4-methylthio-2-oxobutanoic acid

2-oxo-4-Methylthiobutanoic acid, also known as 2-keto-4-methylthiobutyrate or 4-methylthio-2-oxobutanoate, belongs to the class of organic compounds known as thia fatty acids. These are fatty acid derivatives obtained by insertion of a sulfur atom at specific positions in the chain. 2-oxo-4-Methylthiobutanoic acid is slightly soluble (in water) and a weakly acidic compound (based on its pKa). 2-oxo-4-Methylthiobutanoic acid has been primarily detected in urine. Within the cell, 2-oxo-4-methylthiobutanoic acid is primarily located in the cytoplasm and adiposome. 2-oxo-4-Methylthiobutanoic acid exists in all living organisms, ranging from bacteria to humans. In humans, 2-oxo-4-methylthiobutanoic acid is involved in the methionine metabolism pathway. 2-oxo-4-Methylthiobutanoic acid is also involved in several metabolic disorders, some of which include methylenetetrahydrofolate reductase deficiency (MTHFRD), the homocystinuria-megaloblastic anemia due to defect in cobalamin metabolism, CBLG complementation type pathway, methionine adenosyltransferase deficiency, and the hypermethioninemia pathway. Outside of the human body, 2-oxo-4-methylthiobutanoic acid can be found in a number of food items such as lotus, wasabi, watercress, and chickpea. This makes 2-oxo-4-methylthiobutanoic acid a potential biomarker for the consumption of these food products. 4-Methylthio-2-oxobutanoic acid is the direct precursor of methional, which is a potent inducer of apoptosis in a BAF3 murine lymphoid cell line which is interleukin-3 (IL3)-dependent. (PMID 7848263).


CID 25244659

Methionine sulfoxide is an oxidation product of methionine with reactive oxygen species via 2-electron-dependent mechanism. Such oxidants can be generated from activated neutrophils; therefore, methionine sulfoxide can be regarded as a biomarker of oxidative stress in vivo. (PMID 12576054).


Piroxicam

Piroxicam is only found in individuals that have used or taken this drug. It is a cyclooxygenase inhibiting, non-steroidal anti-inflammatory agent (NSAID) that is well established in treating rheumatoid arthritis and osteoarthritis and used for musculoskeletal disorders, dysmenorrhea, and postoperative pain. Its long half-life enables it to be administered once daily. [PubChem]The antiinflammatory effect of Piroxicam may result from the reversible inhibition of cyclooxygenase, causing the peripheral inhibition of prostaglandin synthesis. The prostaglandins are produced by an enzyme called Cox-1. Piroxicam blocks the Cox-1 enzyme, resulting into the disruption of production of prostaglandins. Piroxicam also inhibits the migration of leukocytes into sites of inflammation and prevents the formation of thromboxane A2, an aggregating agent, by the platelets.


Ibandronate

Ibandronate is a nitrogen-containing bisphosphonate in the same class as alendronate and risedronate. Ibandronate inhibits osteoclast-mediated bone resorption. All of the bisphosphonates prevent the breakdown of bone by bone cells called osteoclasts. In persons who are at high risk for osteoporosis, bisphosphonates not only result in increased amounts of bone and bone strength, they also reduce the risk of hip fractures and other bone fractures.

Ibandronate sodium monohydrate
Ibandronic acid
R484
Bondronat
Ibandronate


Simvastatin

Simvastatin is a hypolipidemic drug belonging to the class of pharmaceuticals called 'statins'. It is used to control hypercholesterolemia (elevated cholesterol levels) and to prevent cardiovascular disease. Simvastatin is a synthetic derivate of a fermentation product of Aspergillus terreus; Simvastatin is a powerful lipid-lowering drug that can decrease low density lipoprotein (LDL) levels by up to 50 percent. It is used in doses of 5 mg up to 80 mg. Higher doses (160 mg) have been found to be too toxic, while giving only minimal benefit in terms of lipid lowering. There is no real effect on HDL and triglyceride levels. Simvastatin (INN) is a hypolipidemic drug belonging to the class of pharmaceuticals called 'statins'. It is used to control hypercholesterolemia (elevated cholesterol levels) and to prevent cardiovascular disease. Simvastatin is a synthetic derivate of a fermentation product of Aspergillus terreus; The drug is the form of an inactive lactone that is hydrolized after ingestion to produce the active agent. It is a white, nonhygroscopic, crystalline powder that is practically insoluble in water, and freely soluble in chloroform, methanol and ethanol; Ezetimibe/simvastatin is a combination product to lower lipids and marketed as Vytorin.


Aspirin

Aspirin is only found in individuals who have consumed this drug. Aspirin or acetylsalicylic acid (acetosal) is a drug in the family of salicylates, often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant effect and is used in long-term low-doses to prevent heart attacks and cancer. It was isolated from meadowsweet (Filipendula ulmaria, formerly classified as Spiraea ulmaria) by German researchers in 1839. While their extract was somewhat effective, it also caused digestive problems such as irritated stomach and diarrhoea, and even death when consumed in high doses. In 1853, a French chemist named Charles Frederic Gerhardt neutralized salicylic acid by buffering it with sodium (sodium salicylate) and acetyl chloride, creating acetosalicylic anhydride. Gerhardt's product worked, but he had no desire to market it and abandoned his discovery. In 1897, researcher Arthur Eichengrun and Felix Hoffmann, a research assistant at Friedrich Bayer & Co. in Germany, derivatized one of the hydroxyl functional groups in salicylic acid with an acetyl group (forming the acetyl ester), which greatly reduced the negative effects. This was the first synthetic drug, not a copy of something that existed in nature, and the start of the pharmaceuticals industry. The name 'aspirin' is composed of a- (from the acetyl group) -spir- (from the plant genus Spiraea) and -in (a common ending for drugs at the time). It has also been stated that the name originated by another means. As referring to AcetylSalicylic and 'pir' in reference to one of the scientists who was able to isolate it in crystalline form, Raffaele Piria. Finally 'in' due to the same reasons as stated above. Salicylic acid (which is a naturally occurring substance found in many plants) can be acetylated using acetic anhydride, yielding aspirin and acetic acid as a byproduct. It is a common experiment performed in organic chemistry labs, and generally tends to produce low yields due to the relative difficulty of its extraction from an aqueous state. The trick to getting the reaction to work is to acidify with phosphoric acid and heat the reagents under reflux with a boiling water bath for between 40 minutes and an hour. Aspirin acts as an inhibitor of cyclooxygenase which results in the inhibition of the biosynthesis of prostaglandins. Aspirin also inhibits platelet aggregation and is used in the prevention of arterial and venous thrombosis. (From Martindale, The Extra Pharmacopoeia, 30th ed, p5).

2-(acetyloxy)benzoate
2-(acetyloxy)benzoic acid
2-acetoxybenzenecarboxylic acid
2-acetoxybenzoate
2-acetoxybenzoic acid
2-carboxyphenyl acetate
Acenterine
Acetard
Aceticyl
Acetol
Acetonyl
Acetophen
Acetosal
Acetosalin
Acetylin
Acetylsalicylate
Acetylsalicylic acid
Acetyonyl
Acetysal
Acetysalicylic acid
Acylpyrin
Asatard
Aspergum
Aspirdrops
Aspirin
Benaspir
Bialpirinia
Bufferin
Caprin
Cardioaspirina
Easprin
Ecolen
Ecotrin
Empirin
Endosprin
Endydol
O-(acetyloxy)benzoate
O-(acetyloxy)benzoic acid
O-acetoxybenzoate
O-acetoxybenzoic acid
O-acetylsalicylic acid
O-carboxyphenyl acetate
Persistin
Pharmacin
Polopiryna
Premaspin
Rheumintabletten
Rhodine
Salcetogen
Saletin
Salicylic acid acetate
Salospir
Solprin
Solprin acid
Solpyron
Tasprin
Temperal
Toldex
Triaminicin
Acetylsalicylsaeure
Acide 2-(acetyloxy)benzoique
Acide acetylsalicylique
Acido acetilsalicilico
Acidum acetylsalicylicum
Asa
Azetylsalizylsaeure
2-acetoxybenzenecarboxylate
O-acetylsalicylate
O-carboxyphenyl acetic acid
Salicylate acetate
Salicylic acid acetic acid


Etodolac

Etodolac is only found in individuals that have used or taken this drug. It is a non-steroidal anti-inflammatory drug (NSAID) with anti-inflammatory, analgesic and antipyretic properties. Its therapeutic effects are due to its ability to inhibit prostaglandin synthesis. It is indicated for relief of signs and symptoms of rheumatoid arthritis and osteoarthritis. Similar to other NSAIDs, the anti-inflammatory effects of etodolac result from inhibition of the enzyme cycooxygenase (COX). This decreases the synthesis of peripheral prostaglandins involved in mediating inflammation. Etodolac binds to the upper portion of the COX enzyme active site and prevents its substrate, arachidonic acid, from entering the active site. Etodolac was previously thought to be a non-selective COX inhibitor, but it is now known to be 5 – 50 times more selective for COX-2 than COX-1. Antipyresis may occur by central action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat loss.


Ketoprofen

Ketoprofen is only found in individuals that have used or taken this drug. It is a propionic acid derivative and is a nonsteroidal anti-inflammatory agent (NSAIA) with analgesic and antipyretic properties. The anti-inflammatory effects of ketoprofen are believed to be due to inhibition cylooxygenase-2 (COX-2), an enzyme involved in prostaglandin synthesis via the arachidonic acid pathway. This results in decreased levels of prostaglandins that mediate pain, fever and inflammation. Ketoprofen is a non-specific cyclooxygenase inhibitor and inhibition of COX-1 is thought to confer some of its side effects, such as GI upset and ulceration. Ketoprofen is thought to have anti-bradykinin activity, as well as lysosomal membrane-stabilizing action. Antipyretic effects may be due to action on the hypothalamus, resulting in an increased peripheral blood flow, vasodilation, and subsequent heat dissipation.


Ibuprofen

Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) widely marketed under various trademarks including Act-3, Advil, Brufen, Motrin, Nuprin, and Nurofen. It is used for relief of symptoms of arthritis, primary dysmenorrhoea, and fever; Ibuprofen is an NSAID which is believed to work through inhibition of cyclooxygenase (COX), thus inhibiting prostaglandin synthesis. There are at least 2 variations of cyclooxygenase (COX-1 and COX-2), ibuprofen inhibits both COX-1 and COX-2. It appears that its analgesic, antipyretic, and anti-inflammatory activity are achieved principally through COX-2 inhibition; whereas COX-1 inhibition is responsible for its unwanted effects on platelet aggregation and the GI mucosa. As with other NSAIDs, ibuprofen inhibits platelet aggregation, but is not used therapeutically for this action since it is a minor and reversible effect. -- Wikipedia.


beta-D-Glucuronoside

Ibuprofen glucuronide is a metabolite of ibuprofen. Ibuprofen is a nonsteroidal anti-inflammatory drug (NSAID) used for relief of symptoms of arthritis, fever, as an analgesic (pain reliever), especially where there is an inflammatory component, and dysmenorrhea. Ibuprofen is known to have an antiplatelet effect, though it is relatively mild and somewhat short-lived when compared with aspirin or other better-known antiplatelet drugs. (Wikipedia)


Rofecoxib

Rofecoxib, also known as vioxx or ceoxx, belongs to the class of organic compounds known as stilbenes. These are organic compounds containing a 1,2-diphenylethylene moiety. Stilbenes (C6-C2-C6 ) are derived from the common phenylpropene (C6-C3) skeleton building block. The introduction of one or more hydroxyl groups to a phenyl ring lead to stilbenoids. Rofecoxib is a drug which is used for the treatment of osteoarthritis, rheumatoid arthritis, acute pain in adults, and primary dysmenorrhea, as well as acute treatment of migraine attacks with or without auras. Rofecoxib is considered to be a practically insoluble (in water) and relatively neutral molecule.


Pravastatin

Pravastatin is a member of the drug class of statins, used for lowering cholesterol and preventing cardiovascular disease. Pravastatin was identified originally in a mold called Nocardia autotrophica by researchers of the Sankyo Pharma Inc; An antilipemic fungal metabolite isolated from cultures of Nocardia autotrophica. It acts as a competitive inhibitor of HMG CoA reductase (hydroxymethylglutaryl CoA reductases); In medicine and pharmacology, pravastatin (Pravachol or Selektine) is a member of the drug class of statins, used for lowering cholesterol and preventing cardiovascular disease.


Rosuvastatin

Rosuvastatin is an antilipemic agent that competitively inhibits hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase. HMG-CoA reducuase catalyzes the conversion of HMG-CoA to mevalonic acid, the rate-limiting step in cholesterol biosynthesis. Rosuvastatin belongs to a class of medications called statins and is used to reduce plasma cholesterol levels and prevent cardiovascular disease.


Diclofenac

Diclofenac is only found in individuals that have used or taken this drug. It is a non-steroidal anti-inflammatory agent (NSAID) with antipyretic and analgesic actions. It is primarily available as the sodium salt. [PubChem]The antiinflammatory effects of diclofenac are believed to be due to inhibition of both leukocyte migration and the enzyme cylooxygenase (COX-1 and COX-2), leading to the peripheral inhibition of prostaglandin synthesis. As prostaglandins sensitize pain receptors, inhibition of their synthesis is responsible for the analgesic effects of diclofenac. Antipyretic effects may be due to action on the hypothalamus, resulting in peripheral dilation, increased cutaneous blood flow, and subsequent heat dissipation.


Sulindac

Sulindac is a nonsteroidal anti-inflammatory agent (NSAIA) of the arylalkanoic acid class that is marketed in the U.S. by Merck as Clinoril. Like other NSAIAs, it may be used in the treatment of acute or chronic inflammatory conditions. Sulindac is a prodrug, derived from sulfinylindene, that is converted in vivo to an active sulfide compound by liver enzymes. The sulfide metabolite then undergoes enterohepatic circulation; it is excreted in the bile and then reabsorbed from the intestine. This is thought to help maintain constant blood levels with reduced gastrointestinal side effects. Some studies have shown sulindac to be relatively less irritating to the stomach than other NSAIA's except for drugs of the cyclooxygenase-2 (COX-2) inhibitor class. The exact mechanism of its NSAIA properties is unknown, but it is thought to act on enzymes COX-1 and COX-2, inhibiting prostaglandin synthesis.


Alendronic acid

Alendronic acid, also known as alendronate or acido alendronico, belongs to the class of organic compounds known as bisphosphonates. These are organic compounds containing two phosphonate groups linked together through a carbon atoms. Alendronic acid is a drug which is used for the treatment and prevention of osteoporosis in women and paget's disease of bone in both men and women. Alendronic acid exists as a solid, soluble (in water), and an extremely strong acidic compound (based on its pKa). Alendronic acid has been found in human prostate and intestine tissues. Within the cell, alendronic acid is primarily located in the cytoplasm. In humans, alendronic acid is involved in the alendronate action pathway. Alendronic acid is a potentially toxic compound. Alendronate (Fosamax, Merck) is a bisphosphonate drug used for osteoporosis and several other bone diseases. It is marketed alone as well as in combination with vitamin D (2,800 U, under the name Fosavance).


Celecoxib

Celecoxib (INN) is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. It is marketed by Pfizer under the brand name Celebrex. In some countries, it is branded Celebra. Celecoxib is a non-steroidal anti-inflammatory drug (NSAID) used in the treatment of osteoarthritis, rheumatoid arthritis, acute pain, painful menstruation and menstrual symptoms, and to reduce numbers of colon and rectum polyps in patients with familial adenomatous polyposis. Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs; Celecoxib is a highly selective COX-2 inhibitor and primarily inhibits this isoform of cyclooxygenase, whereas traditional NSAIDs inhibit both COX-1 and COX-2. Celecoxib is approximately 10-20 times more selective for COX-2 inhibition over COX-1. In theory, this specificity allows celecoxib and other COX-2 inhibitors to reduce inflammation (and pain) while minimizing gastrointestinal adverse drug reactions (e.g. stomach ulcers) that are common with non-selective NSAIDs. It also means that it has a reduced effect on platelet aggregation compared to traditional NSAIDs.


Hydroxycelecoxib is only found in individuals that have used or taken Celecoxib. Hydroxycelecoxib is a metabolite of Celecoxib. Hydroxycelecoxib belongs to the family of Phenylpyrazoles. These are compounds containing a phenylpyrazole skeleton, which consists of a pyrazole bound to a phenyl group.


Ketorolac

Ketorolac is only found in individuals that have used or taken this drug. It is a pyrrolizine carboxylic acid derivative structurally related to indomethacin. It is an NSAID and is used principally for its analgesic activity (from Martindale The Extra Pharmacopoeia, 31st ed). Ketorolac is a nonsteroidal anti-inflammatory drug (NSAID) chemically related to indomethacin and tolmetin. Ketorolac tromethamine is a racemic mixture of [-]S- and [+]R-enantiomeric forms, with the S-form having analgesic activity. Its antiinflammatory effects are believed to be due to inhibition of both cylooxygenase-1 (COX-1) and cylooxygenase-2 (COX-2) which leads to the inhibition of prostaglandin synthesis leading to decreased formation of precursors of prostaglandins and thromboxanes from arachidonic acid. The resultant reduction in prostaglandin synthesis and activity may be at least partially responsible for many of the adverse, as well as the therapeutic, effects of these medications. Analgesia is probably produced via a peripheral action in which blockade of pain impulse generation results from decreased prostaglandin activity. However, inhibition of the synthesis or actions of other substances that sensitize pain receptors to mechanical or chemical stimulation may also contribute to the analgesic effect. In terms of the ophthalmic applications of ketorolac - ocular administration of ketorolac reduces prostaglandin E2 levels in aqueous humor, secondary to inhibition of prostaglandin biosynthesis.


nucleoside 5'-triphoshate(3-)

Formamidopyrimidine nucleoside triphosphate belongs to the class of organic compounds known as pentose phosphates. These are carbohydrate derivatives containing a pentose substituted by one or more phosphate groups. Formamidopyrimidine nucleoside triphosphate is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Formamidopyrimidine nucleoside triphosphate exists in all living organisms, ranging from bacteria to humans. In humans, formamidopyrimidine nucleoside triphosphate is involved in pterine biosynthesis pathway. Formamidopyrimidine nucleoside triphosphate is also involved in several metabolic disorders, some of which include the segawa syndrome pathway, hyperphenylalaniemia due to guanosine triphosphate cyclohydrolase deficiency, sepiapterin reductase deficiency, and hyperphenylalaninemia due to 6-pyruvoyltetrahydropterin synthase deficiency (PTPS). Formamidopyrimidine nucleoside triphosphate is involved in folate biosynthesis. Formamidopyrimidine nucleoside triphosphat is created from 2,5-Diaminopyrimidine nucleoside triphosphate by GTP cyclohydrolase I [EC:3.5.4.16].


2,5-Diaminopyrimidine nucleoside triphosphate belongs to the class of organic compounds known as pentose phosphates. These are carbohydrate derivatives containing a pentose substituted by one or more phosphate groups. 2,5-Diaminopyrimidine nucleoside triphosphate is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). 2,5-Diaminopyrimidine nucleoside triphosphate exists in all living organisms, ranging from bacteria to humans. In humans, 2,5-diaminopyrimidine nucleoside triphosphate is involved in pterine biosynthesis pathway. 2,5-Diaminopyrimidine nucleoside triphosphate is also involved in several metabolic disorders, some of which include hyperphenylalaninemia due to 6-pyruvoyltetrahydropterin synthase deficiency (PTPS), hyperphenylalaninemia due to DHPR-deficiency, sepiapterin reductase deficiency, and hyperphenylalaniemia due to guanosine triphosphate cyclohydrolase deficiency. 2,5-Diaminopyrimidine nucleoside triphosphate is involved in folate biosynthesis. 2,5-Diaminopyrimidine nucleoside triphosphate is created from 2,5-Diaminopyrimidine nucleoside triphosphate by GTP cyclohydrolase I [EC:3.5.4.16].


2,5-Diamino-6-(5'-triphosphoryl-3',4'-trihydroxy-2'-oxopentyl)-amino-4-oxopyrimidine is involved in folate biosynthesis. 2,5-Diamino-6-(5'-triphosphoryl-3',4'-trihydroxy-2'-oxopentyl)-amino-4-oxopyrimidine is created from 2,5-Diaminopyrimidine nucleoside triphosphate by GTP cyclohydrolase I [EC:3.5.4.16]. 2,5-Diamino-6-(5'-triphosphoryl-3',4'-trihydroxy-2'-oxopentyl)-amino-4-oxopyrimidine can be converted into 2-Amino-4-hydroxy-6-(erythro-1,2,3-trihydroxypropyl)dihydropteridine. triphosphate by GTP cyclohydrolase I [EC:3.5.4.16]. GTP cyclohydrolase I [EC:3.5.4.16] can also be converted to 6-(3'-Triphosphoryl-1'-methylglyceryl)-7-methyl-7,8-dihydrobiopterin.


7,8-dihydroneopterin 3'-triphosphate

The biosynthesis of tetrahydrobiopterin (BH4) from dihydroneopterin triphosphate (NH2P3) was studied in human liver extract. The phosphate-eliminating enzyme (PEE) was purified approximately 750-fold. The conversion of NH2P3 to BH4 was catalyzed by this enzyme in the presence of partially purified sepiapterin reductase, Mg2+ and NADPH. The PEE is heat stable when heated at 80 degrees C for 5 min. It has a molecular weight of 63 000 daltons. One possible intermediate 6-(1'-hydroxy-2'-oxopropyl)5,6,7,8-tetrahydropterin(2'-oxo-tetrahydropte rin) was formed upon incubation of BH4 in the presence of sepiapterin reductase and NADP+ at pH 9.0. Reduction of this compound with NaBD4 yielded monodeutero threo and erythro-BH4, the deuterium was incorporated at the 2' position. This and the UV spectra were consistent with a 2'-oxo-tetrahydropterin structure. Dihydrofolate reductase (DHFR) catalyzed the reduction of BH2 to BH4 and was found to be specific for the pro-R-NADPH side. The sepiapterin reductase catalyzed the transfer of the pro-S hydrogen of NADPH during the reduction of sepiapterin to BH2. In the presence of crude liver extracts the conversion of NH2P3 to BH4 requires NADPH. Two deuterium atoms were incorporated from (4S-2H)NADHP in the 1' and 2' position of the BH4 side chain. Incorporation of one hydrogen from the solvent was found at position C(6). These results are consistent with the occurrence of an intramolecular redox exchange between the pteridine nucleus and the side chain and formation of 6-pyruvoyl-5,6,7,8-tetrahydropterin(tetrahydro-1'-2'-dioxopterin) as intermediate. PMID: 3930838.


dyspropterin

Dyspropterin belongs to the class of organic compounds known as pterins and derivatives. These are polycyclic aromatic compounds containing a pterin moiety, which consist of a pteridine ring bearing a ketone and an amine group to form 2-aminopteridin-4(3H)-one. Dyspropterin is considered to be a practically insoluble (in water) and relatively neutral molecule. Dyspropterin has been found in human placenta tissue. Within the cell, dyspropterin is primarily located in the nucleus, mitochondria and cytoplasm. Dyspropterin exists in all living organisms, ranging from bacteria to humans. In humans, dyspropterin is involved in pterine biosynthesis pathway. Dyspropterin is also involved in several metabolic disorders, some of which include hyperphenylalaninemia due to 6-pyruvoyltetrahydropterin synthase deficiency (PTPS), the dopa-responsive dystonia pathway, the segawa syndrome pathway, and hyperphenylalaniemia due to guanosine triphosphate cyclohydrolase deficiency. Dyspropterin, an intermediate formed from dihydroneopterin triphosphate in the biosynthetic pathway of tetrahydrobiopterin.


TRIPHOSPHATE

PPPi is a salt or acid that contains three phosphate groups. Triphosphoric acid, also tripolyphosphoric acid, with formula H5P3O10, is a condensed form of phosphoric acid.In polyphosphoric acids, it is the next after pyrophosphoric acid, H4P2O7, also called diphosphoric acid.Compounds such as ATP (adenosine triphosphate) are esters of triphosphoric acid. Polyphosphates are hydrolyzed into smaller units (orthophosphates) in the gut before absorption, which may induce a metabolic acidosis. The acute toxicity of polyphosphonates is low as the lowest LD50 after oral administration is > 1,000 mg/kg body weight.Polyphosphates are moderately irritating to skin and mucous membrane because of their alkalinity. No mutagenic potential was observed when TTP was tested in a Salmonella/microsome assay (Ames test) and in a chromosomal aberration assay in vitro using a Chinese hamster fibroblast cell line (Ishidate et al. 1984). Tetrasodium pyrophosphate was not mutagenic in an in vitro assay using S. cerevisiae strains and S. typhimurium strains with and without the addition of mammalian metabolic activation preparations (IPCS 1982). Reproduction studies in three generations of rats on diets with 0.5% TTP were performed. TTP had no effects on fertility or litter size, or on growth or survival on offspring (Hodge 1964). Tetrasodi.


6-Lactoyltetrahydropterin is a putative intermediate in the de novo synthesis of tetrahydrobiopterin (BH4) pathway, in a reaction involving the enzyme sepiapterin reductase (E.C. 1.1.1.153) in human liver. In brain, an enzyme distinct from sepiapterin reductase catalyzes the TPNH-dependent reduction of 6-pyruvoyl-tetrahydropterin to 6-lactoyl-tetrahydropterin. (PMID: 4004850). In brain, the expression of other enzymes involved in BH4 biosynthesis includes aldose reductase, carbonyl reductase, GTP-cyclohydrolase I, and 6-pyruvoyltetrahydrobiopterin. Sepiapterin reductase expression is increased in Parkinson's disease brain tissue. (PMID: 17270157).


7,8-dihydroneopterin (H(2)Neo) is produced by human monocyte-derived macrophages upon stimulation with Interferon-gamma. Increased amounts of H(2)Neo in human body fluids are found in many disorders, including viral infections and autoimmune diseases. (PMID 12804528 ).


Umanopterin

Neopterin is a pteridine derivative present in body fluids; elevated levels result from immune system activation, malignant disease, allograft rejection, and viral infections. (From Stedman, 26th ed) Neopterin also serves as a precursor in the biosynthesis of biopterin.


11beta,21-Dihydroxy-3,20-oxo-5beta-pregnan-18-al is an intermediate in C21-Steroid hormone metabolism. 11beta,21-Dihydroxy-3,20-oxo-5beta-pregnan-18-al is converted from Aldosterone via the enzyme 3-oxo-5beta-steroid 4-dehydrogenase (EC:1.3.99.6). It is then converted to 3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC:1.1.1.50).


3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al is an intermediate in C21-Steroid hormone metabolism. 3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al is converted from 11beta,21-Dihydroxy-3,20-oxo-5beta-pregnan-18-al via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50).


Aldosterone

Aldosterone is a steroid hormone produced by the adrenal cortex in the adrenal gland to regulate sodium and potassium balance in the blood. Specifically it regulates electrolyte and water balance by increasing the renal retention of sodium and the excretion of potassium. It is synthesized from cholesterol by aldosterone synthase, which is absent in other sections of the adrenal gland. It is the sole endogenous member of the class of mineralocorticoids. Aldosterone increases the permeability of the apical (luminal) membrane of the kidney's collecting ducts to potassium and sodium and activates their basolateral Na+/K+ pumps, stimulating ATP hydrolysis, reabsorbing sodium (Na+) ions and water into the blood, and excreting potassium (K+) ions into the urine.


18-Hydroxycorticosterone is a corticosteroid and a derivative of corticosterone. If it is present in sufficiently high concentrations, it can lead to serious electrolyte imbalances (an electrolyte toxin). 18-Hydroxycorticosterone serves as an intermediate in the synthesis of aldosterone by the enzyme aldosterone synthase in the zona glomerulosa. Chronically high levels of 18-hydroxycorticosterone are associated with at least three inborn errors of metabolism including adrenal hyperplasia type V, corticosterone methyl oxidase I deficiency, and corticosterone methyl oxidase II deficiency. Each of these conditions is characterized by excessive amounts of sodium being released in the urine (salt wasting), along with insufficient release of potassium in the urine, usually beginning in the first few weeks of life. This imbalance leads to low levels of sodium and high levels of potassium in the blood (hyponatremia and hyperkalemia, respectively). Individuals with corticosterone methyloxidase deficiency can also have high levels of acid in the blood (metabolic acidosis). Acidosis typically occurs when arterial pH falls below 7.35. In infants with acidosis the initial symptoms include poor feeding, vomiting, loss of appetite, weak muscle tone (hypotonia), and lack of energy (lethargy). The hyponatremia, hyperkalemia, and metabolic acidosis associated with corticosterone methyloxidase deficiency can cause nausea, vomiting, dehydration, low blood pressure, extreme tiredness (fatigue), and muscle weakness.


Corticosterone

Corticosterone, also known as 17-deoxycortisol, belongs to the class of organic compounds known as 21-hydroxysteroids. These are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Thus, corticosterone is considered to be a steroid lipid molecule. Corticosterone exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. Corticosterone has been found throughout most human tissues, and has also been detected in multiple biofluids, such as blood and urine. Within the cell, corticosterone is primarily located in the cytoplasm, membrane (predicted from logP), mitochondria and endoplasmic reticulum. In humans, corticosterone is involved in the steroidogenesis pathway. Corticosterone is also involved in several metabolic disorders, some of which include 21-hydroxylase deficiency (cyp21), 3-Beta-hydroxysteroid dehydrogenase deficiency, 11-beta-hydroxylase deficiency (cyp11b1), and adrenal hyperplasia type 5 or congenital adrenal hyperplasia due to 17 Alpha-hydroxylase deficiency. Corticosterone is an adrenocortical steroid that has modest but significant activities as a mineralocorticoid and a glucocorticoid. (From Goodman and Gilman\'s The Pharmacological Basis of Therapeutics, 8th ed, p1437).


dihydrocorticosterone

11beta,21-Dihydroxy-5beta-pregnane-3,20-dione is an intermediate in C21-Steroid hormone metabolism. 11beta,21-Dihydroxy-5beta-pregnane-3,20-dione is the 3rd to last step in the synthesis of 3alpha,20alpha,21-Trihydroxy-5beta-pregnane-11-one and is converted from Corticosterone via the enzyme 3-oxo-5beta-steroid 4-dehydrogenase (EC 1.3.99.6). It is then converted to Tetrahydrocorticosterone via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50).


Tetrahydrocorticosterone

Tetrahydrocorticosterone is one of the major urinary metabolites from corticosterone. Premenopausal patients with early breast cancer excrete subnormal amounts of tetrahydrocorticosterone as compared with the normal subjects of corresponding ages. (PMID 1133844).


11-Dehydrocorticosterone is a mineral corticosteroid. The conversion of inactive 11-ketoglucocorticoids such as 11-dehydrocorticosterone) into active 11b-hydroxyglucocorticoids (such as corticosterone) is catalyzed by 11beta-hydroxysteroid dehydrogenase (11b-HSD1, EC 1.1.1.146), which is expressed in many tissues and plays an important role in metabolically relevant tissues such as the liver, adipose tissue, skeletal muscles and possibly kidney. Chronically elevated local glucocorticoid action as a result of increased 11beta-HSD1 activity rather than elevated systemic glucocorticoid levels has been associated with metabolic syndrome, which is characterized by obesity, insulin resistance, type 2 diabetes and cardiovascular complications. Recent studies indicate that compounds inhibiting 11beta-HSD1 activity ameliorate the adverse effects of excessive glucocorticoid concentrations on metabolic processes, providing promising opportunities for the development of therapeutic interventions. 11-dehydrocorticosterone and corticosterone display antinatriuretic activity, although 11-dehydrocorticosterone is generally a more potent sodium retainer than corticosterone. (PMID: 17584152, Endocr Metab Immune Disord Drug Targets. 2007 Jun;7(2):125-40.).


21-Hydroxy-5beta-pregnane-3,11,20-trione is an intermediate in C21-Steroid hormone metabolism. 21-Hydroxy-5beta-pregnane-3,11,20-trione is the. second to last step in the synthesis of 3alpha,20alpha,21-Trihydroxy-5beta-pregnane-11-one and is converted from 11-Dehydrocorticosterone via the enzyme 3-oxo-5beta-steroid 4-dehydrogenase (EC 1.3.99.6). It is then converted to 3alpha,21-Dihydroxy-5beta-pregnane-11,20-dione via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50).


3alpha,21-Dihydroxy-5beta-pregnane-11,20-dione is an intermediate in C21-Steroid hormone metabolism. 3alpha,21-Dihydroxy-5beta-pregnane-11,20-dione is converted from Tetrahydrocorticosterone via the enzyme 11beta-hydroxysteroid dehydrogenase (EC 1.1.1.146). It is then converted to 3alpha,20alpha,21-Trihydroxy-5beta-pregnane-11-one via the enzyme 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53).


11beta-Hydroxyprogesterone is a normal human metabolite. Plasma 11beta-Hydroxyprogesterone concentrations does not vary significantly as a function of age, sex, or phase of the menstrual cycle, in contrast to 17-hydroxyprogesterone. Increased plasma 11beta-Hydroxyprogesterone levels in late-onset adrenal 21-hydroxylase deficiency suggest a mild defect of the mineralocorticoid pathway. 21-hydroxylase deficiency (OMIM 201910) is probably the most frequent (if not the most frequent) autosomal recessive genetic disease, occurring in almost 1% of Caucasians and about 3% of Ashkenazi Jews. 21-hydroxylase deficiency is unusual among genetic diseases in that approximately 95% of the mutant alleles have apparently been generated by recombination between a normally active gene (CYP21) and a closely linked pseudogene (CYP21P). There are 4 recognized clinical forms of congenital adrenal hyperplasia, the majority of cases being associated with 21-hydroxylase deficiency: salt-wasting (SW), simple virilizing (SV), nonclassic (NC) late-onset (also called attenuated and acquired), and cryptic. (PMID: 3546944, 2537337). 11beta-hydroxyprogesterone acts as a mineralocorticoid agonist in stimulating Na+ absorption in mammalian principal cortical collecting duct cells.It activates the transiently expressed hMR in COS-7 cells in a dose-dependent manner (ED(50): 10(-8) M) and, like aldosterone, stimulated Ams I(sc) in mpkCCD(cl4) cells. Docking 11OHP within the hMR-ligand-binding domain homology model revealed that the agonist activity of 11OHP is caused by contacts between its 11 beta-hydroxyl group and Asn770. Furthermore, 11OHP was unable to activate the mutant hMR/N770A, in which Ala is substituted for Asn at position 770. These findings demonstrate that in the absence of the 21-hydroxyl group, the 11 beta-hydroxyl group can produce the contact with the hMR-Asn770 required for the hMR activation leading to stimulated Na(+) absorption.


Plasma 21-deoxycortisol (21DF) is an excellent marker of 21-hydroxylase deficiency. Currently, it is the only marker able to detect heterozygous carriers with 21-hydroxylase deficiency after Adrenocorticotropic Hormone (ACTH) stimulation. The syndrome of congenital adrenal hyperplasia (CAH) comprises the spectrum of autosomal recessive enzymatic disorders that impair cortisol biosynthesis. The hormonal pattern and clinical manifestations result from hyperstimulation of the adrenal cortex by excessive production of ACTH, untied from the negative feedback exerted by reduced cortisol levels, and the ultimate accumulation of F precursors and androgens. These abnormalities predispose the female newborn to ambiguous genitalia (female pseudohermaphroditism) and precocious puberty that may occur in both sexes. CAH due to 21-hydroxylase deficiency (21OHD) comprises nearly 90% of all cases, with an estimated worldwide incidence of 1 in 14,000 live births. Because 21-deoxycortisol (21DF) is an 11b-hydroxylase (11bOH) derivative of 17-hydroxyprogesterone (17OHP), its serum levels are parallel and proportionally elevated in patients with 21OHD but decreased or undetectable in those with 11b-hydroxylase deficiency (11bOHD). Due to the marked buildup of 17OHP in 21OHD, this precursor steroid can proceed directly to 11-hydroxylation, producing distinct elevations of 21DF. (PMID: 16551734, 10731638).


Hydrocortisone

Cortisol is the main glucocorticoid secreted by the adrenal cortex and it is involved in the stress response. Its synthetic counterpart hydrocortisone is used, either as an injection or topically, in the treatment of inflammation, allergy, collagen diseases, asthma, adrenocortical deficiency, shock, and some neoplastic conditions. Hydrocortisone is synthesized from pregnenolone and is used as an immunosuppressive drug given by injection in the treatment of severe allergic reactions such as anaphylaxis and angioedema, in place of prednisolone in patients who need steroid treatment but cannot take oral medication, and peri-operatively in patients on long-term steroid treatment to prevent an Addisonian crisis. Cortisol increases blood pressure, blood sugar levels, may cause infertility in women, and suppresses the immune system. The amount of cortisol present in the serum undergoes diurnal variation, with the highest levels present in the early morning and lower levels in the evening, several hours after the onset of sleep. Cortisol is found to be associated with ACTH deficiency and glucocorticoid deficiency, which are inborn errors of metabolism. Cortisol binds to the cytosolic glucocorticoid receptor. After binding the receptor, the newly formed receptor-ligand complex translocates itself into the cell nucleus where it binds to many glucocorticoid response elements (GRE) in the promoter region of the target genes. The DNA-bound receptor then interacts with basic transcription factors, causing the increase in expression of specific target genes. The anti-inflammatory actions of corticosteroids are thought to involve lipocortins, phospholipase A2 inhibitory proteins which, through inhibition arachidonic acid, control the biosynthesis of prostaglandins and leukotrienes. Specifically, glucocorticoids induce lipocortin-1 (annexin-1) synthesis, which then binds to cell membranes and prevents phospholipase A2 from coming into contact with its substrate arachidonic acid. This leads to diminished eicosanoid production. The cyclooxygenase (both COX-1 and COX-2) expression is also suppressed, potentiating the effect. In other words, the two main products of inflammation, prostaglandins and leukotrienes, are inhibited by the action of glucocorticoids. Glucocorticoids also stimulate the escape of lipocortin-1 into the extracellular space, where it binds to the leukocyte membrane receptors and inhibits various inflammatory events: epithelial adhesion, emigration, chemotaxis, phagocytosis, respiratory burst, and the release of various inflammatory mediators (lysosomal enzymes, cytokines, tissue plasminogen activator, chemokines, etc.) from neutrophils, macrophages, and mastocytes. Additionally, the immune system is suppressed by corticosteroids due to a decrease in the function of the lymphatic system, a reduction in immunoglobulin and complement concentrations, the precipitation of lymphocytopenia, and interference with antigen-antibody binding.

11-hydrocortisone
11-beta-hydrocortisone
11-beta-hydroxycortisone
11a-hydroxycorticosterone
11alpha-hydroxycorticosterone
11b,17,21-trihydroxyprogesterone
11b-hydrocortisone
11b-hydroxycortisone
11beta,17,21-trihydroxyprogesterone
11beta-hydrocortisone
11beta-hydroxycortisone
17-hydroxycorticosterone
17a-hydroxycorticosterone
17alpha-hydroxycorticosterone
4-pregnene-11alpha,21-triol 3,20-dione
4-pregnene-11b,17a,21-triol-3,20-dione
Acticort
Aeroseb hc
Aeroseb-hc
Ala-cort
Ala-scalp
Alacort
Algicirtis
Alphaderm
Amberin
Anflam
Anti-inflammatory hormone
Aquacort
Aquanil hc
Barseb hc
Basan-corti
Caldecort spray
Cetacort
Chronocort
Clear aid
Cleiton
Cobadex
Compound f
Cor-tar-quin
Cort-dome
Cort-quin
Cortanal
Cortenema
Cortesal
Corticreme
Cortifan
Cortifoam
Cortiment
Cortisol alcohol
Cortisolonum
Cortisporin
Cortisporin otico
Cortispray
Cortizol
Cortolotion
Cortonema
Cortoxide
Cremesone
Cremicort-h
Cutisol
Delacort
Derm-aid
Dermil
Dermolate
Dihydrocostisone
Dioderm
Dome-cort
Domolene-hc
Drotic
Ef corlin
Efcorbin
Efcortelan
Efcortelin
Eldercort
Epicort
Epiderm h
Esiderm h
Evacort
Ficortril
Fiocortril
Foille insetti
Genacort
Gyno-cortisone
H-cort
Hc
Heb cort
Heb-cort
Hidalone
Hidro-colisona
Hidrocortisona
Hycort
Hycortol
Hycortole
Hydracort
Hydrasson
Hydro-adreson
Hydro-colisona
Hydrocort
Hydrocortal
Hydrocorticosterone
Hydrocortisone
Hydrocortisone alcohol
Hydrocortisone base
Hydrocortisone free alcohol
Hydrocortisonum
Hydrocortistab
Hydrocortisyl
Hydrocortone
Hydroskin
Hydroxycortisone
Hysone
Hytisone
Hytone
Hytone lotion
Idrocortisone
Incortin-h
Incortin-hydrogen
Kendall's compound f
Komed hc
Kyypakkaus
Lacticare hc
Lacticare-hc
Lactisona
Lubricort
Maintasone
Medicort
Meusicort
Mildison
Milliderm
Neo-cort-dome
Neosporin-h ear
Nutracort
Nystaform-hc
Optef
Otalgine
Otic-neo-cort-dome
Otobiotic
Otocort
Otosone-f
Pediotic suspension
Penecort
Permicort
Polcort h
Preparation h hydrocortisone cream
Prepcort
Prestwick_265
Prevex hc
Proctocort
Proctofoam
Protocort
Racet
Rectoid
Reichstein's substance m
Remederm hc
Sanatison
Scalpicin capilar
Schericur
Scheroson f
Sigmacort
Signef
Stiefcorcil
Synacort
Systral hydrocort
Tarcortin
Timocort
Topicort
Transderma h
Traumaide
Uniderm
Vioform-hydrocortisone
Vosol hc
Vytone
Zenoxone


Cortisone

Cortisone is a naturally occurring glucocorticoid. It has been used in replacement therapy for adrenal insufficiency and as an anti-inflammatory agent. Cortisone itself is inactive. It is converted in the liver into the active metabolite cortisol (Martindale, The Extra Pharmacopoeia, 30th ed, p726). Cortisone is a corticosteroid hormone released by the adrenal gland in response to stress. One of cortisone's effects on the body, and a potentially harmful side effect when administered clinically, is the suppression of the immune system. This is an explanation for the apparent correlation between high stress and sickness (Wikipedia).


desoxycortone

11-Deoxycorticosterone (also called desoxycortone, 21-hydroxyprogesterone, DOC, or simply deoxycorticosterone) is a steroid hormone produced by the adrenal gland that possesses mineralocorticoid activity and acts as a precursor to aldosterone. It is classified as a member of the 21-hydroxysteroids. 21-hydroxysteroids are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Deoxycorticosterone is very hydrophobic, practically insoluble (in water), and relatively neutral. Deoxycorticosterone can be synthesized from progesterone by 21-beta-hydroxylase and is then converted to corticosterone by 11-beta-hydroxylase. Corticosterone is then converted to aldosterone by aldosterone synthase. Deoxycorticosterone stimulates the collecting tubules in the kidney to continue to excrete potassium in much the same way that aldosterone does. Deoxycorticosterone has about 1/20 of the sodium retaining power of aldosterone and about 1/5 the potassium excreting power of aldosterone (Wikipedia). Deoxycorticosterone can be found throughout all human tissues and has been detected in amniotic fluid and blood. When present in sufficiently high levels, deoxycorticosterone can act as a hypertensive agent and a metabotoxin. A hypertensive agent increases blood pressure and causes the production of more urine. A metabotoxin is an endogenously produced metabolite that causes adverse health effects at chronically high levels.  Chronically high levels of deoxycorticosterone are associated with congenital adrenal hyperplasia (CAH) and with adrenal tumors producing deoxycorticosterone (PMID: 20671982). High levels of this mineralocorticoid are associated with resistant hypertension, which can result in polyuria, polydipsia, increased blood volume, edema, and cardiac enlargement. Deoxycorticosterone can be used to treat adrenal insufficiency. In particular, desoxycorticosterone acetate (DOCA) is used as replacement therapy in Addison's disease.


21-hydroxypregnenolone is an essential intermediate in corticosterone synthesis. The hydrolysis of 21-hydroxypregnenolone of fetal origin by steryl-sulfatase (SOS, EC 3.1.6.2), may be important in the biosynthesis of deoxycorticosterone, which is present in the plasma of pregnant women in high concentration. 21-hydroxypregnenolone has been identified in follicular fluid from follicles of women. Pregnenolone is transformed to 21-hydroxypregnenolone by human adrenal microsomal preparations, suggesting the involvement of alternative paths via 17a,21-dihydroxypregnenolone in human. (PMID 974176, 3347051, 3495701, 7382480, 6247575).


Progesterone

The major progestational steroid that is secreted primarily by the corpus luteum and the placenta. Progesterone acts on the uterus, the mammary glands and the brain. It is required in embryo implantation, pregnancy maintenance, and the development of mammary tissue for milk production. Progesterone, converted from pregnenolone, also serves as an intermediate in the biosynthesis of gonadal steroid hormones and adrenal corticosteroids. -- Pubchem; Progesterone is a C-21 steroid hormone involved in the female menstrual cycle, pregnancy (supports gestation) and embryogenesis of humans and other species. Progesterone belongs to a class of hormones called progestagens, and is the major naturally occurring human progestagen. -- Wikipedia; During implantation and gestation, progesterone appears to decrease the maternal immune response to allow for the acceptance of the pregnancy. Progesterone decreases contractility of the uterine smooth muscle. The fetus metabolizes placental progesterone in the production of adrenal mineralo- and glucosteroids. A drop in progesterone levels is possibly one step that facilitates the onset of labor. In addition progesterone inhibits lactation during pregnancy. The fall in progesterone levels following delivery is one of the triggers for milk production. -- Wikipedia.

17a-progesterone
3,20-pregnene-4
4-pregnen-3,20-dione
4-pregnene-3,20-dione
Agolutin
Bio-luton
Cidr
Colprosterone
Corlutin
Corlutina
Corluvite
Corporin
Corpus luteum hormone
Crinone
Crinone progesterone gel
Curretab
Cyclogest
Cyclogesterin
D4-pregnene-3,20-dione
Delalutin
Duraprogen
Estima
Flavolutan
Fologenon
Gesterol
Gesterol 100
Gesterol 50
Gestiron
Gestone
Gestormone
Gestron
Glanducorpin
Gynlutin
Gynoluton
Gynolutone
Hormoflaveine
Hormoluton
Hydroxyprogesterone caproate
Hydroxyprogesterone caproic acid
Lingusorbs
Lipo-lutin
Lucorteum
Lucorteum sol
Lugesteron
Luteal hormone
Luteocrin normale
Luteodyn
Luteogan
Luteohormone
Luteol
Luteopur
Luteosan
Luteostab
Luteovis
Luteum
Lutex
Lutidon
Lutociclina
Lutocuclin m
Lutocyclin
Lutocyclin m
Lutocylin
Lutocylol
Lutoform
Lutogyl
Lutren
Lutromone
Mpa
Membrettes
Methylpregnone
Nalutron
Percutacrine
Percutacrine luteinique
Piaponon
Pranone
Pregn-4-en-3,20-dione
Pregn-4-ene-3,20-dione
Pregnene-3,20-dione
Pregnenedione
Primolut
Prochieve
Progeffik
Progekan
Progestan
Progestasert
Progesterol
Progesterone
Progesteronum
Progestin
Progestogel
Progestol
Progeston
Progestone
Progestosol
Progestron
Progestronol
Projestaject
Prolets
Prolidon
Prolutin
Proluton
Prolutone
Prometrium
Prontogest
Protormone
Syngesterone
Syngestrets
Synovex s
Syntolutan
Utrogest
Utrogestan
Vitarrine
Beta-progesterone
Delta(sup 4)-pregnene-3,20-dione
(s)-4-pregnene-3,20-dione
(s)-pregn-4-en-3,20-dione
(s)-progesterone
17alpha-progesterone
Akrolutin
Delta(4)-pregnene-3,20-dione
Gelbkoerperhormon
Progesteron
17α-progesterone
δ(4)-pregnene-3,20-dione


Pregnenolone

Pregnenolone is a derivative of cholesterol, the product of cytochrome P450 side-chain cleavage (EC 1.14.15.6, CYP11A1. This reaction consists of three consecutive monooxygenations, a 22-hydroxylation, a 20-hydroxylation, and the cleavage of the C20-C22 bond, yielding pregnenolone. Pregnenolone is the precursor to gonadal steroid hormones and the adrenal corticosteroids. This reaction occurs in steroid hormone-producing tissues such as the adrenal cortex, corpus luteum, and placenta. The most notable difference between the placenta and other steroidogenic tissues is that electron supply to CYP11A1 limits the rate at which cholesterol is converted into pregnenolone in the placenta. The limiting component for electron delivery to CYP11A1 is the concentration of adrenodoxin reductase in the mitochondrial matrix which is insufficient to maintain the adrenodoxin pool in a fully reduced state. Pregnenolone is also a neurosteroid, and is produced in the spinal cord; CYP11A1 is the key enzyme catalyzing the conversion of cholesterol into pregnenolone, the rate-limiting step in the biosynthesis of all classes of steroids, and has been localized in sensory networks of the spinal cord dorsal horn. In the adrenal glomerulosa cell, angiotensin II, one of the major physiological regulators of mineralocorticoid synthesis, appears to affect most of the cholesterol transfer to the mitochondrial outer membrane and many steps in the transport to the inner membrane. Thus, it exerts a powerful control over the use of cholesterol for aldosterone production (PMID: 17222962, 15823613, 16632873, 15134809).


Cortodoxone

Cortexolone is the precursor of cortisol. Accumulation of cortexolone can happen in a defect known as congenital adrenal hyperplasia, which is due to 11-beta-hydroxylase deficiency, resulting in androgen excess, virilization, and hypertension (PMID: 2022736). Cortexolone is a 17-hydroxycorticosteroid with glucocorticoid and anti-inflammatory activities (PubChem).


17alpha,21-Dihydroxypregnenolone is an intermediate in the human fetus at midpregnancy that is converted into cortisol (PMID: 4231965). It has also been found as an intermediate in alternative pathways in human adrenal steroidogenesis that take place under in vitro conditions. In normal adrenal slices from patients with hypernephroid kidney carcinomas these pathways bypass cholesterol, pregnenolone, and progesterone, and proceed to 21-hydroxypregnenolone (PMID: 6247575). 17alpha,21-Dihydroxypregnenolone is an intermediate in C21-Steroid hormone metabolism. 17alpha,21-Dihydroxypregnenolone is the 5th to last step in the synthesis of Cortol and is converted from 17alpha-Hydroxypregnenolone via the enzyme cytochrome P450 (EC 1.14.99.10). It is then converted to 11beta,17alpha,21-Trihydroxypregnenolone via the enzyme cytochrome P450 (EC 1.14.15.4).


20alpha,22beta-Dihydroxycholesterol is an intermediate in C21-Steroid hormone metabolism. 20alpha,22beta-Dihydroxycholesterol is the 8th to last step in the synthesis of 3alpha,11beta,21-Trihydroxy-20-oxo-5beta-pregnan-18-al and is converted from 20alpha-Hydroxycholesterol via the enzyme cytochrome P450 (EC 1.14.15.6). It is then converted to Pregnenolone via the enzyme cytochrome P450 (EC 1.14.15.6).


4-Methylpentanal, also known as isocaproaldehyde or isohexanal, belongs to the class of organic compounds known as alpha-hydrogen aldehydes. These are aldehydes with the general formula HC(H)(R)C(=O)H, where R is an organyl group. 4-Methylpentanal is slightly soluble (in water) and an extremely weak acidic (essentially neutral) compound (based on its pKa). Within the cell, 4-methylpentanal is primarily located in the mitochondria and cytoplasm. In humans, 4-methylpentanal is involved in the steroidogenesis pathway. 4-Methylpentanal is also involved in several metabolic disorders, some of which include 3-Beta-hydroxysteroid dehydrogenase deficiency, corticosterone methyl oxidase II deficiency - cmo II, adrenal hyperplasia type 5 or congenital adrenal hyperplasia due to 17 Alpha-hydroxylase deficiency, and the apparent mineralocorticoid excess syndrome pathway. 4-Methylpentanal is an intermediate in the metabolism of C21-Steroid hormone. It is a substrate for Cytochrome P450 11A1 (mitochondrial).


17alpha,20alpha-Dihydroxycholesterol is an intermediate in C21-Steroid hormone metabolism. 17alpha,20alpha-Dihydroxycholesterol is the 8th to last step in the synthesis of Cortolone and is converted from 20alpha-Hydroxycholesterol via the enzyme cytochrome P450 (EC 1.14.99.9). It is then converted to 17alpha-Hydroxypregnenolone via the enzyme cytochrome P450 (EC1.14.15.6).


20alpha-Hydroxycholesterol belongs to the class of organic compounds known as cholesterols and derivatives. Cholesterols and derivatives are compounds containing a 3-hydroxylated cholestane core. Thus, 20alpha-hydroxycholesterol is considered to be a sterol lipid molecule. 20alpha-Hydroxycholesterol is considered to be a practically insoluble (in water) and relatively neutral molecule. 20alpha-Hydroxycholesterol has been found throughout all human tissues, and has also been primarily detected in urine. Within the cell, 20alpha-hydroxycholesterol is primarily located in the membrane (predicted from logP), mitochondria and cytoplasm. In humans, 20alpha-hydroxycholesterol is involved in the steroidogenesis pathway. 20alpha-Hydroxycholesterol is also involved in several metabolic disorders, some of which include corticosterone methyl oxidase II deficiency - cmo II, the apparent mineralocorticoid excess syndrome pathway, corticosterone methyl oxidase I deficiency (cmo I), and the congenital lipoid adrenal hyperplasia (clah) or lipoid cah pathway. 20 alpha-hydroxycholesterol participates in C21-Steroid hormone metabolism. 20 alpha-hydroxycholesterol is produced by the reaction between cholesterol and the enzyme, cholesterol monooxygenase (side-chain-cleaving) [EC:1.14.15.6].


17alpha,21-Dihydroxy-5beta-pregnane-3,11,20-trione is an intermediate in C21-Steroid hormone metabolism. 17alpha,21-Dihydroxy-5beta-pregnane-3,11,20-trione is the second to last step in the synthesis of Cortolone and is converted. from Cortisone via the enzyme Delta4-3-oxosteroid 5beta-reductase (EC 1.3.1.3). It is then converted to Urocortisone via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50).


Dihydrocortisol

Dihydrocortisol is the product of the enzyme Steroid 5-beta-reductase [EC 1.3.1.3], which catalyzes the reduction of progesterone, androstenedione, 17-alpha-hydroxyprogesterone, testosterone, aldosterone, corticosterone and cortisol to 5-beta-reduced metabolites. A deficiency in this enzyme is associated with congenital defect in bile acid synthesis. (OMIM 235555). Dihydrocortisol is the substrate of the enzyme 3-alpha-hydroxysteroid dehydrogenase[EC:1.1.1.225 1.1.1.213 1.3.1.20 1.1.1.50], and is an iintermediate in the Bile acid biosynthesis, C21-Steroid hormone metabolism, Androgen and estrogen metabolism, and in the Metabolism of xenobiotics by cytochrome P450. (KEGG).


tetrahydrocortisol

Tetrahydrocortisol, also known as dihydrocortison or urocortisol, belongs to the class of organic compounds known as 21-hydroxysteroids. These are steroids carrying a hydroxyl group at the 21-position of the steroid backbone. Tetrahydrocortisol is considered to be a practically insoluble (in water) and relatively neutral molecule. Tetrahydrocortisol has been found in human hepatic tissue, and has also been primarily detected in urine. Within the cell, tetrahydrocortisol is primarily located in the membrane (predicted from logP) and cytoplasm. In humans, tetrahydrocortisol is involved in the steroidogenesis pathway. Tetrahydrocortisol is also involved in several metabolic disorders, some of which include 11-beta-hydroxylase deficiency (cyp11b1), adrenal hyperplasia type 5 or congenital adrenal hyperplasia due to 17 Alpha-hydroxylase deficiency, the apparent mineralocorticoid excess syndrome pathway, and corticosterone methyl oxidase II deficiency - cmo II. Tetrahydrocortisol is the most powerful natural angiostatic steroid. It is involved in C21-Steroid hormone metabolism pathway (KEGG).


11beta,17alpha,21-Trihydroxypregnenolone is an intermediate in C21-Steroid hormone metabolism. 11beta,17alpha,21-Trihydroxypregnenolone is the 4th to last step in the synthesis of Cortol and is converted from 17alpha,21-Dihydroxypregnenolone via the enzyme cytochrome P450 (EC:1.14.15.4). It is then converted to Cortisol via the enzyme 3beta-hydroxy-delta5-steroid dehydrogenase (EC 1.1.1.145) and the enzyme steroid delta-isomerase (EC 5.3.3.1).


5a-Pregnane-3,20-dione, also known as 3,20-allopregnanedione or 5-a-dihydroprogesterone, belongs to the class of organic compounds known as gluco/mineralocorticoids, progestogins and derivatives. These are steroids with a structure based on a hydroxylated prostane moiety. Thus, 5a-pregnane-3,20-dione is considered to be a steroid lipid molecule. 5a-Pregnane-3,20-dione exists as a solid and is considered to be practically insoluble (in water) and relatively neutral. 5a-Pregnane-3,20-dione has been found in human hepatic and testicle tissues, and has also been detected in multiple biofluids, such as blood and urine. Within the cell, 5a-pregnane-3,20-dione is primarily located in the membrane (predicted from logP) and cytoplasm. In humans, 5a-pregnane-3,20-dione is involved in the steroidogenesis pathway. 5a-Pregnane-3,20-dione is also involved in several metabolic disorders, some of which include corticosterone methyl oxidase I deficiency (cmo I), 11-beta-hydroxylase deficiency (cyp11b1), adrenal hyperplasia type 3 or congenital adrenal hyperplasia due to 21-hydroxylase deficiency, and 21-hydroxylase deficiency (cyp21). 5a-Pregnane-3,20-dione is a biologically active 5-alpha-reduced metabolite of plasma progesterone. It is the immediate precursor of 5-alpha-pregnan-3-alpha-ol-20-one (allopregnanolone), a neuroactive steroid that binds with GABA(A) receptor.


3alpha-Hydroxy-5beta-pregnane-20-one is an intermediate in C21-Steroid hormone metabolism. 3alpha-Hydroxy-5beta-pregnane-20-one is converted from 5beta-Pregnane-3,20-dione via the enzyme 3-alpha-hydroxysteroid dehydrogenase (EC 1.1.1.50). It is then converted to Pregnanediol via the enzyme 3alpha(or 20beta)-hydroxysteroid dehydrogenase (EC 1.1.1.53).


Tyramine

Tyramine is a monoamine compound derived from the amino acid tyrosine. Tyramine is metabolized by the enzyme monoamine oxidase. In foods, it is often produced by the decarboxylation of tyrosine during fermentation or decay. Foods containing considerable amounts of tyramine include fish, chocolate, alcoholic beverages, cheese, soy sauce, sauerkraut, and processed meat. A large dietary intake of tyramine can cause an increase in systolic blood pressure of 30 mmHg or more. Tyramine acts as a neurotransmitter via a G protein-coupled receptor with high affinity for tyramine called TA1. The TA1 receptor is found in the brain as well as peripheral tissues including the kidney. An indirect sympathomimetic, Tyramine can also serve as a substrate for adrenergic uptake systems and monoamine oxidase so it prolongs the actions of adrenergic transmitters. It also provokes transmitter release from adrenergic terminals.


Homovanillin

3 -Methoxy-4-hydroxyphenylacetaldehyde is an intermediary aldehyde of dopamine metabolism, metabolized by the class I human liver alcohol dehydrogenases (ADHs). ADH catalyzes both ethanol and acetaldehyde, and the dopamine intermediates compete for the same site of ADH, a basis for the ethanol-induced in vivo alterations of dopamine metabolism. (PMID 2432930).


4-hydroxyphenylacetic acid

p-Hydroxyphenylacetic acid is an oxidative deaminated metabolite of p-tyramine. Also a metabolite of tyrosine via enteric bacteria. The bacterial origin of this compound was confirmed by the finding that this compound in urine decreased significantly after the use of the antibiotic neomycin.

(4-hydroxy-phenyl)-essigsaeure
(4-hydroxy-phenyl)-acetate
(4-hydroxy-phenyl)-acetic acid
(4-hydroxyphenyl)acetate
(4-hydroxyphenyl)acetic acid
(p-hydroxyphenyl)acetate
(p-hydroxyphenyl)acetic acid
(p-hydroxyphenyl)-acetate
(p-hydroxyphenyl)-acetic acid
4-hydroxy-benzeneacetate
4-hydroxy-benzeneacetic acid
4-hydroxybenzeneacetate
4-hydroxybenzeneacetic acid
4-hydroxyphenylacetate
4-hydroxyphenylacetic acid
4-hydroxyphenyl-acetic acid
Parahydroxy phenylacetate
Parahydroxy phenylacetic acid
Parahydroxyphenylacetate
P-hydroxyphenylacetate
P-hydroxyphenylacetic acid
4-carboxymethylphenol


L-dopaquinone

Dopaquinone, also known as o-dopaquinone or L-dopaquinone, is a member of the class of compounds known as L-alpha-amino acids. L-alpha-amino acids are alpha-amino acids which have the L-configuration of the alpha-carbon atom. Dopaquinone is slightly soluble (in water) and a moderately acidic compound (based on its pKa). L-Dopaquinone is a metabolite of L-DOPA and a precursor of melanin. Melanin is synthesized from tyrosine by hydroxylation to dihydroxyphenylalanine (DOPA) and subsequent oxidation to dopaquinone. Both reactions are catalyzed by the enzyme tyrosinase, which is the rate-limiting step. Dopaquinone has an ortho-quinone ring, which is known to be neurotoxic and highly reactive with many other compounds (PMID: 413870). Dopaquinone typically combines with cysteine to form pheomelanin (a pigment-polymer). Alternatively, dopaquinone can be converted to leucodopachrome and eventually to eumelanin (also a pigment-polymer). Dopaquinone can be found in skin and feces. Within the cell, dopaquinone is primarily located in the cytoplasm. Dopaquinone is involved in several metabolic disorders, some of which include transient tyrosinemia, hawkinsinuria, tyrosinemia type I, and alkaptonuria. Chronically high levels of dopaquinone are associated with Parkinson's disease (PD). Many Parkinson's patients are treated with L-DOPA. However, long-term treatment with L-DOPA may actually worsen symptoms or result in neurotic and psychotic symptoms. These may be due to dopachrome and dopaquinone accumulating in the brain of L-DOPA treated patients (PMID: 19131041, PMID: 12373519).


leucodopachrome

Leucodopachrome is an indolic intermediate in the melanogenesis pathway, the non-enzymatic product of dopaquinone through cyclization in a reaction whose operation is determined by a pH greater than 4 (melanin synthesis in human pigment cell lysates is maximal at pH 6.8). Leucodopachrome participates in redox exchange with dopaquinone to give the eumelanin precursor dopachrome plus DOPA. Dopaquinone (the quinone intermediate resulting from tyrosinase-mediated oxidation of tyrosine, monophenol dihydroxyphenylalanine:oxygen oxidoreductase, EC 1.14.18.1) could be a toxic metabolite in melanin biosynthesis (PMID: 6807981, 1445949, 413870, 11461115, 11171088, 12755639).


L-dopachrome

Dopachrome is a cyclization product of L-DOPA and is an intermediate in the biosynthesis of melanin. Dopaquinone has an ortho-quinone ring, which is known to be neurotoxic and highly reactive with many other compounds (PMID: 413870). Dopachrome spontaneously gives rise to 5,6-dihydroxyindole (DHI) or it can be enzymatically metabolized by dopachrome tautomerase to give 5,6-dihydroxyindole-2-carboxylic acid (DHICA). DHI and its oxidation products are also toxic to cells. Many Parkinson's patients are treated with L-DOPA. However, long-term treatment with L-DOPA may actually worsen symptoms or may result in neurotic and psychotic symptoms. These may be due to dopachrome and dopaquinone accumulating in the brain of L-DOPA treated patients (PMID: 19131041, PMID: 12373519).


DIHYDROXYINDOLE

5,6-Dihydroxyindole, also known as DHI or dopamine lutine, belongs to the class of organic compounds known as hydroxyindoles. These are organic compounds containing an indole moiety that carries a hydroxyl group. 5,6-Dihydroxyindole is slightly soluble (in water) and a very weakly acidic compound (based on its pKa). In humans, 5,6-dihydroxyindole is involved in the tyrosine metabolism pathway and the disulfiram action pathway. 5,6-Dihydroxyindole is also involved in several metabolic disorders, some of which include tyrosinemia, transient, OF the newborn pathway, monoamine oxidase-a deficiency (mao-a), the tyrosinemia type I pathway, and the alkaptonuria pathway. 5,6-Dihydroxyindole is a substrate for Tyrosinase.

Aminochrome
Dhi
Dopaminochrome
Dopamine lutine


Indole-5,6-quinone, also known as IQ, belongs to the class of organic compounds known as indoles and derivatives. These are organic compounds containing an indole, which is a bicyclic ring system made up of a six-membered benzene ring fused to a five-membered nitrogen-containing pyrrole ring. Indole-5,6-quinone is soluble (in water) and a strong basic compound (based on its pKa). In humans, indole-5,6-quinone is involved in the tyrosine metabolism pathway and the disulfiram action pathway. Indole-5,6-quinone is also involved in several metabolic disorders, some of which include the alkaptonuria pathway, the hawkinsinuria pathway, dopamine beta-hydroxylase deficiency, and monoamine oxidase-a deficiency (mao-a). Indole-5,6-quinone is involved in the tyrosine metabolism pathway. More specifically, indole-5,6-quinone is an intermediate in the production of melanin. Indole-5,6-quinone is produced from 5,6-dihydroxyindole by tyrosinase [EC:1.14.18.1].

1h-indole-5,6-dione
Indole-5,6 quinone
Iq
Indolequinone


5,6-dihydroxyindole-2-carboxylic acid

5,6-Dihydroxyindole-2-carboxylic acid, also known as 5,6-dhica or DHI2C, belongs to the class of organic compounds known as indolecarboxylic acids and derivatives. Indolecarboxylic acids and derivatives are compounds containing a carboxylic acid group (or a derivative thereof) linked to an indole. 5,6-Dihydroxyindole-2-carboxylic acid is slightly soluble (in water) and a weakly acidic compound (based on its pKa). Within the cell, 5,6-dihydroxyindole-2-carboxylic acid is primarily located in the cytoplasm. In humans, 5,6-dihydroxyindole-2-carboxylic acid is involved in the disulfiram action pathway and the tyrosine metabolism pathway. 5,6-Dihydroxyindole-2-carboxylic acid is also involved in several metabolic disorders, some of which include dopamine beta-hydroxylase deficiency, the tyrosinemia type I pathway, the alkaptonuria pathway, and monoamine oxidase-a deficiency (mao-a). 5,6-Dihydroxyindole-2-carboxylic acid is an intermediate in the metabolism of Tyrosine. It is a substrate for Dopachrome tautomerase.


Thuringione

Normetanephrine, also known as normetadrenaline, belongs to the class of organic compounds known as methoxyphenols. Methoxyphenols are compounds containing a methoxy group attached to the benzene ring of a phenol moiety. Normetanephrine exists as a solid, slightly soluble (in water), and a very weakly acidic compound (based on its pKa). Normetanephrine has been found in human brain and endocrine gland tissues, and has also been primarily detected in feces, urine, blood, and cerebrospinal fluid. Within the cell, normetanephrine is primarily located in the cytoplasm. In humans, normetanephrine is involved in the tyrosine metabolism pathway and the disulfiram action pathway. Normetanephrine is also involved in several metabolic disorders, some of which include the tyrosinemia type I pathway, tyrosinemia, transient, OF the newborn pathway, dopamine beta-hydroxylase deficiency, and the alkaptonuria pathway. Normetanephrine is a methylated metabolite of norepinephrine that is excreted in the urine and found in certain tissues. It is a marker for tumors.


3,4-Dihydroxymandelaldehyde is the monoamine oxidase (MAO) aldehyde metabolite of both norepinephrine and epinephrine. 3,4- dihydroxymandelaldehyde generates a free radical and activates mitochondrial permeability transition, a mechanism implicated in neuron death. There is an increasing body of evidence suggesting that these compounds are neurotoxic, and it has been recently hypothesized that neurodegenerative disorders may be associated with increased levels of this biogenic aldehyde. It is possible to speculate that reduced detoxification of 3,4- dihydroxymandelaldehyde from impaired or deficient aldehyde dehydrogenase function may be a contributing factor in the suggested neurotoxicity of these compounds. Aldehyde dehydrogenases are a group of NAD(P)+ -dependent enzymes that catalyze the oxidation of aldehydes, such as those derived from catecholamines, to their corresponding carboxylic acids. To date, 19 aldehyde dehydrogenase genes have been identified in the human genome. Mutations in these genes and subsequent inborn errors in aldehyde metabolism are the molecular basis of several diseases. Several pharmaceutical agents and environmental toxins are also known to disrupt or inhibit aldehyde dehydrogenase function. (PMID: 17379813, 14697885, 11164826).


Methylamine

Methylamine occurs endogenously from amine catabolism and its tissue levels increase in some pathological conditions, including diabetes. Interestingly, methylamine and ammonia levels are reciprocally controlled by a semicarbazide-sensitive amine oxidase activity that deaminates methylamine to formaldehyde with the production of ammonia and hydrogen peroxide. Methylamine also targets the voltage-operated neuronal potassium channels, probably inducing release of neurotransmitter(s). Semicarbazide-sensitive amine oxidase (SSAO) catalyzes the deamination of primary amines. Such deamination has been shown capable of regulating glucose transport in adipose cells. It has been independently discovered that the primary structure of vascular adhesion protein-1 (VAP-1) is identical to SSAO. Increased serum SSAO activities have been found in patients with diabetic mellitus, vascular disorders, and Alzheimer's disease. The SSAO-catalyzed deamination of endogenous substrates like methylamine led to production of toxic formaldehyde. Chronic elevated methylamine increases the excretion of malondialdehyde and microalbuminuria. Amine oxidase substrates such as methylamine have been shown to stimulate glucose uptake by increasing the recruitment of the glucose transporter GLUT4 from vesicles within the cell to the cell surface. Inhibition of this effect by the presence of semicarbazide and catalase led to the suggestion that the process is mediated by the hydrogen peroxide produced in the oxidation of these amines (PMID: 16049393, 12686132, 17406961).

Aminomethane
Anhydrous methylamine
Carbinamine
Imizin
Mma
Mercurialin
Methanamine
Methyl group
Methyl of gamma-n-methylasparagine
Methylamine
Methylamine anhydrous
Methylamine aqueous solution
Methylamine solution
Methylamine solutions
Methylaminen
Metilamine
Metyloamina
Monomethylamine
N-methylamine
Nma
Nme


Metanephrine is a metabolite of epinephrine created by action of catechol O-methyltransferase on epinephrine. Technically it is a product of epinephrine O-methylation. It is a commonly occurring, pharmacologically and physiologically inactive metabolite of epinephrine. The measurement of plasma free metanephrines is considered to be the best tool in the diagnosis of pheochromocytoma, a rare kind of adrenal medullary neoplasm. In adrenal chromaffin cells, leakage of norepinephrine and epinephrine from storage granules leads to substantial intracellular production of the O-methylated metabolite metanephrine. In fact, the adrenals constitute the single largest source out of any organ system including the liver for circulating metanephrine. In humans, about 93 percent of circulating metanephrine is derived from catecholamines metabolized within adrenal chromaffin cells. (PMID 15317907).


3-Methoxy-4-hydroxyphenylglycolaldehyde is the monoamine oxidase (MAO) aldehyde metabolite of metanephrine. Metanephrine is an O-methylated metabolite formed by catechol-O-methyltransferase (COMT) from epinephrine. Catecholamines play an important role in platelet activation and aggregation, epinephrine being the most potent one. Catecholamines are substantially increased during stress, exercise or smoking and could result in clinically important platelet activation if their action was not rapidly regulated. The inhibitory effects of methoxy phenolic derivatives on epinephrine-induced platelet aggregation may possibly be attributed to their free radical scavenging properties. There is substantial evidence to conclude that an internal rapid autoregulation of epinephrine-induced platelet aggregation, caused by its metabolic degradation products, takes place in vivo. (PMID: 11958479, 9706478).


3,4-dihydroxymandelic acid

3,4-Dihydroxymandelic acid is is a minor metabolite of norepinephrine in humans (PMID 12649306). Patients with neuroblastoma experience elevated levels of 3,4-Dihydroxymandelic acid and other Catecholamines metabolites, and their presence in urine is a good indicator for diagnosis and follow-up (PMID 8193481).


3,4-Dihydroxyphenylglycol (DOPEG) is a normal norepinephrine metabolite present in CSF, plasma and urine in humans (PMID 6875564). In healthy individuals there is a tendency for free DOPEG to increase and for conjugated DOPEG to decrease with age; plasmatic DOPEG levels are significantly lower in depressed patients as compared to healthy controls (PMID 6671452).


2-Hydroxy-3-(4-hydroxyphenyl)propenoic acid is an intermediate in tyrosine metabolism. It is reversibly converted from 4-hydroxyphenylpyruvate via phenylpyruvate tautomerase. 2-Hydroxy-3-(4-hydroxyphenyl)propenoic acid is typically a terminal product of tyrosine metabolism.


Guaiacol

Guaiacol is a phenolic compound with a methoxy group and is the monomethyl ether of catechol. Guaiacol is readily oxidized by the heme iron of peroxidases including the peroxidase of cyclooxygenase (COX) enzymes. It therefore serves as a reducing co-substrate for COX reactions. Guaiacol is a phenolic natural product first isolated from Guaiac resin and the oxidation of lignin. It is a yellowish aromatic oil that is now commonly derived from guaiacum or wood creosote. It is used medicinally as an expectorant, antiseptic, and local anesthetic. Guaiacol is used in traditional dental pulp sedation, and has the property of inducing cell proliferation; guaiacol is a potent scavenger of reactive oxygen radicals and its radical scavenging activity may be associated with its effect on cell proliferation. Guaiacol is also used in the preparation of synthetic vanillin. Guaiacol is also present in wood smoke, as a product of pyrolysis of lignin. Guaiacol has been found in the urine of patients with neuroblastoma and pheochromocytoma. (PMID 4344880, 16152729).

1-hydroxy-2-methoxybenzene
2-hydroxyanisole
2-methoxy-phenol
2-methoxyphenol
Anastil
Catechol monomethyl ether
Creodon
Guaiacol
Guaiacol (liquid) extra pure
Guaiastil
Guaicol
Guaicolina
Guajakol
Guajol
Guasol
Guiacol
Methoxyphenol
Methylcatachol
Methylcatechol
O-guaiacol
O-hydroxyanisole
O-methoxy-phenol
O-methoxyphenol
O-methyl catechol
Pyrocatechol monomethyl ether
Pyroguaiac acid


catechol

Pyrocatechol, often known as catechol or benzene-1,2-diol, is a benzenediol, with formula C6H4(OH)2. It was first prepared in 1839 by H. Reinsch by distilling catechin (the juice of Mimosa catechu). This colourless compound occurs naturally, but about 20000 tons are manufactured each year, mainly as precursors to pesticides, flavors, and fragrances. Its sulfonic acid is often present in the urine of many mammals. Small amounts of catechol occur naturally in fruits and vegetables, along with the enzyme polyphenol oxidase. Upon mixing the enzyme with the substrate and exposure to oxygen (as when a potato or apple is cut), the colorless catechol oxidizes to reddish-brown benzoquinone derivatives. The enzyme is inactivated by adding an acid, such as lemon juice, or by refrigeration. Excluding oxygen also prevents the browning reaction. Catechol melts at 28 oC and boils at 250 oC. It is employed in medicine as an expectorant. The dimethyl ether or veratrol is also used in medicine. Many other pyrocatechin derivatives have been suggested for therapeutic application.

1,2-dihydroxybenzene
2-hydroxyphenol
Catechol
Durafur developer c
Fouramine pch
Fourrine 68
O-benzenediol
O-dihydroxybenzene
O-dioxybenzene
O-hydroquinone
O-hydroxyphenol
O-phenylenediol
Oxyphenate
Oxyphenic acid
Pelagol grey c
Phthalhydroquinone
Phthalic alcohol
Pyrocatechin
Pyrocatechine
Pyrocatechol


3,4-Dihydroxyphenylacetaldehyde (DOPAL) is a metabolite of the monoamine oxidase-catalyzed oxidative deamination of dopamine. Aldehydes are highly reactive molecules formed during the biotransformation of numerous endogenous and exogenous compounds, including biogenic amines. DOPAL generates a free radical and activates mitochondrial permeability transition, a mechanism implicated in neuron death. There is an increasing body of evidence suggesting that these compounds are neurotoxic, and it has been recently hypothesized that neurodegenerative disorders may be associated with increased levels of this biogenic aldehyde. It is possible to speculate that reduced detoxification of 3,4- dihydroxymandelaldehyde from impaired or deficient aldehyde dehydrogenase function may be a contributing factor in the suggested neurotoxicity of these compounds. Aldehyde dehydrogenases are a group of NAD(P)+ -dependent enzymes that catalyze the oxidation of aldehydes, such as those derived from catecholamines, to their corresponding carboxylic acids. To date, 19 aldehyde dehydrogenase genes have been identified in the human genome. Mutations in these genes and subsequent inborn errors in aldehyde metabolism are the molecular basis of several diseases. Several pharmaceutical agents and environmental toxins (i.e.: 4-hydroxy-2-nonenal) are also known to disrupt or inhibit aldehyde dehydrogenase function. (PMID: 17379813, 14697885, 11164826, 16956664.


Dopac

3,4-dihydroxyphenylacetic acid (DOPAC) is a phenolic acid. DOPAC is a neuronal metabolite of dopamine (DA). DA undergoes monoamine oxidase-catalyzed oxidative deamination to 3,4-dihydroxyphenylacetaldehyde (DOPAL), which is metabolized primarily to DOPAC via aldehyde dehydrogenase (ALDH2). The biotransformation of DOPAL is critical as previous studies have demonstrated this DA-derived aldehyde to be a reactive electrophile and toxic to dopaminergic cells. Known inhibitors of mitochondrial ALDH2, such as 4-hydroxy-2-nonenal (4HNE) inhibit ALDH2-mediated oxidation of the endogenous neurotoxin DOPAL. 4HNE is one of the resulting products of oxidative stress, thus linking oxidative stress to the uncontrolled production of an endogenous neurotoxin relevant to Parkinson's disease. In early onset Parkinson disease there is markedly reduced activities of both monoamine oxidase (MAO) A and B. The amount of DOPAC, which is produced during dopamine oxidation by MAO, is greatly reduced as a result of increased parkin overexpression. Administration of methamphetamine to animals causes loss of DA terminals in the brain, and significant decreases in Dopamine and dihydroxyphenylacetic acid (DOPAC) in the striata. Renal dopamine produced in the residual tubular units may be enhanced during a sodium challenge, thus behaving appropriately as a compensatory natriuretic hormone; however the renal dopaminergic system in patients afflicted with renal parenchymal disorders should address parameters other than free urinary dopamine, namely the urinary excretion of L-DOPA and metabolites. DOPAC is one of the major phenolic acids formed during human microbial fermentation of tea, citrus, and soy flavonoid supplements. DOPAC exhibits a considerable antiproliferative effect in LNCaP prostate cancer and HCT116 colon cancer cells. The antiproliferative activity of DOPAC may be due to its catechol structure. A similar association of the catechol moiety in the B-ring with antiproliferative activity was demonstrated for flavanones. (PMID: 16956664, 16455660, 8561959, 11369822, 10443478, 16365058).

(3,4-dihydroxyphenyl)acetate
(3,4-dihydroxyphenyl)acetic acid
(3,4-dihydroxyphenyl)-acetic acid
2-(3,4-dihydroxyphenyl)acetic acid
3,4-dhpop
3,4-dihydroxy-benzeneacetic acid
3,4-dihydroxy-phenylacetic acid
3,4-dihydroxybenzeneacetate
3,4-dihydroxybenzeneacetic acid
3,4-dihydroxyphenyl acetate
3,4-dihydroxyphenyl acetic acid
3,4-dihydroxyphenylacetate
3,4-dihydroxyphenylacetic acid
Dhy
Dopac
Dihydroxyphenylacetate
Dihydroxyphenylacetic acid
Dopacetate
Dopacetic acid
Haa
Homogentisic acid
Homoprotocatechuate
Homoprotocatechuic acid


homovanillic acid

Homovanillic acid is a dopamine metabolite occurring in human biofluids. A high proportion of patients with neuroblastoma excrete increased amounts of it in their urine. Homovanillic acid is a major catecholamine metabolite. It is used as a reagent to detect oxidative enzymes.(Wikipedia).

(4-hydroxy-3-methoxyphenyl)acetate
(4-hydroxy-3-methoxyphenyl)acetic acid
3-methoxy-4-hydroxy-phenylacetic acid
3-methoxy-4-hydroxyphenylacetate
3-methoxy-4-hydroxyphenylacetic acid
4-hydroxy-3-methoxybenzeneacetate
4-hydroxy-3-methoxybenzeneacetic acid
4-hydroxy-3-methoxyphenylacetic acid
4-hydroxy 3-methoxyphenylacetic acid
Homovanilate
Homovanilic acid
Homovanillate
Homovanillinic acid
Vanilacetate
Vanilacetic acid
Hva
Vanillacetic acid
Vanillacetate


Intracellular messenger formed by the action of phospholipase C on phosphatidylinositol 4,5-bisphosphate, which is one of the phospholipids that make up the cell membrane. Inositol 1,4,5-trisphosphate is released into the cytoplasm where it releases calcium ions from internal stores within the cell's endoplasmic reticulum. These calcium ions stimulate the activity of B kinase or calmodulin. (PubChem). Inositol 1,4,5-trisphosphate (InsP3) is traditionally considered to be the messenger that initiates the increase and spreading of the activating Ca2+ wave. In line with this hypothesis, recent evidence suggests that the penetrating sperm delivers into mammalian eggs a novel isoform of phospholipase C (PLC), which promotes the formation of InsP3. The mechanism by which the interacting sperm triggers the production of NAADP and subsequently that of InsP3 remains obscure. (PMID: 15362223).


1D-Myo-inositol 1,4,5,6-tetrakisphosphate has been shown to regulate Cl- transport, to be a phosphoinositide 3-kinase antagonist, and to bind tightly to some pleckstrin homology domains, and finally, it may contribute to transcriptional regulation. Inositol phosphates comprise a large family of intracellular signals which play many important roles in cell biology. These biological actions can be quite specific to one particular inositol phosphate. 1D-myo-Inositol 1,4,5,6-tetrakisphosphate (Ins(1,4,5,6)P4) is phosphorylated by inositolphosphate-multikinase (IPMK; this enzyme has the capacity to regulate the cellular levels of Ins(1,4,5,6)P4 in mammalian cells. (PMID: 16376887, 10720331, 8809047, 9405634).


myo-Inositol 1,3,4,5,6-pentakisphosphate (Ins(1,3,4,5,6)P(5)), an inositol polyphosphate of emerging significance in cellular signalling, and its C-2 epimer scyllo-inositol pentakisphosphate (scyllo-InsP(5)) were synthesised from the same myo-inositol-based precursor. (PMID: 16755629). InsP6, Ins(1,3,4,5,6)P5 and their close metabolic relatives, which are amongst the more abundant intracellular inositol polyphosphates, in chromatin organization, DNA maintenance, gene transcription, nuclear mRNA transport, membrane trafficking and control of cell proliferation. (PMID: 14992690).


1D-myo-inositol 1,3,4-trisphosphate

Inositol 1,3,4-trisphosphate, also known as 1,3,4-itp or I3S, belongs to the class of organic compounds known as inositol phosphates. Inositol phosphates are compounds containing a phosphate group attached to an inositol (or cyclohexanehexol) moiety. Inositol 1,3,4-trisphosphate is soluble (in water) and an extremely strong acidic compound (based on its pKa). Within the cell, inositol 1,3,4-trisphosphate is primarily located in the cytoplasm. In humans, inositol 1,3,4-trisphosphate is involved in the inositol metabolism pathway and the inositol phosphate metabolism pathway. Inositol 1,3,4-trisphosphate is a specific regulator of cellular signaling.


1D-Myo-inositol 1,3,4,6-tetrakisphosphate, also known as ins-1,3,4,6-p4, belongs to the class of organic compounds known as inositol phosphates. Inositol phosphates are compounds containing a phosphate group attached to an inositol (or cyclohexanehexol) moiety. 1D-Myo-inositol 1,3,4,6-tetrakisphosphate is soluble (in water) and an extremely strong acidic compound (based on its pKa). Within the cell, 1D-myo-inositol 1,3,4,6-tetrakisphosphate is primarily located in the nucleus. In humans, 1D-myo-inositol 1,3,4,6-tetrakisphosphate is involved in the inositol metabolism pathway and the inositol phosphate metabolism pathway. 1D-Myo-inositol 1,3,4,6-tetrakisphosphate is a substrate for Tyrosine-protein kinase BTK and Inositol polyphosphate multikinase.


1D-myo-inositol 3,4-bisphosphate

1D-Myo-inositol 3,4-bisphosphate belongs to the class of organic compounds known as inositol phosphates. Inositol phosphates are compounds containing a phosphate group attached to an inositol (or cyclohexanehexol) moiety. 1D-Myo-inositol 3,4-bisphosphate is soluble (in water) and an extremely strong acidic compound (based on its pKa). Within the cell, 1D-myo-inositol 3,4-bisphosphate is primarily located in the cytoplasm. In humans, 1D-myo-inositol 3,4-bisphosphate is involved in the inositol phosphate metabolism pathway and the inositol metabolism pathway. 1D-myo-Inositol 3,4-bisphosphate is an intermediate in inositol phosphate metabolism. 1D-myo-Inositol 3,4-bisphosphate is converted from 1D-myo-inositol-3-phosphate via inositol polyphosphate-4-phosphatase [EC:3.1.3.66].


1D-myo-inositol 3-phosphate

1D-myo-Inositol 3-phosphate is involved in the inositol phosphate metabolism and the phosphatidylinositol signaling systems. With regards to the inositol phosphate metabolism system, 1D-myo-Inositol 3-phosphate is created from D-myo-Inositol 3,4-bisphosphate by inositol polyphosphate-4-phosphatase (EC:3.1.3.66) and is converted to myo-Inositol by myo-inositol-1(or 4)-monophosphatase (EC:3.1.3.25). Within the phosphatidylinositol signaling system, 1D-myo-Inositol 3-phosphate is created from D-myo-Inositol 3,4-bisphosphate by inositol polyphosphate-4-phosphatase (EC:3.1.3.66) and is converted to myo-Inositol by myo-inositol-1(or 4)-monophosphatase (EC:3.1.3.25).

1d-myo-inositol 3-monophosphate
1l-myo-inositol 1-phosphate
D-myo-inositol 3-monophosphate
D-myo-inositol 3-phosphate
Inositol 3-monophosphate
Inositol 3-phosphate
L-myo-inositol 1-phosphate
Myo-inositol 3-monophosphate
Myo-inositol 3-phosphate


Inositol

myo-Inositol is an inositol isoform. Inositol is a derivative of cyclohexane with six hydroxyl groups, making it a polyol. It also is known as a sugar alcohol, having exactly the same molecular formula as glucose or other hexoses. Inositol exists in nine possible stereoisomers, of which cis-1,2,3,5-trans-4,6-cyclohexanehexol, or myo-inositol is the most widely occurring form in nature. The other known inositols include scyllo-inositol, muco-inositol, D-chiro-inositol, L-chiro-inositol, neo-inositol, allo-inositol, epi-inositol and cis-inositol. myo-Inositol is found naturally in many foods (particularly in cereals with high bran content) and can be used as a sweetner as it has half the sweetness of sucrose (table sugar). myo-Inositol was once considered a member of the vitamin B complex and given the name: vitamin B8. However, because it is produced by the human body from glucose, it is not an essential nutrient, and therefore cannot be called a vitamin. myo-Inositol is a precursor molecule for a number of secondary messengers including various inositol phosphates. In addition, inositol/myo-inositol is an important component of the lipids known as phosphatidylinositol (PI) phosphatidylinositol phosphate (PIP). myo-Inositol is synthesized from glucose, via glucose-6-phosphate (G-6-P) in two steps. First, G-6-P is isomerised by an inositol-3-phosphate synthase enzyme to myo-inositol 1-phosphate, which is then dephosphorylated by an inositol monophosphatase enzyme to give free myo-inositol. In humans, myo-inositol is primarily synthesized in the kidneys at a rate of a few grams per day. myo-Inositol can be used in the management of preterm babies who have or are at a risk of infant respiratory distress syndrome. It is also used as a treatment for polycystic ovary syndrome (PCOS). It works by increasing insulin sensitivity, which helps to improve ovarian function and reduce hyperandrogenism. Reduced levels of myo-inositol have been found in the spinal fluid of depressed patients and levels are significantly reduced in brain samples of suicide victims.


1D-Myo-inositol 1,4-bisphosphate is a substrate for Inositol polyphosphate 1-phosphatase, Phosphatidylinositol 4,5-bisphosphate 5-phosphatase A, Skeletal muscle and kidney enriched inositol phosphatase and Type I inositol-1,4,5-trisphosphate 5-phosphatase.

1d-myo-inositol 1,4-bisphosphate
D-myo-inositol 1,4-bisphosphate
Inositol 1,4-bisphosphate
Myo-inositol 1,4-bisphosphate
D-myo-inositol-1,4-bisphosphate
D-myo-inositol 1,4-bisphosphoric acid


1D-myo-inositol 4-phosphate

D-Myo-inositol 4-phosphate, also known as inositol 4-phosphoric acid, belongs to the class of organic compounds known as inositol phosphates. Inositol phosphates are compounds containing a phosphate group attached to an inositol (or cyclohexanehexol) moiety. D-Myo-inositol 4-phosphate is soluble (in water) and a moderately acidic compound (based on its pKa). Within the cell, D-myo-inositol 4-phosphate is primarily located in the cytoplasm. In humans, D-myo-inositol 4-phosphate is involved in the inositol phosphate metabolism pathway and the inositol metabolism pathway. D-Myo-inositol 4-phosphate is a substrate for Inositol monophosphatase, Inositol polyphosphate 1-phosphatase and Inositol monophosphatase 2.

1d-myo-inositol 4-monophosphate
1d-myo-inositol 4-phosphate
D-myo-inositol-4-phosphate
D-myoinositol 4-phosphate
Inositol 4-phosphate
Myo-inositol 4-phosphate
D-myo-inositol 4-phosphate
1d-myo-inositol 4-monophosphoric acid
1d-myo-inositol 4-phosphoric acid
D-myo-inositol 4-phosphoric acid


Phosphatidylinositol (3,4,5)-trisphosphate (PtdIns(3,4,5)P3) commonly abbreviated to PIP3 is the product of the class I phosphoinositide 3-kinases (PI 3-kinases) activity on phosphatidylinositol (4,5)-bisphosphate. PtdIns(3,4,5)P3 is dephophosphorylated by the phosphatase, PTEN on the 3 position and by SHIPs (SH2-containing inositol phosphatase) on the 5' position of the inositol ring.
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The PH domain in a number of proteins binds to PtdIns(3,4,5)P3. Such proteins include Akt/PKB, PDK1, Btk1 and ARNO. The generation of PtdIns(3,4,5)P3 at the plasma membrane upon the activation of class I PI 3-kinases causes these proteins to translocate to the plasma membrane and accordingly affects their activity. The PH domain allows binding between PtdIns(3,4,5)P3 and G-protein coupled receptor kinases (GRKs). This enhances the binding of the GRK to the plasma membrane. (Wikipedia)
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1-Phosphatidyl-1D-myo-inositol 3-phosphate, also known as PTDINS3P, belongs to the class of organic compounds known as inositol phosphates. Inositol phosphates are compounds containing a phosphate group attached to an inositol (or cyclohexanehexol) moiety. 1-Phosphatidyl-1D-myo-inositol 3-phosphate is soluble (in water) and a moderately acidic compound (based on its pKa). 1-Phosphatidyl-1D-myo-inositol 3-phosphate has been found in human skeletal muscle tissue. Within the cell, 1-phosphatidyl-1D-myo-inositol 3-phosphate is primarily located in the cytoplasm. In humans, 1-phosphatidyl-1D-myo-inositol 3-phosphate is involved in the inositol metabolism pathway. 1-Phosphatidyl-1D-myo-inositol 3-phosphate is a substrate for FYVE finger-containing phosphoinositide kinase and Neutrophil cytosol factor 4.


1-Phosphatidyl-D-myo-inositol is an intermediate in inositol phosphate metabolism (KEGG ID C04637). It is generated from 1-phosphatidyl-1D-myo-inositol-5P via the enzyme 1-phosphatidylinositol-5-phosphate 4-kinase [EC:2.7.1.149] and then converted to 1D-myo-inositol-1,4,5P3 via the enzyme 1-phosphatidylinositol-4,5-bisphosphate phosphodiesterase [EC:3.1.4.11].


Inositol phosphates are a family of water-soluble intracellular signaling molecules derived from membrane inositol phospholipids. They undergo a variety of complex interconversion pathways, and their levels are dynamically regulated within the cytosol in response to a variety of agonists. D-Myo-inositol (3,4,5,6) tetrakisphosphate (Ins(3,4,5,6)P4) has a direct biphasic (activation/inhibition) effect on an epithelial Ca2+-activated chloride channel. The effect of Ins(3,4,5,6)P4 is not mimicked by other inositol tetrakisphosphate isomers, is dependent on the prevailing calcium concentration, and is influenced when channels are phosphorylated by calmodulin kinase II. The predominant effect of Ins(3,4,5,6)P4 on phosphorylated channels is inhibitory at levels of intracellular calcium observed in stimulated cells. Ins(3,4,5,6)P4 activity acts to inhibit calcium-dependent chloride secretion. The secretion of fluid and electrolytes across intestinal epithelial cells in response to Ca2+-dependent secretagogues is a tightly regulated process that is subject to both positive and negative influences. Agonists of Gq protein-coupled receptor (GqPCRs) appear to have the ability to evoke antisecretory mechanisms. One is mediated by the generation of Ins(3,4,5,6)P4 and serves to chronically downregulate epithelial responsiveness to subsequent challenge with Ca2+-dependent agonists. (PMID: 12388102, 11408264).


Phytate Sodium

Myo-Inositol hexakisphosphate is an intermediate in inositol phosphate metabolism. It can be generated from D-myo-Inositol 1,3,4,5,6-pentakisphosphate via the enzyme inositol-pentakisphosphate 2-kinase (EC:2.7.1.158). Myo-Inositol hexakisphosphate is also known as phytic acid. It can be used clinically as a complexing agent for removal of traces of heavy metal ions. It acts also as a hypocalcemic agent. Phytic acid is a strong chelator of important minerals such as calcium, magnesium, iron and zinc and can therefore contribute to mineral deficiencies in developing countries. For people with a particularly low intake of essential minerals, especially young children and those in developing countries, this effect can be undesirable. However, dietary mineral chelators help prevent over-mineralization of joints, blood vessels, and other parts of the body, which is most common in older persons. The Journal of Environmental Nutrition (April 2004 volume 27 issue 4) has also stated phytic acid may be considered a phytonutrient, providing an antioxidant effect.


Inositol 1,3,4,5-tetrakisphopsphate (IP4) is a second messenger responsible for mediating Ca2+ entry through plasma membrane and mobilize intracellular Ca2+ by acting synergistically with inositol 1,4,5-trisphosphate (IP3). Inositol 1,4,5-trisphosphate 3-kinase (IP3K, EC 2.7.1.127) phosphorylates IP3 to IP4. Evidence shows that IP4 can activate a protein with ras- and rap-GAP activity and finally inactivate the G protein. This indicates that IP4 regulates Ca2+ influx in a GTP-dependent way, which potentially links the IP3 signaling pathway to GTP-regulated signaling mechanisms. IP4 is demonstrated to be a common regulator in Ca2+ homeostasis. IP4 can bind with high affinity to several intracellular proteins: synaptotagmin (I and II), Gap1, Btk, and centaurin-alpha-and may interact with synaptotagmin to inhibit synaptic transmission. IP4 also acts as a mediator in neuronal death in the ischemic hippocampus. IP4 production is not always associated with modification in calcium concentration, and control of calcium mobilization is not the sole function proposed for IP4. IP4 define an essential signaling pathway for T cell precursor responsiveness and development. In the thymus, IP4 is essential during positive and negative selection of double-positive thymocytes, and in the control of thymocyte reactivity to antigens. 1D-Myo-inositol 1,3,4,5-tetrakisphosphate is also a substrate for Type I inositol-1,4,5-trisphosphate 5-phosphatase, Phosphatidylinositol 4,5-bisphosphate 5-phosphatase A and Skeletal muscle and kidney enriched inositol phosphatase. (PMID: 15740635, 14517551).


alpha-D-glucuronic acid

Glucuronic acid is a carboxylic acid that has the structure of a glucose molecule that has had its sixth carbon atom (of six total) oxidized. The salts of glucuronic acid are known as glucuronates. Glucuronic acid is highly soluble in water. In humans, glucuronic acid is often linked to toxic or poisonous substances to allow for subsequent elimination, and to hormones to allow for easier transport. These linkages involve O-glycosidic bonds. The process is known as glucuronidation, and the resulting substances are known as glucuronides (or glucuronosides). Glucuronidation uses UDP-glucuronic acid (glucuronic acid linked via a glycosidic bond to uridine diphosphate) as an intermediate. UDP-glucuronic acid is formed in the liver of all animals.

D-(+)-glucuronate
D-(+)-glucuronic acid
D-glucuronate
Gcu
Glucosiduronate
Glucosiduronic acid
Glucuronate
Glucuronic acid
Alpha-d-glucopyranuronic acid
Alpha-d-glucuronic acid
Alpha-delta-glucopyranuronic acid
Alpha-delta-glucuronic acid
Delta-(+)-glucuronate
Delta-(+)-glucuronic acid
Delta-glucuronate
D-glucuronic acid
Glcaa
Glcaalpha
A-d-glucuronate
A-d-glucuronic acid
Alpha-d-glucuronate
α-d-glucuronate
α-d-glucuronic acid