses or at biomonitored levels from low environmental exposures are unknown. Intentional overdoses and unintentional high dose occupational exposures to chlorophenoxy acid herbicides have resulted in weakness, headache, dizziness, nausea, abdominal pain, myotonia, hypotension, renal and hepatic injury, and delayed neuropathy. Cometabolism of 2,4,5-T is possible to produce 3,5-dichlorocatechol which, in turn, can be degraded by Pseudomonas bacteria. IARC considers the chlorophenoxyacetic acids group of chemicals as possibly carcinogenic to humans. In 1963 a production vessel for 2,4,5-T exploded in the Philips-Duphar plant in the Netherlands. Six workers that cleaned up afterwards got seriously intoxicated and developed chloracne. After twelve years, four of the six cleaners had died.


2,4,5-Trihydroxyamphetamine
2,4,5-Trihydroxyamphetamine (THM) is a neurotoxin and a metabolite of MDMA. It comes from the ring-hydroxylation of 3,4-methylenedioxyamphetamine (MDA).


2,4,5-Trihydroxyamphetamine
In one paper, it was shown to reduce hippocampal tryptophan hydroxylase activity by 54% after short-term treatment. In another study, it was shown to significantly reduce striatal tyrosine hydroxylase activity.


2,4,5-Trihydroxycinnamic acid
2,4,5-Trihydroxycinnamic acid is a hydroxycinnamic acid found in rooibos tea. cis-2,4,5-Trihydroxycinnamic acid can be isolated from seeds of Alisma orientale.


2,4,5-Trihydroxymethamphetamine
2,4,5-Trihydroxymethamphetamine (THMA) is a neurotoxin and a metabolite of MDMA. It has structural similarity to the dopamine neurotoxin 6-hydroxydopamine, and produces lasting serotonin deficits when administered centrally.


2,4,5-Trimethoxyphenethylamine
2,4,5-Trimethoxyphenethylamine (2C-O or 2C-OMe) or is a phenethylamine of the 2C family and was first synthesized by Jansen in 1931. It is a positional isomer of the drug mescaline (3,4,5-trimethoxy).


2,4,5-Trimethoxyphenethylamine, Chemistry
2C-O is a member of a class of chemical compounds commonly known as phenethylamines. Its full chemical name is 2-(2,4,5-trimethoxyphenyl)ethanamine; it is also known as 2,4,5-trimethoxyphenethylamine and 2,4,5-TMPEA.


2,4,5-Trimethoxyphenethylamine, Effects
Although not centrally active itself, 2C-O appeared to potentiate the action of mescaline when employed as pretreatment 45 minutes prior to the administration of mescaline.


2,4,5-Trimethoxyphenethylamine, Law, Canada
As of October 31, 2016, 2C-O is a controlled substance (Schedule III) in Canada.


2,4,5-Trimethoxyphenethylamine, Law, United States
2C-O is a Schedule I substance, as a positional isomer of mescaline.


2,4,5-Trimethoxyphenethylamine, Law, United Kingdom
2C-O and all other compounds featured in PiHKAL are Class A drugs in the United Kingdom.


2,4,5-Trimethoxypropiophenone
2,4,5-Trimethoxypropiophenone is a natural phenylpropanoid and precursor in the synthesis of α-asarone.


2,4,5-Trimethoxypropiophenone, Natural occurrence
2,4,5-Trimethoxypropiophenone is a component of several plant species' essential oils. The chemical has been identified in Piper marginatum, Acorus tatarinowii, and Asarum maximum.


2,4,6-Tri-tert-butylphenol
2,4,6-Tri-tert-butylphenol (2,4,6-TTBP) is a phenol symmetrically substituted with three tert-butyl groups and thus strongly sterically hindered. 2,4,6-TTBP is a readily oxidizable aromatic compound and a weak acid. It oxidizes to give the deep-blue 2,4,6-tri-tert-butylphenoxy radical. 2,4,6-TTBP is related to 2,6-di-tert-butylphenol, which is widely used as an antioxidant in industrial applications. These compounds are colorless solids.


2,4,6-Tri-tert-butylphenol, Preparation
The preparation of 2,4,6-tri-tert-butylphenol has been studied extensively. As early as 1890, Wilhelm Koenigs described the acid-catalyzed reaction of phenol with isobutylene. Many other reports have appeared. Yields up to 90%  have been reported. Typical side products are the result of incomplete alkylation: 4-tert-butylphenol (4-TBP), 2,4-di-tert-butylphenol (2,4-DTBP), 2,6-di-tert-butylphenol (2,6-DTBP). 2,5-Di-tert-butylphenol (2,5-DTB) has been observed. 2,4,6-tri-tert-butylphenol is also found as a by-product in the synthesis of the disubstitution products 2,4-DTBP and 2,6-DTBP, which are more widely used antioxidants.


2,4,6-Tri-tert-butylphenol, Preparation
A synthesis of 2,4,6-tri-tert-butylphenol has been described that is also suitable as a teaching experiment. Methyl tert-butyl ether is used as the alkylating agent and sulfuric acid as catalyst. 2,4,6-TTBP is being obtained in 69% yield.


2,4,6-Tri-tert-butylphenol, Properties
2,4,6-Tri-tert-butylphenol is a white solid which dissolves in many organic solvents, but not in aqueous or alcoholic alkaline solutions. The green-blue coloring with iron(III)chloride, which is characteristic for phenols, does not occur in 2,4,6-TTBP. The compound is oxidizable in air but practically non-biodegradable.


2,4,6-Tri-tert-butylphenol, Properties
As an electron-rich aromatic, 2,4,6-tri-tert-butylphenol can also be easily oxidized electrochemically. In the alkaline, the phenolate anion formed is first oxidized in a reversible reaction to the phenoxy radical. The stable radical is oxidized by further electron withdrawal to the phenoxonium cation, which reacts in water to give 2,4,6-tri-tert-butyl-4-hydroxy-2,5-cyclohexadienone.


2,4,6-Tri-tert-butylphenol, Properties
In acidic media, the hydroxydienone is dealkylated with the cleavage of the tert-butyl group in the 4-position to the 2,6-di-tert-butylhydroquinone, which is oxidized to the end product 2,6-di-tert-butyl-1,4-benzoquinone.


2,4,6-Tri-tert-butylphenol, Properties
The oxidation of 2,4,6-tri-tert-butylphenol in the alkaline to the intensely blue-colored phenoxy radical can also occur with potassium ferricyanide. The 2,4,6-tri-tert-butylphenoxy radical forms blue crystals on cooling to -70 ° C, which are stable at room temperature for several weeks and only gradually turn yellow. The phenoxy radical reacts with oxygen as a diradical to form a 4,4'-linked peroxide forming yellow crystals.


2,4,6-Tri-tert-butylphenol, Applications
The electron-rich 2,4,6-tri-tert-butylphenol can easily be oxidized to the phenoxy radical, which in the 4-position adds phenols, as well as alcohols and thiols to the corresponding cyclohexadienones. The cyclohexadienones, also referred to in the literature as chinolethers, cleave the 4-position tert-butyl group upon heating under acidic conditions and aromatizes back to the substituted phenol.


2,4,6-Tri-tert-butylphenol, Applications
The reaction can be used for the synthesis of 2,6-di-tert-butyl-4-methoxyphenol, which is frequently used as an antioxidant.


2,4,6-Tri-tert-butylphenol, Applications
2,4,6-TTBP is used as stabilizers, free-radical scavengers and antioxidants in technical applications, such as in fuels, hydraulic fluids and lubricating oils, as well as in elastomeric and thermoplastic polymers. Because of its pronounced persistence, its high tendency for bioaccumulation and aquatic toxicity, 2,4,6-TTBP is only of low industrial use and is even forbidden, for example, in Japan.


2,4,6-Tri-tert-butylphenol, Applications
The phenoxy radical of 2,4,6-TTBP is also described as a sterically demanding protecting group in a reagent for the transfer of a nucleophilic dimethylaminomethyl-group [(CH3)2-N-CH2-] to form tertiary amines.


2,4,6-Tribromoaniline
2,4,6-Tribromoaniline is a chemical compound with a formula of  C6H4Br3N. It is used in organic synthesis of pharmaceuticals, agrochemicals and fire-extinguishing agents.


2,4,6-Tribromoaniline, Synthesis
2,4,6-Tribromoaniline can be prepared by treating bromine water with aniline in a solution of acetic acid or dilute hydrochloric acid:


2,4,6-Tribromoanisole
2,4,6-Tribromoanisole (TBA) is a chemical compound that is a brominated derivative of anisole. It is one of the chemicals responsible for cork taint.


2,4,6-Tribromoanisole
Tribromoanisole is a fungal metabolite of 2,4,6-tribromophenol, which is used as a fungicide. It can be found in minute traces on packaging materials stored in the presence of fiberboard treated with 2,4,6-tribromophenol. These traces can cause an unpleasant mustiness in packaged foods.


2,4,6-Tribromoanisole
Tribromoanisole is usually produced when naturally occurring airborne fungi or bacteria (usually Aspergillus sp., Penicillium sp., Actinomycetes, Botrytis cinerea, Rhizobium sp., or Streptomyces) are presented with brominated phenolic compounds, which they then convert into bromoanisole derivatives. The bromophenols can originate from various contaminants including those found in some pesticides and wood preservatives. They can also migrate from other objects such as shipping pallets treated by bromophenols.


2,4,6-Tribromoanisole
Tribromoanisole has a very low odor detection threshold. It is 0.08-0.3 parts per trillion (ppt) in water and 2-6 ppt in wine (or 3.4-7.9 ng/l) so even very minute amounts can be detected. It causes unpleasant earthy, musty and moldy aromas.


2,4,6-Tribromoanisole, Consumer product recalls
There have been several events in which consumer products were recalled due to odors caused by tribromoanisole on product packaging. In 2010 and 2011, Johnson & Johnson voluntarily recalled some over-the-counter products, including Tylenol, due to an odor caused by tribromoanisole. In this case, a supplier had used 2,4,6-tribromophenol to treat wooden pallets on which product packaging materials were transported and stored. In 2010 and in 2011, Pfizer recalled bottles of Lipitor after reports of an odor linked to the packaging bottles. Pfizer said the bottles were supplied by a third-party manufacturer and determined the cause to be exposure of the bottles to low levels of tribromoanisole as they were shipped or stored.


2,4,6-Tribromophenol
2,4,6-Tribromophenol (TBP) is a brominated derivative of phenol. It is used as a fungicide, as a wood preservative, and an intermediate in the preparation of flame retardants.


2,4,6-Tribromophenol, Production
Although natural TBP has been identified in ocean sediments as a metabolite of marine fauna, the commercial product is prepared industrially. In 2001, the production volume of TBP was estimated to be 2500 tonnes/year in Japan and 9500 tonnes/year worldwide. TBP can be prepared by the controlled reaction of elemental bromine with phenol:


2,4,6-Tribromophenol, Uses
The predominant use of TBP is as an intermediate in the preparation of flame retardants such as brominated epoxy resins. TBP is reacted with sodium hydroxide to form the sodium salt, which is used as a fungicide and wood preservative.


2,4,6-Tribromophenol, Uses, Bismuth salt
The bismuth salt is the active ingredient in Xeroform dressing.


2,4,6-Tribromophenol, Metabolism
Microbial metabolism in products treated with TBP is known to produce 2,4,6-tribromoanisole (TBA),  which has a musty odor. In 2010 and 2011, Pfizer and Johnson & Johnson voluntarily recalled some products due to TBA odors from wooden pallets which were treated with TBP.


2,4,6-Trichloroaniline
2,4,6-Trichloroaniline is a chemical compound with a formula of C6H4Cl3N. It is useful as an intermediate in chemical reactions.


2,4,6-Trichloroaniline, Preparation
Dry aniline are dissolved in dry carbon tetrachloride, and placed in a flask fitted with a mechanical stirrer. The flask is surrounded by an efficient freezing mixture, so that the temperature is about -10 °C. Through one of the side tubes is passed dry gaseous chlorine mixed with dry carbon dioxide (equal volumes). A white crystalline deposit of 2,4,6-trichloroaniline is thrown down, but if the temperature rises, oxidants are added, or the materials are not absolutely dry, the product is contaminated with aniline black (polyaniline).


2,4,6-Trichloroaniline, Safety
Occupational exposure to 2,4,6-trichloroaniline may occur through inhalation and dermal contact with this compound at workplaces where 2,4,6-trichloroaniline is produced or used (SRC). The general population may be exposed to 2,4,6-trichloroaniline via drinking water and dermal contact with this compound in dyestuffs, pigments, and pesticides containing 2,4,6-trichloroaniline. 2,4,6 -trichloroaniline can be toxic when inhaled or ingested orally. The lethal dose is 2400 mg/kg for a rat.


2,4,6-Trichloroaniline, Safety
Upon heating, 2,4,6-trichloroaniline will not undergo combustions, but may release hydrogen chloride, nitrogen oxides or carbon monoxide (when burned), which is irritating or toxic.


2,4,6-Trichloroanisole
2,4,6-Trichloroanisole (TCA) is a chemical compound that is a chlorinated derivative of anisole. TCA is a fungal metabolite of 2,4,6-trichlorophenol, which is used as a fungicide. It can be found in minute traces on packaging materials stored in the presence of fiberboard treated with trichlorophenol.


2,4,6-Trichloroanisole
TCA is the chemical primarily responsible for cork taint in wines. TCA has also been implicated as a major component of the "Rio defect" in coffees from Central and South America, which refers to a taste described as medicinal, phenolic, or iodine-like.


2,4,6-Trichloroanisole
TCA is usually produced when naturally occurring airborne fungi and bacteria (usually Aspergillus sp., Penicillium sp., Actinomycetes, Botrytis cinerea, Rhizobium sp., or Streptomyces) are presented with chlorinated phenolic compounds, which they then convert into chlorinated anisole derivatives. The chlorophenols can originate from various contaminants such as those found in some pesticides and wood preservatives. Chlorophenols can also be a product of the chlorine bleaching process used to sterilize or bleach wood, paper, and other materials; they can be synthesized by reaction of hypochlorites with lignin. They can also migrate from other objects such as shipping pallets treated by chlorophenols.


2,4,6-Trichloroanisole
The odor of TCA is not directly perceived. Instead, the molecule distorts the perception of smell by suppressing olfactory signal transduction. The effect occurs at very low concentrations (single parts per trillion), so even very minute amounts of TCA can be detected. It causes unpleasant earthy, musty and moldy aromas.


2,4,6-Trichlorophenol
2,4,6-Trichlorophenol, also known as TCP, phenaclor, Dowicide 2S, Dowcide 2S, omal, is a chlorinated phenol that has been used as a fungicide, herbicide, insecticide, antiseptic, defoliant, and glue preservative. It is a clear to yellowish crystalline solid with a strong, phenolic odor. It decomposes on heating to produce toxic and corrosive fumes including hydrogen chloride and chlorine.


2,4,6-Trichlorophenol, Health effects
In animal models, consumption of 2,4,6-trichlorophenol leads to an increased incidence of lymphomas, leukemia, and liver cancer. It is classified as Group B2 (probable human carcinogen) by the United States Environmental Protection Agency. The technical grade of this substance may contain polychlorinated dibenzodioxins (PCDDs), polychlorinated dibenzofurans (PCDFs), and other contaminants.


2,4,6-Trichlorophenol, Environmental effects
2,4,6-Trichlorophenol is an environmental pollutant that has been found in fresh water lakes such as the Great Lakes.


2,4,6-Trihydroxyacetophenone
2,4,6-Trihydroxyacetophenone (THAP) is a chemical compound that is a derivative of phloroglucinol.


2,4,6-Trihydroxyacetophenone
In an animal model, THAP was reported to enhance cholesterol 7 alpha-hydroxylase (CYP7A1) activity.


2,4,6-Trihydroxyacetophenone
THAP is also used as a matrix in matrix-assisted laser desorption/ionization (MALDI) for the analysis of acidic glycans and glycopeptides in negative ion mode.


2,4,6-Trihydroxyacetophenone, Derivatives
THAP is a chemical precursor that can be used to form part of the backbone of 5,7-dihydroxyflavones like noreugenin, apigenin, luteolin, diosmetin, naringenin, and hesperetin.


2,4,6-Trimethylaniline
2,4,6-Trimethylaniline is an organic compound with formula (CH3)3C6H2NH2. It is an aromatic amine that is of commercial interest as a precursor to dyes. It is prepared by selective mononitration of mesitylene, avoiding oxidation of the methyl groups. The resulting nitro compound is reduced to the aniline.


2,4,6-Trimethylaniline, Coordination chemistry
Trimethylaniline is a building block to a variety of bulky ligands. Condensation with glyoxal gives the 1,2-diimine ligands. An example is glyoxal-bis(mesitylimine), a yellow solid that is synthesized by condensation of 2,4,6-trimethylaniline and glyoxal. The diimine is a useful precursor to popular NHC ligands including IMes. N-heterocyclic carbenes, as found in 2nd generation Grubbs' catalyst, are also prepared from this compound.


2,4,6-Trimethylpyridine
2,4,6-Trimethylpyridine (2,4,6-collidine) is an organic compound which belongs to the heterocycles (more precisely, heteroaromatics). It consists of a pyridine ring substituted with three methyl groups. It belongs to the substance group of the collidines, a group of six constitutional isomers. 2,4,6-trimethylpyridine is the most well-known isomer of this group.


2,4,6-Trimethylpyridine, Properties
The compound has a refractive index of 1.4959 (25 °C).


2,4,6-Trimethylpyridine, Preparation
2,4,6-Trimethylpyridine was isolated from Dippel's oil in 1854. A synthesis can be carried out analogously to the Hantzsch's dihydropyridine synthesis from ethyl acetoacetate (as β-ketocarbonyl compound), acetaldehyde and ammonia in the ratio 2: 1: 1.


2,4,6-Trimethylpyridine, Use
By oxidation of the methyl groups with potassium permanganate collidinic acid is obtained.


2,4,6-Trimethylpyridine, Use
2,4,6-Trimethylpyridine is used in organic syntheses (for example, for dehydrohalogenation), by binding the formed hydrogen halides.


2,4,6-Trinitroaniline
2,4,6-Trinitroaniline, C6H4N4O6, abbreviated as TNA and also known as picramide, a nitrated amine. Materials in this group range from slight to strong oxidizing agents. If mixed with reducing agents, including hydrides, sulfides and nitrides, they may begin a vigorous reaction that culminates in a detonation. The aromatic nitro compounds may explode in the presence of a base such as sodium hydroxide or potassium hydroxide even in the presence of water or organic solvents. The explosive tendencies of aromatic nitro compounds are increased by the presence of multiple nitro groups. The appearance of trinitroaniline varies from yellow to orange to red depending on its purity and concentration.


2,4,6-Trinitroaniline, Applications/Uses
Trinitroaniline is only used in modern times in the small warheads of some explosive devices such as mortars. In World War II it was used by Imperial Japanese Navy as Type 97 bakuyaku (Model 1931 explosive) in some versions of gun projectiles instead of less stable burster schimose. It was also used in the Yokosuka MXY-7 Ohka, a kamikaze antishipping human-guided rocket aircraft.


2,4,6-Trinitroaniline, Health and safety
Trinitroaniline is dangerously explosive. Symptoms of exposure to this compound may include skin and eye irritation, headache, drowsiness, weakness, cyanosis, and respiratory distress.


2,4,6-Trinitrobenzenesulfonic acid
Trinitrobenzenesulfonic acid (C6H3N3O9S) is a nitroaryl oxidizing acid. Due to its extreme oxidative properties, if mixed with reducing agents including hydrides, sulfides, and nitrides, it may begin a vigorous reaction that culminates in almost immediate detonation. The aromatic nitro compounds may explode in the presence of a base such as sodium hydroxide or potassium hydroxide even in the presence of water or organic solvents because of the explosive tendencies of aromatic nitro compounds which increase in the presence of multiple nitro groups. Not much is known about this compound, but it is used as a peptide terminal amino group neutralizer and is currently being investigated for its effects on the immune system.


2,4,6-Trinitrobenzenesulfonic acid, Uses
Its primary usage is primarily to neutralize peptide terminal amino groups in scientific research. Occasionally it is used as a detonator for certain other explosive compounds.


2,4,6-Trinitrobenzenesulfonic acid, Uses
It is also used to induce colitis in the colon of laboratory animals in order to model inflammatory bowel disease and post-infectious irritable bowel syndrome.


2,4,6-Trinitrobenzenesulfonic acid, Health concerns and safety precautions
The primary hazard of working with 2,4,6-trinitrobenzenesulfonic acid is the risk of instantaneous explosion. 2,4,6-Trinitrobenzenesulfonic acid is an extremely sensitive compound especially when mixed with other compounds, exposed to heat, or exposed to rapid temperature or pressure changes. The toxicological properties of this compound have not been investigated, so all health effects are unknown. To best prevent bodily harm or injury it is recommended that all direct contact be avoided and the compound be kept under extremely strict environmentally controlled conditions.


2,4,6-Trinitrobenzenesulfonic acid, Health concerns and safety precautions
In case of spillage it is recommended that a local fire department be called in advance prior to any attempt at cleaning. In case of fire it is recommended that the material be left to burn and the surrounding area be evacuated. If fire fighting is required it is recommended that a fully positive pressure self-contained breathing apparatus be used along with either foam or CO2 extinguishers.


2,4,6-Tris(trinitromethyl)-1,3,5-triazine
2,4,6-Tris(trinitromethyl)-1,3,5-triazine is a chemical compound that is a derivative of triazine first prepared in 1995. It is synthesized by destructive nitration of 2,4,6-tricarboxyl-1,3,5-triazine. It is noteworthy for having more nitro groups than it does carbon atoms, thus potentially being useful as an oxygen source, or added to oxygen-poor explosives to increase their power.


2,4,6-Tris(trinitromethyl)-1,3,5-triazine
Derivatives have been prepared by nucleophilic displacement of the nitro groups with azide and hydrazine.


2,4,7-trihydroxy-1,4-benzoxazin-3-one-glucoside 7-O-methyltransferase
2,4,7-trihydroxy-1,4-benzoxazin-3-one-glucoside 7-O-methyltransferase (EC , BX7 (gene), OMT BX7) is an enzyme with systematic name S-adenosyl-L-methionine:(2R)-4,7-dihydroxy-3-oxo-3,4-dihydro-2H-1,4-benzoxazin-2-yl β-D-glucopyranoside 7-O-methyltransferase. This enzyme catalyses the following chemical reaction


2,4,7-trihydroxy-1,4-benzoxazin-3-one-glucoside 7-O-methyltransferase
The enzyme is involved in the biosynthesis of the protective and allelopathic benzoxazinoid DIMBOA, e.g. from the family Poaceae (grasses).


2,4-Bis(4-hydroxybenzyl)phenol
2,4-Bis(4-hydroxybenzyl)phenol is a phenolic compound produced by the saprophytic orchid Gastrodia elata and by the myco-heterotroph orchid Galeola faberi.


2,4-DB
2,4-DB or 4-(2,4-dichlorophenoxy)butyric acid is a selective systemic phenoxy herbicide used to control many annual and perennial broad-leaf weeds in alfalfa, peanuts, soybeans, and other crops. Its active metabolite, 2,4-D, inhibits growth at the tips of stems and roots. It is classified in toxicity class III. It shows some evidence of toxicity to dogs and cats, such as changes in body weight and reduced numbers of offspring, when fed 25-80 milligrams per kilogram of body weight for prolonged periods. Tests of carcinogenicity in this range yielded differing results. It is moderately toxic to fish.


2,4-Diacetylphloroglucinol
2,4-Diacetylphloroglucinol or Phl is a natural phenol found in several bacteria:


2,4-Diaminotoluene
2,4-Diaminotoluene is an organic compound with the formula C6H3(NH2)2CH3. It is one isomer of six with this formula. It is a white solid although commercial samples are often yellow-tan.


2,4-Diaminotoluene, Preparation
It is prepared by hydrogenation of 2,4-dinitrotoluene using a nickel catalyst. Commercial samples often contain up to 20% of the 2,6-isomer.


2,4-Diaminotoluene, Preparation
A laboratory method involves reduction of 2,4-dinitrotoluene with iron powder.


2,4-Diaminotoluene, Use
It is mainly used as a precursor to toluene diisocyanate, a precursor to polyurethane.


2,4-Diaminotoluene, Use
Its reaction with benzenediazonium chloride gives the cationic azo dye Basic Orange 1. Condensation of 2,4-diaminotoluene with acetaldehyde gives the acridine dye called Basic Yellow 9.


2,4-Dibromophenol
2,4-Dibromophenol is a brominated derivative of phenol with the molecular formula C6H4Br2O. It belongs to the bromobenzenes, which are organic compounds containing bromine atoms attached to a benzene ring.


2,4-Dibromophenol, Properties
At room temperature, 2,4-dibromophenol is a solid with needle-like crystals. It melts at 38 °C (100.4 °F) and boils at 238.5 °C (461.3 °F). it has a molecular weight of 251.905 g/mol. It is soluble in water, ethanol, ether and benzene and slightly soluble in carbon tetrachloride.


2,4-Dibromophenol, Occurrence
2,4-Dibromophenol is found in certain molluscs and crustaceans, as well as the acorn worm Saccoglossus bromophenolosus, which is named after it.


2,4-Dichlorobenzyl alcohol
2,4-Dichlorobenzyl alcohol is a mild antiseptic, able to kill bacteria and viruses associated with mouth and throat infections. It is a common ingredient in throat lozenges such as Cofsils, Strepsils, Lorsept, and Gorpils. It is also an ingredient in the European product Neo Borocillina. A low-pH throat lozenge containing dichlorobenzyl alcohol (1.2 mg) and amylmetacresol (0.6 mg) has been found to deactivate respiratory syncytial virus and SARS-Cov, but not adenovirus or rhinovirus. A dentifrice containing 10% sodium benzoate and 0.3% dichlorobenzyl alcohol maintains antimicrobial activity for 5 to 10 minutes after brushing.


2,4-Dichlorophenol
2,4-Dichlorophenol (2,4-DCP) is a chlorinated derivative of phenol with the molecular formula Cl2C6H3OH. It is a white solid that is mildly acidic (pKa = 7.9). It is produced on a large scale as a precursor to  the herbicide 2,4-dichlorophenoxyacetic acid (2,4-D).


2,4-Dichlorophenol, Production and use
Annual worldwide production is estimated at 88 million pounds. It is also a photo-degradation product of the common antibacterial and antifungal agent triclosan along with the dioxin 2,8-dichlorodibenzo-p-dioxin.


2,4-Dichlorophenol, Safety
The LD50 is 580 mg/kg (rats, oral). Liquid (molten) 2,4-DCP is readily absorbed through the skin. Solid 2,4-DCP does not readily absorb through skin and has a lower NFPA H=3 rating (versus H=4 for molten 2,4-DCP). This is primarily caused by instantaneous kidney failure, liver failure, and failure of various other organs.


2,4-Dichlorophenoxyacetic acid
2,4-Dichlorophenoxyacetic acid is an organic compound with the chemical formula C8H6Cl2O3 which is usually referred to by its ISO  common name 2,4-D. It is a systemic herbicide which kills most broadleaf weeds by causing uncontrolled growth in them but most grasses such as cereals, lawn turf, and grassland are relatively unaffected.


2,4-Dichlorophenoxyacetic acid
2,4-D is one of the oldest and most widely available herbicides and defoliants in the world, having been commercially available since 1945, and is now produced by many chemical companies since the patent on it has long since expired. It can be found in numerous commercial lawn herbicide mixtures, and is widely used as a weedkiller on cereal crops, pastures, and orchards. Over 1,500 herbicide products contain 2,4-D as an active ingredient.


2,4-Dichlorophenoxyacetic acid, History
The discovery of 2,4-D as well as the similar hormone herbicides 2,4,5-T, and MCPA occurred during World War II and was a case of multiple discovery by four groups working independently under wartime secrecy in the United Kingdom and the United States: William G. Templeman and associates at Imperial Chemical Industries (ICI) in the UK; Philip S. Nutman and associates at Rothamsted Research in the UK; Franklin D. Jones and associates at the American Chemical Paint Company; and Ezra Kraus, John W. Mitchell, and associates at the University of Chicago and the United States Department of Agriculture.


2,4-Dichlorophenoxyacetic acid, History
All four groups were subject to wartime secrecy laws and did not follow the usual procedures of publication and patent disclosure. In December 1942, following a meeting at the Ministry of Agriculture the Rothamsted and ICI workers pooled resources and Nutman moved to Jealott's Hill to join the ICI effort. The first scientific publication describing the 2,4-D structure and plant growth regulating activity was by Percy W. Zimmerman and Albert E. Hitchcock at the Boyce Thompson Institute, who were not the original inventors. The precise sequence of early 2,4-D discovery events and publications has been discussed.


2,4-Dichlorophenoxyacetic acid, History
William Templeman found that when indole-3-acetic acid (IAA), the naturally occurring auxin, was used at high concentrations, it could stop plant growth. In 1940, he published his finding that IAA killed broadleaf plants within a cereal field. MCPA was discovered at about that time by his ICI group.


2,4-Dichlorophenoxyacetic acid, History
In the USA, a similar search for an acid with a longer half life, i.e., a metabolically and environmentally more stable compound, led to 2,4-dichlorophenoxyacetic acid (2,4-D) and 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), both phenoxy herbicides and analogs of IAA. Robert Pokorny, an industrial chemist for the C.B. Dolge Company in Westport, Connecticut, published their synthesis in 1941.


2,4-Dichlorophenoxyacetic acid, History
All the novel auxins were developed as part of a clandestine wartime effort to create chemical warfare agents and / or selective herbicides; although 2,4-D was not used this way during the war. Britain and the United States were looking for a chemical to starve Germany and Japan into submission by killing their potato and rice crops, but 2,4-D was found to be ineffective for that purpose, because both crops tolerate it. Within a year after the war ended, 2,4-D was commercially released as an herbicide to control broadleaf weeds in grain crops such as rice and wheat, and in the 1950s it was registered in the United States to control size and enhance skin color in potatoes without affecting yields.


2,4-Dichlorophenoxyacetic acid, History
The first publication of 2,4-D's use as a selective herbicide came in 1944. The ability of 2,4-D to control broadleaf weeds in turf was documented soon thereafter, in 1944. Starting in 1945, the American Chemical Paint Company brought 2,4-D to market as an herbicide called "Weedone". It revolutionized weed control, as it was the first compound that, at low doses, could selectively control dicotyledons (broadleaf plants), but not most monocotyledons — narrowleaf crops, such as  wheat, maize (corn), rice, and similar cereal grass crops. At a time when labor was scarce and the need for increased food production was large, it literally "replaced the hoe".


2,4-Dichlorophenoxyacetic acid, History
2,4-D is one of the ingredients in Agent Orange, an herbicide that was widely used during the Malayan Emergency and the Vietnam War. However, 2,3,7,8-Tetrachlorodibenzodioxin (TCDD), a contaminant in the production of another ingredient in Agent Orange, 2,4,5-T, was the cause of the adverse health effects associated with Agent Orange.


2,4-Dichlorophenoxyacetic acid, History
In the 2000s, Dow AgroSciences developed a new choline salt version of 2,4-D (2,4-D choline) that Dow included in its "Enlist Duo" herbicide along with glyphosate and an agent that reduces drift; the choline salt form of 2,4-D is less volatile than 2,4-D.


2,4-Dichlorophenoxyacetic acid, Manufacture
2,4-D is a member of the phenoxy family of herbicides.


2,4-Dichlorophenoxyacetic acid, Manufacture
2,4-D is manufactured from chloroacetic acid and 2,4-dichlorophenol, which is itself produced by chlorination of phenol. Alternatively, it is produced by the chlorination of phenoxyacetic acid. The production processes may create several contaminants including di-, tri-, and tetrachlorodibenzo-p-dioxin isomers and N-nitrosamines, as well as monochlorophenol.


2,4-Dichlorophenoxyacetic acid, Mode of action
2,4-D acts by mimicking the action of the plant growth hormone auxin, which results in uncontrolled growth and eventually death in susceptible plants. It is absorbed through the leaves and is translocated to the meristems of the plant. Uncontrolled, unsustainable growth ensues, causing stem curl-over, leaf withering, and eventual plant death. 2,4-D is typically applied as an amine salt, but more potent ester versions exist, as well.


2,4-Dichlorophenoxyacetic acid, Applications
2,4-D is primarily used as a selective herbicide which kills many terrestrial and aquatic broadleaf weeds, but not grasses. As it was discovered in the 1940s, a patent no longer governs the manufacture and sale of 2,4-D, and any company is free to produce it. Thus, it is sold in various formulations under a wide variety of brand names. 2,4-D can be found in commercial lawn herbicide mixtures, which often contain other active ingredients including mecoprop and dicamba. Over 1,500 herbicide products contain 2,4-D as an active ingredient.


2,4-Dichlorophenoxyacetic acid, Applications
A wide variety of different sectors uses products containing 2,4-D to kill weeds and unwanted vegetation. In agriculture, it was the first herbicide found to be capable of selectively killing weeds but not crops. It has been used since 1945 to control broad-leafed weeds in pastures, orchards, and cereal crops such as corn, oats, rice, and wheat. Cereals, in particular, have excellent tolerance to 2,4-D when it is applied before planting. 2,4-D is the cheapest way for farmers to control winter annual weeds by spraying in the fall, often at the lowest recommended rate. This is particularly effective before planting beans, peas, lentils, and chickpeas. The estimated use of 2,4-D in US agriculture is mapped by the US Geological Survey. In 2017, the latest date for which figures are available, this reached 40,000,000 pounds (18,000,000 kg) annually.


2,4-Dichlorophenoxyacetic acid, Applications
In domestic lawn and garden maintenance, 2,4-D is commonly used for weed control in lawns and other turf. It is used to kill unwanted weeds such as dandelions, plantain, clover, and chickweed. In forestry, it is used for stump treatment, trunk injection, and selective control of brush in conifer forests. Along roadways, railways, and power lines, it is used to control weeds and brush which might interfere with safe operation and damage equipment. Along waterways, it is used to control aquatic weeds that might interfere with boating, fishing, and swimming or clog irrigation and hydroelectric equipment. It is often used by government agencies to control the spread of invasive, noxious, and non-native weed species and prevent them from crowding out native species, and also to control many poisonous weeds such as poison ivy and poison oak.


2,4-Dichlorophenoxyacetic acid, Applications
A 2010 monitoring study conducted in the US and Canada found that "current exposures to 2,4-D are below applicable exposure guidance values."


2,4-Dichlorophenoxyacetic acid, Applications
2,4-D has been used in laboratories for plant research as a supplement in plant cell culture media such as MS medium since at least 1962. 2,4-D is used in plant cell cultures as a dedifferentiation (callus induction) hormone. It is classified as an auxin plant hormone derivative.


2,4-Dichlorophenoxyacetic acid, Health effects
Men who work with 2,4-D are at risk for abnormally shaped sperm and thus fertility problems; the risk depends on the amount and duration of exposure and other personal factors.


2,4-Dichlorophenoxyacetic acid, Health effects, Acute toxicity
According to the U.S. Environmental Protection Agency, "The toxicity of 2,4-D depends on its chemical forms, including salts, esters, and an acid form. 2,4-D generally has low toxicity for humans, except certain acid and salt forms can cause eye irritation. Swimming is restricted for 24 hours after application of certain 2,4-D products applied to control aquatic weeds to avoid eye irritation." As of 2005 the median lethal dose or LD50 determined in acute toxicity rat studies was 639 mg/kg.


2,4-Dichlorophenoxyacetic acid, Health effects, Acute toxicity
Urinary alkalinisation has been used in acute poisoning, but evidence to support its use is poor.


2,4-Dichlorophenoxyacetic acid, Health effects, Cancer risk
The  International Agency for Research on Cancer classifies 2,4-D as a possible carcinogen to humans while the United States Environmental Protection Agency does not. The International Agency for Research on Cancer (IARC), said 2,4-D was classified as "possibly carcinogenic to humans (Group 2B), based on inadequate evidence in humans and limited evidence in experimental animals".


2,4-Dichlorophenoxyacetic acid, Health effects, Cancer risk
In June 2015 the World Health Organization's International Agency for Research on Cancer confirmed its 1987 classification of  2,4-D as a possible carcinogen.


2,4-Dichlorophenoxyacetic acid, Health effects, Cancer risk
On August 8, 2007, the EPA issued a ruling that existing data do not support a link between human cancer and 2,4-D exposure.