Protopine
Protopine is a dibenzazecine alkaloid isolated from Fumaria vaillantii. It has a role as a plant metabolite. Protopine is a natural product found in Corydalis heterocarpa var. japonica, Fumaria capreolata, and other organisms with data available. Protopine is a benzylisoquinoline alkaloid occurring in opium poppies and other plants of the family papaveraceae. It has been found to inhibit histamine H1 receptors and platelet aggregation, and acts as an opioid analgesic. See also: Sanguinaria canadensis root (part of); Chelidonium majus flowering top (part of). Protopine is a benzylisoquinoline alkaloid occurring in opium poppies and other plants of the family papaveraceae. It has been found to inhibit histamine H1 receptors and platelet aggregation, and acts as an opioid analgesic [HMDB] Protopine is a benzylisoquinoline alkaloid occurring in opium poppies and other plants of the family papaveraceae. It has been found to inhibit histamine H1 receptors and platelet aggregation, and acts as an opioid analgesic. Protopine is an alkaloid occurring in opium poppy,[2] Corydalis tubers[3] and other plants of the family papaveraceae, like Fumaria officinalis.[4] Protopine is metabolically derived from the benzylisoquinoline alkaloid (S)-Reticuline through a progressive series of five enzymatic transformations: 1) berberine bridge enzyme to (S)-Scoulerine; 2) (S)-cheilanthifoline synthase/CYP719A25 to (S)-Cheilanthifoline; 3) (S)-stylopine synthase/CYP719A20 to (S)-Stylopine; 4) (S)-tetrahydroprotoberberine N-methyltransferase to (S)-cis-N-Methylstylopine; and ultimately, 5) N-methylstylopine hydroxylase to protopine.[5] It has been found to inhibit histamine H1 receptors and platelet aggregation, and acts as an analgesic.[6][7] Protopine (Corydinine), an isoquinoline alkaloid, is a specific reversible and competitive inhibitor of acetylcholinesterase. Protopine exhibits anti-inflammation, anti-microbial, anti-angiogenic and anti-tumour activity[1][2]. Protopine (Corydinine), an isoquinoline alkaloid, is a specific reversible and competitive inhibitor of acetylcholinesterase. Protopine exhibits anti-inflammation, anti-microbial, anti-angiogenic and anti-tumour activity[1][2].
L-Threonine
L-threonine is an optically active form of threonine having L-configuration. It has a role as a nutraceutical, a micronutrient, a Saccharomyces cerevisiae metabolite, a plant metabolite, an Escherichia coli metabolite, a human metabolite, an algal metabolite and a mouse metabolite. It is an aspartate family amino acid, a proteinogenic amino acid, a threonine and a L-alpha-amino acid. It is a conjugate base of a L-threoninium. It is a conjugate acid of a L-threoninate. It is an enantiomer of a D-threonine. It is a tautomer of a L-threonine zwitterion. An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. L-Threonine is a metabolite found in or produced by Escherichia coli (strain K12, MG1655). Threonine is an essential amino acid in humans (provided by food), Threonine is an important residue of many proteins, such as tooth enamel, collagen, and elastin. An important amino acid for the nervous system, threonine also plays an important role in porphyrin and fat metabolism and prevents fat buildup in the liver. Useful with intestinal disorders and indigestion, threonine has also been used to alleviate anxiety and mild depression. (NCI04) Threonine is an essential amino acid in humans. It is abundant in human plasma, particularly in newborns. Severe deficiency of threonine causes neurological dysfunction and lameness in experimental animals. Threonine is an immunostimulant which promotes the growth of thymus gland. It also can probably promote cell immune defense function. This amino acid has been useful in the treatment of genetic spasticity disorders and multiple sclerosis at a dose of 1 gram daily. It is highly concentrated in meat products, cottage cheese and wheat germ. The threonine content of most of the infant formulas currently on the market is approximately 20\\\\\\% higher than the threonine concentration in human milk. Due to this high threonine content the plasma threonine concentrations are up to twice as high in premature infants fed these formulas than in infants fed human milk. The whey proteins which are used for infant formulas are sweet whey proteins. Sweet whey results from cheese production. Threonine catabolism in mammals appears to be due primarily (70-80\\\\\\%) to the activity of threonine dehydrogenase (EC 1.1.1.103) that oxidizes threonine to 2-amino-3-oxobutyrate, which forms glycine and acetyl CoA, whereas threonine dehydratase (EC 4.2.1.16) that catabolizes threonine into 2-oxobutyrate and ammonia, is significantly less active. Increasing the threonine plasma concentrations leads to accumulation of threonine and glycine in the brain. Such accumulation affects the neurotransmitter balance which may have consequences for the brain development during early postnatal life. Thus, excessive threonine intake during infant feeding should be avoided. (A3450). An essential amino acid occurring naturally in the L-form, which is the active form. It is found in eggs, milk, gelatin, and other proteins. See also: Amlisimod (monomer of) ... View More ... Threonine (Thr) or L-threonine is an alpha-amino acid. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon). Amino acids are organic compounds that contain amino (–NH2) and carboxyl (–COOH) functional groups, along with a side chain (R group) specific to each amino acid. L-threonine is one of 20 proteinogenic amino acids, i.e., the amino acids used in the biosynthesis of proteins. Threonine is found in all organisms ranging from bacteria to plants to animals. It is classified as a polar, uncharged (at physiological pH), aliphatic amino acid. Threonine is sometimes considered as a branched chain amino acid. Threonine was actually the last of the 20 amino acids to be discovered (in 1938). It was named threonine because it was similar in structure to threonic acid, a four-carbon monosaccharide. Threonine is an essential amino acid in humans, meaning the body cannot synthesize it and that it must be obtained from the diet. Foods high in threonine include cottage cheese, poultry, fish, meat, lentils, black turtle bean and sesame seeds. Adult humans require about 20 mg/kg body weight/day. In plants and microorganisms, threonine is synthesized from aspartic acid via alpha-aspartyl-semialdehyde and homoserine. In proteins, the threonine residue is susceptible to numerous posttranslational modifications. The hydroxyl side-chain can undergo O-linked glycosylation and phosphorylation through the action of a threonine kinase. Threonine is abundant in human plasma, particularly in newborns. Severe deficiency of threonine causes neurological dysfunction and lameness in experimental animals. Threonine is an immunostimulant which promotes the growth of thymus gland. It also can probably promote cell immune defense function. The threonine content of most of the infant formulas currently on the market is approximately 20\\\\\\% higher than the threonine concentration in human milk. Due to this high threonine content the plasma threonine concentrations are up to twice as high in premature infants fed these formulas than in infants fed human milk. The whey proteins which are used for infant formulas are sweet whey proteins. Sweet whey results from cheese production. Increasing the threonine plasma concentrations leads to accumulation of threonine and glycine in the brain. Such accumulation affects the neurotransmitter balance which may have consequences for the brain development during early postnatal life. Thus, excessive threonine intake during infant feeding should be avoided. (PMID 9853925). Threonine is metabolized in at least two ways. In many animals it is converted to pyruvate via threonine dehydrogenase. An intermediate in this pathway can undergo thiolysis with CoA to produce acetyl-CoA and glycine. In humans the gene for threonine dehydrogenase is an inactive pseudogene, so threonine is converted to alpha-ketobutyrate. From wide variety of protein hydrolysates. Dietary supplement, nutrient L-Threonine. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=72-19-5 (retrieved 2024-07-01) (CAS RN: 72-19-5). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0). DL-Threonine, an essential amino acid, has the potential to treat hypostatic leg ulceration[1]. L-Threonine is a natural amino acid, can be produced by microbial fermentation, and is used in food, medicine, or feed[1]. L-Threonine is a natural amino acid, can be produced by microbial fermentation, and is used in food, medicine, or feed[1].
L-Dopa
L-dopa is an optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinsons disease It has a role as a prodrug, a hapten, a neurotoxin, an antiparkinson drug, a dopaminergic agent, an antidyskinesia agent, an allelochemical, a plant growth retardant, a human metabolite, a mouse metabolite and a plant metabolite. It is a dopa, a L-tyrosine derivative and a non-proteinogenic L-alpha-amino acid. It is a conjugate acid of a L-dopa(1-). It is an enantiomer of a D-dopa. It is a tautomer of a L-dopa zwitterion. Levodopa is a prodrug of dopamine that is administered to patients with Parkinsons due to its ability to cross the blood-brain barrier. Levodopa can be metabolised to dopamine on either side of the blood-brain barrier and so it is generally administered with a dopa decarboxylase inhibitor like carbidopa to prevent metabolism until after it has crossed the blood-brain barrier. Once past the blood-brain barrier, levodopa is metabolized to dopamine and supplements the low endogenous levels of dopamine to treat symptoms of Parkinsons. The first developed drug product that was approved by the FDA was a levodopa and carbidopa combined product called Sinemet that was approved on May 2, 1975. 3,4-Dihydroxy-L-phenylalanine is a metabolite found in or produced by Escherichia coli (strain K12, MG1655). Levodopa is an Aromatic Amino Acid. Levodopa is an amino acid precursor of dopamine with antiparkinsonian properties. Levodopa is a prodrug that is converted to dopamine by DOPA decarboxylase and can cross the blood-brain barrier. When in the brain, levodopa is decarboxylated to dopamine and stimulates the dopaminergic receptors, thereby compensating for the depleted supply of endogenous dopamine seen in Parkinsons disease. To assure that adequate concentrations of levodopa reach the central nervous system, it is administered with carbidopa, a decarboxylase inhibitor that does not cross the blood-brain barrier, thereby diminishing the decarboxylation and inactivation of levodopa in peripheral tissues and increasing the delivery of dopamine to the CNS. L-Dopa is used for the treatment of Parkinsonian disorders and Dopa-Responsive Dystonia and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. Peripheral tissue conversion may be the mechanism of the adverse effects of levodopa. It is standard clinical practice to co-administer a peripheral DOPA decarboxylase inhibitor - carbidopa or benserazide - and often a catechol-O-methyl transferase (COMT) inhibitor, to prevent synthesis of dopamine in peripheral tissue.The naturally occurring form of dihydroxyphenylalanine and the immediate precursor of dopamine. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. It is used for the treatment of parkinsonian disorders and is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. [PubChem]L-Dopa is the naturally occurring form of dihydroxyphenylalanine and the immediate precursor of dopamine. Unlike dopamine itself, L-Dopa can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. In particular, it is metabolized to dopamine by aromatic L-amino acid decarboxylase. Pyridoxal phosphate (vitamin B6) is a required cofactor for this decarboxylation, and may be administered along with levodopa, usually as pyridoxine. The naturally occurring form of DIHYDROXYPHENYLALANINE and the immediate precursor of DOPAMINE. Unlike dopamine itself, it can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to DOPAMINE. It is used for the treatment of PARKINSONIAN DISORDERS and is usually given with agents that inhibit its conversion to dopamine outside ... L-DOPA, also known as levodopa or 3,4-dihydroxyphenylalanine is an alpha amino acid. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon). L-DOPA is found naturally in both animals and plants. It is made via biosynthesis from the amino acid L-tyrosine by the enzyme tyrosine hydroxylase.. L-DOPA is the precursor to the neurotransmitters dopamine, norepinephrine (noradrenaline), and epinephrine (adrenaline), which are collectively known as catecholamines. The Swedish scientist Arvid Carlsson first showed in the 1950s that administering L-DOPA to animals with drug-induced (reserpine) Parkinsonian symptoms caused a reduction in the intensity of the animals symptoms. Unlike dopamine itself, L-DOPA can be taken orally and crosses the blood-brain barrier. It is rapidly taken up by dopaminergic neurons and converted to dopamine. In particular, it is metabolized to dopamine by aromatic L-amino acid decarboxylase. Pyridoxal phosphate (vitamin B6) is a required cofactor for this decarboxylation, and may be administered along with levodopa, usually as pyridoxine. As a result, L-DOPA is a drug that is now used for the treatment of Parkinsonian disorders and DOPA-Responsive Dystonia. It is usually given with agents that inhibit its conversion to dopamine outside of the central nervous system. It is standard clinical practice in treating Parkinsonism to co-administer a peripheral DOPA decarboxylase inhibitor - carbidopa or benserazide - and often a catechol-O-methyl transferase (COMT) inhibitor, to prevent synthesis of dopamine in peripheral tissue. Side effects of L-DOPA treatment may include: hypertension, arrhythmias, nausea, gastrointestinal bleeding, disturbed respiration, hair loss, disorientation and confusion. L-DOPA can act as an L-tyrosine mimetic and be incorporated into proteins by mammalian cells in place of L-tyrosine, generating protease-resistant and aggregate-prone proteins in vitro and may contribute to neurotoxicity with chronic L-DOPA administration. L-phenylalanine, L-tyrosine, and L-DOPA are all precursors to the biological pigment melanin. The enzyme tyrosinase catalyzes the oxidation of L-DOPA to the reactive intermediate dopaquinone, which reacts further, eventually leading to melanin oligomers. An optically active form of dopa having L-configuration. Used to treat the stiffness, tremors, spasms, and poor muscle control of Parkinsons disease DOPA. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=59-92-7 (retrieved 2024-07-01) (CAS RN: 59-92-7). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0). DL-Dopa is a beta-hydroxylated derivative of phenylalanine. DL-Dopa is a beta-hydroxylated derivative of phenylalanine.
K-Strophanthidin
Strophanthidin is a 3beta-hydroxy steroid, a 14beta-hydroxy steroid, a 5beta-hydroxy steroid, a 19-oxo steroid, a member of cardenolides and a steroid aldehyde. It is functionally related to a 5beta-cardanolide. Strophanthidin is a natural product found in Crossosoma bigelovii, Adonis aestivalis, and other organisms with data available. 3 beta,5,14-Trihydroxy-19-oxo-5 beta-card-20(22)-enolide. The aglycone cardioactive agent isolated from Strophanthus Kombe, S. gratus and other species; it is a very toxic material formerly used as digitalis. Synonyms: Apocymarin; Corchorin; Cynotoxin; Corchorgenin. D020011 - Protective Agents > D002316 - Cardiotonic Agents > D002301 - Cardiac Glycosides D020011 - Protective Agents > D002316 - Cardiotonic Agents > D013328 - Strophanthins Strophanthidin is a naturally available cardiac glycoside[1]. Strophanthidin 0.1 and 1 nmol/L increases and 1~100 μmol/L inhibits the Na+/K+-ATPase activities, but Strophanthidin 10 and 100 nmol/L does not affect Na+/K+-ATPase activities in cardiac sarcolemmal[2]. Strophanthidin increases both diastolic and systolic intracellular Ca2+ concentration[3]. Strophanthidin is a naturally available cardiac glycoside[1]. Strophanthidin 0.1 and 1 nmol/L increases and 1~100 μmol/L inhibits the Na+/K+-ATPase activities, but Strophanthidin 10 and 100 nmol/L does not affect Na+/K+-ATPase activities in cardiac sarcolemmal[2]. Strophanthidin increases both diastolic and systolic intracellular Ca2+ concentration[3].
Primuliten
5-Hydroxyflavone is a member of flavones. 5-Hydroxyflavone is a natural product found in Conchocarpus heterophyllus, Primula denticulata, and Lophomyrtus bullata with data available. relative retention time with respect to 9-anthracene Carboxylic Acid is 1.263 relative retention time with respect to 9-anthracene Carboxylic Acid is 1.268 5-Hydroxyflavone, a flavonoid ligand, shows no cytotoxic activity against MCF-7, FaDU, MDA-MB-435S, U87, RPE-1, and HEK293 cells[1]. 5-Hydroxyflavone, a flavonoid ligand, shows no cytotoxic activity against MCF-7, FaDU, MDA-MB-435S, U87, RPE-1, and HEK293 cells[1].
Biotin
Biotin (also known as vitamin B7 or vitamin H) is one of the B vitamins.[1][2][3] It is involved in a wide range of metabolic processes, both in humans and in other organisms, primarily related to the utilization of fats, carbohydrates, and amino acids.[4] The name biotin, borrowed from the German Biotin, derives from the Ancient Greek word βίοτος (bíotos; 'life') and the suffix "-in" (a suffix used in chemistry usually to indicate 'forming').[5] Biotin appears as a white, needle-like crystalline solid.[6] Biotin is an organic heterobicyclic compound that consists of 2-oxohexahydro-1H-thieno[3,4-d]imidazole having a valeric acid substituent attached to the tetrahydrothiophene ring. The parent of the class of biotins. It has a role as a prosthetic group, a coenzyme, a nutraceutical, a human metabolite, a Saccharomyces cerevisiae metabolite, an Escherichia coli metabolite, a mouse metabolite, a cofactor and a fundamental metabolite. It is a member of biotins and a vitamin B7. It is a conjugate acid of a biotinate. A water-soluble, enzyme co-factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk. Biotin is a metabolite found in or produced by Escherichia coli (strain K12, MG1655). Biotin is a natural product found in Lysinibacillus sphaericus, Aspergillus nidulans, and other organisms with data available. Biotin is hexahydro-2-oxo-1H-thieno(3,4-d)imidazole-4-pentanoic acid. Growth factor present in minute amounts in every living cell. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk. The biotin content of cancerous tissue is higher than that of normal tissue. Biotin is an enzyme co-factor present in minute amounts in every living cell. Biotin is also known as vitamin H or B7 or coenzyme R. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk. Biotin has been recognized as an essential nutrient. Our biotin requirement is fulfilled in part through diet, through endogenous reutilization of biotin and perhaps through capture of biotin generated in the intestinal flora. The utilization of biotin for covalent attachment to carboxylases and its reutilization through the release of carboxylase biotin after proteolytic degradation constitutes the biotin cycle. Biotin deficiency is associated with neurological manifestations, skin rash, hair loss and metabolic disturbances that are thought to relate to the various carboxylase deficiencies (metabolic ketoacidosis with lactic acidosis). It has also been suggested that biotin deficiency is associated with protein malnutrition, and that marginal biotin deficiency in pregnant women may be teratogenic. Biotin acts as a carboxyl carrier in carboxylation reactions. There are four biotin-dependent carboxylases in mammals: those of propionyl-CoA (PCC), 3-methylcrotonyl-CoA (MCC), pyruvate (PC) and acetyl-CoA carboxylases (isoforms ACC-1 and ACC-2). All but ACC-2 are mitochondrial enzymes. The biotin moiety is covalently bound to the epsilon amino group of a Lysine residue in each of these carboxylases in a domain 60-80 amino acids long. The domain is structurally similar among carboxylases from bacteria to mammals. There are four biotin-dependent carboxylases in mammals: those of propionyl-CoA (PCC), 3-methylcrotonyl-CoA (MCC), pyruvate (PC) and acetyl-CoA carboxylases (isoforms ACC-1 and ACC-2). All but ACC-2 are mitochondrial enzymes. The biotin moiety is covalently bound to the epsilon amino group of a Lys residue in each of these carboxylases in a domain 60-80 amino acids long. The domain is structurally similar among carboxylases from bacteria to mammals. Evidence is emerging that biotin participates in processes other than classical carboxylation reactions. Specifically, novel roles for biotin in cell signaling, gene expression, and chromatin structure have been identified in recent years. Human cells accumulate biotin by using both the sodium-dependent multivitamin transporter and monocarboxylate transporter 1. These transporters and other biotin-binding proteins partition biotin to compartments involved in biotin signaling: cytoplasm, mitochondria, and nuclei. The activity of cell signals such as biotinyl-AMP, Sp1 and Sp3, nuclear factor (NF)-kappaB, and receptor tyrosine kinases depends on biotin supply. Consistent with a role for biotin and its catabolites in ... Biotin is an enzyme co-factor present in minute amounts in every living cell. Biotin is also known as coenzyme R and vitamin H or B7. It occurs mainly bound to proteins or polypeptides and is abundant in liver, kidney, pancreas, yeast, and milk. Biotin has been recognized as an essential nutrient. Humans fulfill their biotin requirement through their diet through endogenous reutilization of biotin and perhaps through the capture of biotin generated in the intestinal flora. The utilization of biotin for covalent attachment to carboxylases and its reutilization through the release of carboxylase biotin after proteolytic degradation constitutes the biotin cycle. Biotin deficiency is associated with neurological manifestations, skin rash, hair loss, and metabolic disturbances that are thought to relate to the various carboxylase deficiencies (metabolic ketoacidosis with lactic acidosis). It has also been suggested that biotin deficiency is associated with protein malnutrition, and that marginal biotin deficiency in pregnant women may be teratogenic. Biotin acts as a carboxyl carrier in carboxylation reactions. There are four biotin-dependent carboxylases in mammals: those of propionyl-CoA (PCC), 3-methylcrotonyl-CoA (MCC), pyruvate (PC), and acetyl-CoA carboxylases (isoforms ACC-1 and ACC-2). All but ACC-2 are mitochondrial enzymes. The biotin moiety is covalently bound to the epsilon amino group of a lysine residue in each of these carboxylases in a domain 60-80 amino acids long. The domain is structurally similar among carboxylases from bacteria to mammals. Evidence is emerging that biotin participates in processes other than classical carboxylation reactions. Specifically, novel roles for biotin in cell signalling, gene expression, and chromatin structure have been identified in recent years. Human cells accumulate biotin by using both the sodium-dependent multivitamin transporter and monocarboxylate transporter 1. These transporters and other biotin-binding proteins partition biotin to compartments involved in biotin signalling: cytoplasm, mitochondria, and nuclei. The activity of cell signals such as biotinyl-AMP, Sp1 and Sp3, nuclear factor (NF)-kappaB, and receptor tyrosine kinases depends on biotin supply. Consistent with a role for biotin and its catabolites in modulating these cell signals, greater than 2000 biotin-dependent genes have been identified in various human tissues. Many biotin-dependent gene products play roles in signal transduction and localize to the cell nucleus, consistent with a role for biotin in cell signalling. Posttranscriptional events related to ribosomal activity and protein folding may further contribute to the effects of biotin on gene expression. Finally, research has shown that biotinidase and holocarboxylase synthetase mediate covalent binding of biotin to histones (DNA-binding proteins), affecting chromatin structure; at least seven biotinylation sites have been identified in human histones. Biotinylation of histones appears to play a role in cell proliferation, gene silencing, and the cellular response to DNA repair. Roles for biotin in cell signalling and chromatin structure are consistent with the notion that biotin has a unique significance in cell biology (PMID: 15992684, 16011464). Present in many foods; particularly rich sources include yeast, eggs, liver, certain fish (e.g. mackerel, salmon, sardines), soybeans, cauliflower and cow peas. Dietary supplement. Isolated from various higher plant sources, e.g. sweet corn seedlings and radish leaves An organic heterobicyclic compound that consists of 2-oxohexahydro-1H-thieno[3,4-d]imidazole having a valeric acid substituent attached to the tetrahydrothiophene ring. The parent of the class of biotins. [Raw Data] CB004_Biotin_pos_50eV_CB000006.txt [Raw Data] CB004_Biotin_pos_30eV_CB000006.txt [Raw Data] CB004_Biotin_pos_40eV_CB000006.txt [Raw Data] CB004_Biotin_pos_20eV_CB000006.txt [Raw Data] CB004_Biotin_pos_10eV_CB000006.txt [Raw Data] CB004_Biotin_neg_10eV_000006.txt [Raw Data] CB004_Biotin_neg_20eV_000006.txt Biosynthesis Biotin, synthesized in plants, is essential to plant growth and development.[22] Bacteria also synthesize biotin,[23] and it is thought that bacteria resident in the large intestine may synthesize biotin that is absorbed and utilized by the host organism.[18] Biosynthesis starts from two precursors, alanine and pimeloyl-CoA. These form 7-keto-8-aminopelargonic acid (KAPA). KAPA is transported from plant peroxisomes to mitochondria where it is converted to 7,8-diaminopelargonic acid (DAPA) with the help of the enzyme, BioA. The enzyme dethiobiotin synthetase catalyzes the formation of the ureido ring via a DAPA carbamate activated with ATP, creating dethiobiotin with the help of the enzyme, BioD, which is then converted into biotin which is catalyzed by BioB.[24] The last step is catalyzed by biotin synthase, a radical SAM enzyme. The sulfur is donated by an unusual [2Fe-2S] ferredoxin.[25] Depending on the species of bacteria, Biotin can be synthesized via multiple pathways.[24] Biotin (Vitamin B7) is a water-soluble B vitamin and serves as a coenzyme for five carboxylases in humans, involved in the synthesis of fatty acids, isoleucine, and valine, and in gluconeogenesis. Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids[1][2][3]. Biotin, vitamin B7 and serves as a coenzyme for five carboxylases in humans, involved in the synthesis of fatty acids, isoleucine, and valine, and in gluconeogenesis. Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids[1][2][3]. Biotin (Vitamin B7) is a water-soluble B vitamin and serves as a coenzyme for five carboxylases in humans, involved in the synthesis of fatty acids, isoleucine, and valine, and in gluconeogenesis. Biotin is necessary for cell growth, the production of fatty acids, and the metabolism of fats and amino acids[1][2][3].
Adenosine triphosphate
Adenosine triphosphate, also known as atp or atriphos, is a member of the class of compounds known as purine ribonucleoside triphosphates. Purine ribonucleoside triphosphates are purine ribobucleotides with a triphosphate group linked to the ribose moiety. Adenosine triphosphate is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Adenosine triphosphate can be found in a number of food items such as lichee, alpine sweetvetch, pecan nut, and black mulberry, which makes adenosine triphosphate a potential biomarker for the consumption of these food products. Adenosine triphosphate can be found primarily in blood, cellular cytoplasm, cerebrospinal fluid (CSF), and saliva, as well as throughout most human tissues. Adenosine triphosphate exists in all living species, ranging from bacteria to humans. In humans, adenosine triphosphate is involved in several metabolic pathways, some of which include phosphatidylethanolamine biosynthesis PE(16:0/18:4(6Z,9Z,12Z,15Z)), carteolol action pathway, phosphatidylethanolamine biosynthesis PE(20:3(5Z,8Z,11Z)/15:0), and carfentanil action pathway. Adenosine triphosphate is also involved in several metabolic disorders, some of which include lysosomal acid lipase deficiency (wolman disease), phosphoenolpyruvate carboxykinase deficiency 1 (PEPCK1), propionic acidemia, and the oncogenic action of d-2-hydroxyglutarate in hydroxygluaricaciduria. Moreover, adenosine triphosphate is found to be associated with rachialgia, neuroinfection, stroke, and subarachnoid hemorrhage. Adenosine triphosphate is a non-carcinogenic (not listed by IARC) potentially toxic compound. Adenosine triphosphate is a drug which is used for nutritional supplementation, also for treating dietary shortage or imbalanc. Adenosine triphosphate (ATP) is a complex organic chemical that participates in many processes. Found in all forms of life, ATP is often referred to as the "molecular unit of currency" of intracellular energy transfer. When consumed in metabolic processes, it converts to either the di- or monophosphates, respectively ADP and AMP. Other processes regenerate ATP such that the human body recycles its own body weight equivalent in ATP each day. It is also a precursor to DNA and RNA . ATP is able to store and transport chemical energy within cells. ATP also plays an important role in the synthesis of nucleic acids. ATP can be produced by various cellular processes, most typically in mitochondria by oxidative phosphorylation under the catalytic influence of ATP synthase. The total quantity of ATP in the human body is about 0.1 mole. The energy used by human cells requires the hydrolysis of 200 to 300 moles of ATP daily. This means that each ATP molecule is recycled 2000 to 3000 times during a single day. ATP cannot be stored, hence its consumption must closely follow its synthesis (DrugBank). Metabolism of organophosphates occurs principally by oxidation, by hydrolysis via esterases and by reaction with glutathione. Demethylation and glucuronidation may also occur. Oxidation of organophosphorus pesticides may result in moderately toxic products. In general, phosphorothioates are not directly toxic but require oxidative metabolism to the proximal toxin. The glutathione transferase reactions produce products that are, in most cases, of low toxicity. Paraoxonase (PON1) is a key enzyme in the metabolism of organophosphates. PON1 can inactivate some organophosphates through hydrolysis. PON1 hydrolyzes the active metabolites in several organophosphates insecticides as well as, nerve agents such as soman, sarin, and VX. The presence of PON1 polymorphisms causes there to be different enzyme levels and catalytic efficiency of this esterase, which in turn suggests that different individuals may be more susceptible to the toxic effect of organophosphate exposure (T3DB). ATP is an adenosine 5-phosphate in which the 5-phosphate is a triphosphate group. It is involved in the transportation of chemical energy during metabolic pathways. It has a role as a nutraceutical, a micronutrient, a fundamental metabolite and a cofactor. It is an adenosine 5-phosphate and a purine ribonucleoside 5-triphosphate. It is a conjugate acid of an ATP(3-). An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. Adenosine triphosphate is a metabolite found in or produced by Escherichia coli (strain K12, MG1655). Adenosine-5-triphosphate is a natural product found in Chlamydomonas reinhardtii, Arabidopsis thaliana, and other organisms with data available. Adenosine Triphosphate is an adenine nucleotide comprised of three phosphate groups esterified to the sugar moiety, found in all living cells. Adenosine triphosphate is involved in energy production for metabolic processes and RNA synthesis. In addition, this substance acts as a neurotransmitter. In cancer studies, adenosine triphosphate is synthesized to examine its use to decrease weight loss and improve muscle strength. Adenosine triphosphate (ATP) is a nucleotide consisting of a purine base (adenine) attached to the first carbon atom of ribose (a pentose sugar). Three phosphate groups are esterified at the fifth carbon atom of the ribose. ATP is incorporated into nucleic acids by polymerases in the processes of DNA replication and transcription. ATP contributes to cellular energy charge and participates in overall energy balance, maintaining cellular homeostasis. ATP can act as an extracellular signaling molecule via interactions with specific purinergic receptors to mediate a wide variety of processes as diverse as neurotransmission, inflammation, apoptosis, and bone remodelling. Extracellular ATP and its metabolite adenosine have also been shown to exert a variety of effects on nearly every cell type in human skin, and ATP seems to play a direct role in triggering skin inflammatory, regenerative, and fibrotic responses to mechanical injury, an indirect role in melanocyte proliferation and apoptosis, and a complex role in Langerhans cell-directed adaptive immunity. During exercise, intracellular homeostasis depends on the matching of adenosine triphosphate (ATP) supply and ATP demand. Metabolites play a useful role in communicating the extent of ATP demand to the metabolic supply pathways. Effects as different as proliferation or differentiation, chemotaxis, release of cytokines or lysosomal constituents, and generation of reactive oxygen or nitrogen species are elicited upon stimulation of blood cells with extracellular ATP. The increased concentration of adenosine triphosphate (ATP) in erythrocytes from patients with chronic renal failure (CRF) has been observed in many studies but the mechanism leading to these abnormalities still is controversial. (A3367, A3368, A3369, A3370, A3371). Adenosine triphosphate is a metabolite found in or produced by Saccharomyces cerevisiae. An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter. Adenosine triphosphate (ATP) is a nucleotide consisting of a purine base (adenine) attached to the first carbon atom of ribose (a pentose sugar). Three phosphate groups are esterified at the fifth carbon atom of the ribose. ATP is incorporated into nucleic acids by polymerases in the processes of DNA replication and transcription. ATP contributes to cellular energy charge and participates in overall energy balance, maintaining cellular homeostasis. ATP can act as an extracellular signaling molecule via interactions with specific purinergic receptors to mediate a wide variety of processes as diverse as neurotransmission, inflammation, apoptosis, and bone remodelling. Extracellular ATP and its metabolite adenosine have also been shown to exert a variety of effects on nearly every cell type in human skin, and ATP seems to play a direct role in triggering skin inflammatory, regenerative, and fibrotic responses to mechanical injury, an indirect role in melanocyte proliferation and apoptosis, and a complex role in Langerhans cell-directed adaptive immunity. During exercise, intracellular homeostasis depends on the matching of adenosine triphosphate (ATP) supply and ATP demand. Metabolites play a useful role in communicating the extent of ATP demand to the metabolic supply pathways. Effects as different as proliferation or differentiation, chemotaxis, release of cytokines or lysosomal constituents, and generation of reactive oxygen or nitrogen species are elicited upon stimulation of blood cells with extracellular ATP. The increased concentration of adenosine triphosphate (ATP) in erythrocytes from patients with chronic renal failure (CRF) has been observed in many studies but the mechanism leading to these abnormalities still is controversial. (PMID: 15490415, 15129319, 14707763, 14696970, 11157473). 5′-ATP. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=56-65-5 (retrieved 2024-07-01) (CAS RN: 56-65-5). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0).
Decanoyl-CoA (n-C10:0CoA)
Decanoyl CoA is a human liver acyl-CoA ester. It is selected to determine apparent kinetic constants for human liver acyl-CoA due to its relevance to the human diseases with cellular accumulation of this esters, especially to metabolic defects in the acyl-CoA dehydrogenation steps of the branched-chain amino acids, lysine, 5-hydroxy lysine, tryptophan, and fatty acid oxidation pathways. It is concluded that the substrate concentration is decisive for the glycine conjugate formation and that the occurrence in urine of acylglycines reflects an intramitochondrial accumulation of the corresponding acyl-CoA ester. (PMID: 3707752) [HMDB] Decanoyl CoA is a human liver acyl-CoA ester. It is selected to determine apparent kinetic constants for human liver acyl-CoA due to its relevance to the human diseases with cellular accumulation of this esters, especially to metabolic defects in the acyl-CoA dehydrogenation steps of the branched-chain amino acids, lysine, 5-hydroxy lysine, tryptophan, and fatty acid oxidation pathways. It is concluded that the substrate concentration is decisive for the glycine conjugate formation and that the occurrence in urine of acylglycines reflects an intramitochondrial accumulation of the corresponding acyl-CoA ester. (PMID: 3707752). COVID info from COVID-19 Disease Map Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Tolbutamide
Tolbutamide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It is structurally similar to acetohexamide, chlorpropamide and tolazamide and belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Tolbutamide appears to be metabolized in the liver. Tolbutamide and its metabolites are excreted in urine (75-85\\%) and feces. CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4159; ORIGINAL_PRECURSOR_SCAN_NO 4157 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8370; ORIGINAL_PRECURSOR_SCAN_NO 8367 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8423; ORIGINAL_PRECURSOR_SCAN_NO 8420 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8415; ORIGINAL_PRECURSOR_SCAN_NO 8413 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4159; ORIGINAL_PRECURSOR_SCAN_NO 4156 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4203; ORIGINAL_PRECURSOR_SCAN_NO 4202 ORIGINAL_ACQUISITION_NO 8354; CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_PRECURSOR_SCAN_NO 8351 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8415; ORIGINAL_PRECURSOR_SCAN_NO 8412 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4133; ORIGINAL_PRECURSOR_SCAN_NO 4130 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8326; ORIGINAL_PRECURSOR_SCAN_NO 8324 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 8354; ORIGINAL_PRECURSOR_SCAN_NO 8351 CONFIDENCE standard compound; INTERNAL_ID 693; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4161; ORIGINAL_PRECURSOR_SCAN_NO 4157 A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent V - Various > V04 - Diagnostic agents > V04C - Other diagnostic agents > V04CA - Tests for diabetes D007004 - Hypoglycemic Agents
11,12-Epoxyeicosatrienoic acid
11,12-Epoxyeicosatrienoic acid (CAS: 81276-02-0) is an epoxyeicosatrienoic acid (EET). Induction of CYP2C8 in native coronary artery endothelial cells by beta-naphthoflavone enhances the formation of 11,12-epoxyeicosatrienoic acid, as well as endothelium-derived hyperpolarizing factor-mediated hyperpolarization and relaxation. Transfection of coronary arteries with CYP2C8 antisense oligonucleotides resulted in decreased levels of CYP2C and attenuated the endothelium-derived hyperpolarizing factor-mediated vascular responses. Thus, a CYP-epoxygenase product is an essential component of the endothelium-derived hyperpolarizing factor-mediated relaxation in the porcine coronary artery, and CYP2C8 fulfills the criteria for the coronary endothelium-derived hyperpolarization factor synthase. The role of EETs in the regulation of the cerebral circulation has become more important since it was realized that EETs are produced in another specialized cell type of the brain, the astrocytes. It has become evident that EETs released from astrocytes may mediate cerebral functional hyperemia. Molecular and pharmacological evidence has shown that neurotransmitter release and spillover onto astrocytes can generate EETs. Since these EETs may reach the vasculature via astrocyte foot-processes, they have the same potential as their endothelial counterparts to hyperpolarize and dilate cerebral vessels. P450 enzymes contain heme in their catalytic domain and nitric oxide (NO) appears to bind to these heme moieties and block formation of P450 products, including EETs. Thus, there appears to be crosstalk between P450 enzymes and NO/NO synthase. The role of fatty acid metabolites and cerebral blood flow becomes even more complex in light of data demonstrating that cyclooxygenase products can act as substrates for P450 enzymes (PMID: 17494091, 17434916, 17406062, 17361113, 15581597, 11413051, 10519554). EETs function as autocrine and paracrine mediators. During inflammation, a large amount of arachidonic acid (AA) is released into the cellular milieu and cyclooxygenase enzymes convert this AA to prostaglandins that in turn sensitize pain pathways. However, AA is also converted into natural EETs by cytochrome P450 enzymes. Cytochrome P450 (CYP) epoxygenases convert arachidonic acid into four epoxyeicosatrienoic acid (EET) regioisomers, 5,6-, 8,9-, 11,12-, and 14,15-EET. EETs produce vascular relaxation by activating smooth muscle large-conductance Ca2+-activated K+ channels. In particular, 11,12-epoxy-5Z,8Z,14Z-eicosatrienoic acid has been shown to play a role in the recovery of depleted Ca2+ pools in cultured smooth muscle cells (PMID: 9368016). In addition, EETs have anti-inflammatory effects on blood vessels and in the kidney, promote angiogenesis, and protect ischemic myocardium and the brain. EET levels are typically regulated by soluble epoxide hydrolase (sEH), the major enzyme degrading EETs. Specifically, soluble epoxide hydrolase (sEH) converts EETs into dihydroxyeicosatrienoic acids. 11,12-EpETrE or 11,12-epoxy-5Z,8Z,14Z-eicosatrienoic acid is an epoxyeicosatrienoic acid or an EET derived from arachadonic acid. EETs function as autacrine and paracrine mediators. During inflammation, a large amount of arachidonic acid (AA) is released into the cellular milieu and cyclooxygenase enzymes convert this AA to prostaglandins that in turn sensitize pain pathways. However, AA is also converted to natural epoxyeicosatrienoic acids (EETs) by cytochrome P450 enzymes. Cytochrome P450 (CYP) epoxygenases convert arachidonic acid to four epoxyeicosatrienoic acid (EET) regioisomers, 5,6-, 8,9-, 11,12-, and 14,15-EET. EETs produce vascular relaxation by activating smooth muscle large-conductance Ca2+-activated K+ channels. In particular, 11,12-epoxy-5Z,8Z,14Z-eicosatrienoic acid has been show to play a role in the recovery of depleted Ca2+ pools in cultured smooth muscle cells (PMID: 9368016). In addition, EETs have antiinflammatory effects on blood vessels and in the kidney, promote angiogenesis, and protect ischemic myocardium and brain. EET levels are typically regulated by soluble epoxide hydrolase (sEH), the major enzyme degrading EETs. Specifically, soluble epoxide hydrolase (sEH) converts EETs to dihydroxyeicosatrienoic acids. [HMDB] D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents
Betaxolol
Betaxolol is only found in individuals that have used or taken this drug. It is a cardioselective beta-1-adrenergic antagonist with no partial agonist activity. [PubChem]Betaxolol selectively blocks catecholamine stimulation of beta(1)-adrenergic receptors in the heart and vascular smooth muscle. This results in a reduction of heart rate, cardiac output, systolic and diastolic blood pressure, and possibly reflex orthostatic hypotension. Betaxolol can also competitively block beta(2)-adrenergic responses in the bronchial and vascular smooth muscles, causing bronchospasm. C - Cardiovascular system > C07 - Beta blocking agents > C07A - Beta blocking agents > C07AB - Beta blocking agents, selective S - Sensory organs > S01 - Ophthalmologicals > S01E - Antiglaucoma preparations and miotics > S01ED - Beta blocking agents C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C72900 - Adrenergic Antagonist D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D013565 - Sympatholytics D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D018674 - Adrenergic Antagonists D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents Betaxolol is a selective beta1 adrenergic receptor blocker that can be used for the research of hypertension and glaucoma.
Disopyramide
A class I anti-arrhythmic agent (one that interferes directly with the depolarization of the cardiac membrane and thus serves as a membrane-stabilizing agent) with a depressant action on the heart similar to that of guanidine. It also possesses some anticholinergic and local anesthetic properties. [PubChem] C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BA - Antiarrhythmics, class ia D002317 - Cardiovascular Agents > D026941 - Sodium Channel Blockers > D061567 - Voltage-Gated Sodium Channel Blockers C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
Flecainide
A potent anti-arrhythmia agent, effective in a wide range of ventricular and atrial arrhythmias and tachycardias. Paradoxically, however, in myocardial infarct patients with either symptomatic or asymptomatic arrhythmia, flecainide exacerbates the arrhythmia and is not recommended for use in these patients. [PubChem] C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BC - Antiarrhythmics, class ic D002317 - Cardiovascular Agents > D026941 - Sodium Channel Blockers > D061567 - Voltage-Gated Sodium Channel Blockers C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents CONFIDENCE standard compound; EAWAG_UCHEM_ID 3020 CONFIDENCE standard compound; INTERNAL_ID 2276 D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
Glimepiride
Glimepiride is only found in individuals that have used or taken this drug. It is the first III generation sulphonyl urea it is a very potent sulphonyl urea with long duration of action.The mechanism of action of glimepiride in lowering blood glucose appears to be dependent on stimulating the release of insulin from functioning pancreatic beta cells, and increasing sensitivity of peripheral tissues to insulin. Glimepiride likely binds to ATP-sensitive potassium channel receptors on the pancreatic cell surface, reducing potassium conductance and causing depolarization of the membrane. Membrane depolarization stimulates calcium ion influx through voltage-sensitive calcium channels. This increase in intracellular calcium ion concentration induces the secretion of insulin. A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent D007155 - Immunologic Factors > D007166 - Immunosuppressive Agents D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D007004 - Hypoglycemic Agents
Glyburide
Glyburide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating β cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic β cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Glyburide has been shown to decrease fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels (reflective of the last 8-10 weeks of glucose control). Glyburide appears to be completely metabolized, likely in the liver. Although its metabolites exert a small hypoglycemic effect, their contribution to glyburides hypoglycemic effect is thought to be clinically unimportant. Glyburide metabolites are excreted in urine and feces in approximately equal proportions. The half-life of glyburide appears to be unaffected in those with a creatinine clearance of greater than 29 ml/min/1.73m2. CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9286; ORIGINAL_PRECURSOR_SCAN_NO 9285 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4592; ORIGINAL_PRECURSOR_SCAN_NO 4588 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4591; ORIGINAL_PRECURSOR_SCAN_NO 4588 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4577; ORIGINAL_PRECURSOR_SCAN_NO 4575 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9326; ORIGINAL_PRECURSOR_SCAN_NO 9324 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9318; ORIGINAL_PRECURSOR_SCAN_NO 9316 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4570; ORIGINAL_PRECURSOR_SCAN_NO 4568 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9279; ORIGINAL_PRECURSOR_SCAN_NO 9277 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4585; ORIGINAL_PRECURSOR_SCAN_NO 4583 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9315; ORIGINAL_PRECURSOR_SCAN_NO 9314 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 9303; ORIGINAL_PRECURSOR_SCAN_NO 9301 CONFIDENCE standard compound; INTERNAL_ID 1211; DATASET 20200303_ENTACT_RP_MIX504; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 4550; ORIGINAL_PRECURSOR_SCAN_NO 4548 A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent CONFIDENCE standard compound; INTERNAL_ID 2354 CONFIDENCE standard compound; INTERNAL_ID 8511 INTERNAL_ID 8511; CONFIDENCE standard compound D007004 - Hypoglycemic Agents Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
Repaglinide
Repaglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to cells of the pancreas to stimulate insulin release. Repaglinide induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naive to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Repaglinide is extensively metabolized in the liver and excreted in bile. Repaglinide metabolites do not possess appreciable hypoglycemic activity. Approximately 90\\% of a single orally administered dose is eliminated in feces and 8\\% in urine. C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C98079 - Meglitinide Antidiabetic Agent A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins D007004 - Hypoglycemic Agents
Nandrolone decanoate
Nandrolone decanoate is only found in individuals that have used or taken this drug. It is a C18 steroid with androgenic and anabolic properties. It is generally prepared from alkyl ethers of estradiol to resemble testosterone but less one carbon at the 19 position. It is a schedule III drug in the U.S. Nandrolone is an androgen receptor agonist. The drug bound to the receptor complexes which allows it to enter the nucleus and bind directly to specific nucleotide sequences of the chromosomal DNA. The areas of binding are called hormone response elements (HREs), and influence transcriptional activity of certain genes, producing the androgen effects. D006730 - Hormones, Hormone Substitutes, and Hormone Antagonists > D006728 - Hormones > D045930 - Anabolic Agents C147908 - Hormone Therapy Agent > C548 - Therapeutic Hormone > C1636 - Therapeutic Steroid Hormone D050071 - Bone Density Conservation Agents
9-Hydroxyphenanthrene
This compound belongs to the family of Phenanthrenes and Derivatives. These are polycyclic compounds containing a phenanthrene moiety, which is a tricyclic aromatic compound with three non-linearly fused benzene. D004791 - Enzyme Inhibitors > D047428 - Protein Kinase Inhibitors
Diazoxide
Diazoxide is only found in individuals that have used or taken this drug. It is a benzothiadiazine derivative that is a peripheral vasodilator used for hypertensive emergencies. It lacks diuretic effect, apparently because it lacks a sulfonamide group. [PubChem]As a diuretic, diazoxide inhibits active chloride reabsorption at the early distal tubule via the Na-Cl cotransporter, resulting in an increase in the excretion of sodium, chloride, and water. Thiazides like diazoxide also inhibit sodium ion transport across the renal tubular epithelium through binding to the thiazide sensitive sodium-chloride transporter. This results in an increase in potassium excretion via the sodium-potassium exchange mechanism. The antihypertensive mechanism of diazoxide is less well understood although it may be mediated through its action on carbonic anhydrases in the smooth muscle or through its action on the large-conductance calcium-activated potassium (KCa) channel, also found in the smooth muscle. As a antihypoglycemic, diazoxide inhibits insulin release from the pancreas, probably by opening potassium channels in the beta cell membrane. V - Various > V03 - All other therapeutic products > V03A - All other therapeutic products > V03AH - Drugs for treatment of hypoglycemia C - Cardiovascular system > C02 - Antihypertensives > C02D - Arteriolar smooth muscle, agents acting on > C02DA - Thiazide derivatives C78274 - Agent Affecting Cardiovascular System > C29707 - Vasodilating Agent D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents KEIO_ID D051; [MS2] KO008936 KEIO_ID D051
2,4-Dinitrophenol
CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3673; ORIGINAL_PRECURSOR_SCAN_NO 3671 CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3652; ORIGINAL_PRECURSOR_SCAN_NO 3650 CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3645; ORIGINAL_PRECURSOR_SCAN_NO 3640 CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3674; ORIGINAL_PRECURSOR_SCAN_NO 3673 CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3657; ORIGINAL_PRECURSOR_SCAN_NO 3655 CONFIDENCE standard compound; INTERNAL_ID 447; DATASET 20200303_ENTACT_RP_MIX506; DATA_PROCESSING MERGING RMBmix ver. 0.2.7; DATA_PROCESSING PRESCREENING Shinyscreen ver. 0.8.0; ORIGINAL_ACQUISITION_NO 3632; ORIGINAL_PRECURSOR_SCAN_NO 3630 D010575 - Pesticides > D005659 - Fungicides, Industrial > D004140 - Dinitrophenols CONFIDENCE Reference Standard (Level 1); INTERNAL_ID 8070 CONFIDENCE Reference Standard (Level 1); INTERNAL_ID 8823 D004791 - Enzyme Inhibitors > D014475 - Uncoupling Agents CONFIDENCE standard compound; INTERNAL_ID 2302 D004396 - Coloring Agents KEIO_ID D097
Fosinopril
Fosinopril is a phosphinic acid-containing ester prodrug that belongs to the angiotensin-converting enzyme (ACE) inhibitor class of medications. It is rapidly hydrolyzed to fosinoprilat, its principle active metabolite. Fosinoprilat inhibits ACE, the enzyme responsible for the conversion of angiotensin I (ATI) to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). Fosinopril may be used to treat mild to moderate hypertension, as an adjunct in the treatment of congestive heart failure, and to slow the rate of progression of renal disease in hypertensive individuals with diabetes mellitus and microalbuminuria or overt nephropathy. C - Cardiovascular system > C09 - Agents acting on the renin-angiotensin system > C09A - Ace inhibitors, plain > C09AA - Ace inhibitors, plain D004791 - Enzyme Inhibitors > D011480 - Protease Inhibitors > D000806 - Angiotensin-Converting Enzyme Inhibitors D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents CONFIDENCE standard compound; EAWAG_UCHEM_ID 3324
Nateglinide
Nateglinide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the meglitinide class of short-acting insulin secretagogues, which act by binding to cells of the pancreas to stimulate insulin release. Nateglinide is an amino acid derivative that induces an early insulin response to meals decreasing postprandial blood glucose levels. It should only be taken with meals and meal-time doses should be skipped with any skipped meal. Approximately one month of therapy is required before a decrease in fasting blood glucose is seen. Meglitnides may have a neutral effect on weight or cause a slight increase in weight. The average weight gain caused by meglitinides appears to be lower than that caused by sulfonylureas and insulin and appears to occur only in those naive to oral antidiabetic agents. Due to their mechanism of action, meglitinides may cause hypoglycemia although the risk is thought to be lower than that of sulfonylureas since their action is dependent on the presence of glucose. In addition to reducing postprandial and fasting blood glucose, meglitnides have been shown to decrease glycosylated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Meglitinides appear to be more effective at lowering postprandial blood glucose than metformin, sulfonylureas and thiazolidinediones. Nateglinide is extensively metabolized in the liver and excreted in urine (83\\%) and feces (10\\%). The major metabolites possess less activity than the parent compound. One minor metabolite, the isoprene, has the same potency as its parent compound. C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C98079 - Meglitinide Antidiabetic Agent A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins D007004 - Hypoglycemic Agents
Dermorphin
D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D009294 - Narcotics D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics D018377 - Neurotransmitter Agents > D018847 - Opioid Peptides Dermorphin is a natural heptapeptide μ-opioid receptor (MOR) agonist found in amphibian skin. Inhibition of neuropathic pain[1]. Dermorphin is a natural heptapeptide μ-opioid receptor (MOR) agonist found in amphibian skin. Inhibition of neuropathic pain[1]. Dermorphin is a natural heptapeptide μ-opioid receptor (MOR) agonist found in amphibian skin. Inhibition of neuropathic pain[1].
Medetomidine
D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D006993 - Hypnotics and Sedatives C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D000322 - Adrenergic Agonists D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics COVID info from clinicaltrial, clinicaltrials, clinical trial, clinical trials N - Nervous system > N05 - Psycholeptics > N05C - Hypnotics and sedatives Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS Dexmedetomidine ((+)-Medetomidine) is a potent, selective and orally active agonist of α2-adrenoceptor, with a Ki of 1.08 nM. Dexmedetomidine shows 1620-fold selectivity against α1-adrenoceptor. Dexmedetomidine exhibits anxiolysis, sedation, and modest analgesia effects[1][2][3]. Medetomidine is an orally active α2-adrenoceptor agonist (Ki: 1.08 nM). Medetomidine has sedative and analgesic effects. Medetomidine can cause peripheral vasoconstriction through the activation of α2 adrenoceptors on blood vessels[1][2][3][4].
Nalbuphine
Nalbuphine is only found in individuals that have used or taken this drug. It is a narcotic used as a pain medication. It appears to be an agonist at kappa opioid receptors and an antagonist or partial agonist at mu opioid receptors. [PubChem]The exact mechanism of action is unknown, but is believed to interact with an opiate receptor site in the CNS (probably in or associated with the limbic system). The opiate antagonistic effect may result from competitive inhibition at the opiate receptor, but may also be a result of other mechanisms. Nalbuphine is thought primarily to be a kappa agonist. It is also a partial mu antagonist analgesic, with some binding to the delta receptor and minimal agonist activity at the sigma receptor. D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D009294 - Narcotics D002492 - Central Nervous System Depressants > D009294 - Narcotics > D053610 - Opiate Alkaloids N - Nervous system > N02 - Analgesics > N02A - Opioids > N02AF - Morphinan derivatives D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents C78272 - Agent Affecting Nervous System > C67413 - Opioid Receptor Agonist D002491 - Central Nervous System Agents > D000700 - Analgesics
Clofilium
C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D026902 - Potassium Channel Blockers D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators
Dofetilide
Dofetilide is a class III antiarrhythmic agent that is approved by the Food and Drug Administration (FDA) for the maintenance of sinus rhythm in individuals prone to the formation of atrial fibrillation and flutter, and for the chemical cardioversion to sinus rhythm from atrial fibrillation and flutter. [Wikipedia] C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BD - Antiarrhythmics, class iii C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D026902 - Potassium Channel Blockers D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
Nicorandil
C - Cardiovascular system > C01 - Cardiac therapy > C01D - Vasodilators used in cardiac diseases COVID info from clinicaltrial, clinicaltrials, clinical trial, clinical trials C78274 - Agent Affecting Cardiovascular System > C29707 - Vasodilating Agent D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents D018977 - Micronutrients > D014815 - Vitamins Same as: D01810 Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Cyanidin 3-rutinoside
Cyanidin 3-rutinoside is found in asparagus. Antirrhinin is an anthocyanin. It is the 3-rutinoside of cyanidin. It can be found in blackcurrant Antirrhinin is an anthocyanin. It is the 3-rutinoside of cyanidin. It can be found in blackcurrant. Acquisition and generation of the data is financially supported in part by CREST/JST. [Raw Data] CBA67_Keracyanine_pos_30eV.txt [Raw Data] CBA67_Keracyanine_pos_40eV.txt [Raw Data] CBA67_Keracyanine_pos_50eV.txt [Raw Data] CBA67_Keracyanine_pos_10eV.txt [Raw Data] CBA67_Keracyanine_neg_40eV.txt [Raw Data] CBA67_Keracyanine_neg_20eV.txt [Raw Data] CBA67_Keracyanine_neg_10eV.txt [Raw Data] CBA67_Keracyanine_neg_30eV.txt [Raw Data] CBA67_Keracyanine_neg_50eV.txt [Raw Data] CBA67_Keracyanine_pos_20eV.txt
Tamarixetin
Tamarixetin is a monomethoxyflavone that is quercetin methylated at position O-4. Isolated from Cyperus teneriffae. It has a role as a metabolite and an antioxidant. It is a 7-hydroxyflavonol, a monomethoxyflavone and a tetrahydroxyflavone. It is functionally related to a quercetin. Tamarixetin is a natural product found in Ageratina altissima, Chromolaena odorata, and other organisms with data available. See also: Trifolium pratense flower (part of). A monomethoxyflavone that is quercetin methylated at position O-4. Isolated from Cyperus teneriffae. Tamarixetin (4'-O-Methyl Quercetin) is a natural flavonoid derivative of quercetin, with anti-oxidative and anti-inflammatory effects. Tamarixetin protects against cardiac hypertrophy[1][2]. Tamarixetin (4'-O-Methyl Quercetin) is a natural flavonoid derivative of quercetin, with anti-oxidative and anti-inflammatory effects. Tamarixetin protects against cardiac hypertrophy[1][2].
Ergonovine
Ergonovine is only found in individuals that have used or taken this drug. It is an ergot alkaloid with uterine and vascular smooth muscle contractile properties. [PubChem]Ergonovine directly stimulates the uterine muscle to increase force and frequency of contractions. With usual doses, these contractions precede periods of relaxation; with larger doses, basal uterine tone is elevated and these relaxation periods will be decreased. Contraction of the uterine wall around bleeding vessels at the placental site produces hemostasis. Ergonovine also induces cervical contractions. The sensitivity of the uterus to the oxytocic effect is much greater toward the end of pregnancy. The oxytocic actions of ergonovine are greater than its vascular effects. Ergonovine, like other ergot alkaloids, produces arterial vasoconstriction by stimulation of alpha-adrenergic and serotonin receptors and inhibition of endothelial-derived relaxation factor release. It is a less potent vasoconstrictor than ergotamine. As a diagnostic aid (coronary vasospasm), ergonovine causes vasoconstriction of coronary arteries. G - Genito urinary system and sex hormones > G02 - Other gynecologicals > G02A - Uterotonics > G02AB - Ergot alkaloids C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist C78272 - Agent Affecting Nervous System > C66884 - Dopamine Agonist D012102 - Reproductive Control Agents > D010120 - Oxytocics
11,12-DiHETrE
11,12-DiHETrE is a Cytochrome P450 (P450) eicosanoid. Arachidonic acid may be oxygenated by cytochrome P450 in several ways. Epoxidation of the double bonds leads to the regio- and enantioselective formation of four epoxyeicosatrienoic acids (EETs), which are hydrolyzed by epoxide hydrolase to vicinal diols (DHETs). 11,12-DiHETrE excretion is increased in healthy pregnant women compared with nonpregnant female volunteers, and increased even further in patients with pregnancy-induced hypertension (PIH). The physiological significance of arachidonic acid epoxides has been debated and it is unknown whether they play a role in pregnancy and parturition. Vasodilative effects, inhibition of cyclooxygenase, or inhibition of platelet aggregation by EETs have been observed only at micromolar concentrations. On the other hand, effects on the stimulus-secretion coupling during hormone release have been found in the nanomolar and picomolar range. (PMID: 9440131, 2198572) [HMDB] 11,12-DiHETrE is a Cytochrome P450 (P450) eicosanoid. Arachidonic acid may be oxygenated by cytochrome P450 in several ways. Epoxidation of the double bonds leads to the regio- and enantioselective formation of four epoxyeicosatrienoic acids (EETs), which are hydrolyzed by epoxide hydrolase to vicinal diols (DHETs). 11,12-DiHETrE excretion is increased in healthy pregnant women compared with nonpregnant female volunteers, and increased even further in patients with pregnancy-induced hypertension (PIH). The physiological significance of arachidonic acid epoxides has been debated and it is unknown whether they play a role in pregnancy and parturition. Vasodilative effects, inhibition of cyclooxygenase, or inhibition of platelet aggregation by EETs have been observed only at micromolar concentrations. On the other hand, effects on the stimulus-secretion coupling during hormone release have been found in the nanomolar and picomolar range. (PMID: 9440131, 2198572).
Glyceric acid 1,3-biphosphate
Glyceric acid 1,3-biphosphate (CAS: 1981-49-3), also known as 1,3-bisphosphoglycerate (1,3BPG) or PGAP, is a 3-carbon organic molecule present in most, if not all living creatures. It primarily exists as a metabolic intermediate in glycolysis during respiration. 1,3BPG has been recognized as regulatory signal implicated in the control of metabolism, oxygen affinity of red cells, and other cellular functions. 1,3BPG concentration in erythrocytes changes in a number of pathological conditions, such as inherited phosphoglycerate kinase deficiency in erythrocytes (involved in the synthesis and breakdown of 1,3BPG) (PMID: 3555887). Glyceric acid 1,3-biphosphate is phosphorylated at the number 1 and 3 carbons. The result of this phosphorylation gives 1,3BPG important biological properties such as the ability to phosphorylate ADP to form the energy storage molecule ATP (Wikipedia). 3-phospho-d-glyceroyl phosphate, also known as 1,3-bisphospho-D-glycerate or D-glycerate 1,3-diphosphate, is a member of the class of compounds known as acyl monophosphates. Acyl monophosphates are organic compounds containing a monophosphate linked to an acyl group. They have the general structure R-CO-P(O)(O)OH, R=H or organyl. 3-phospho-d-glyceroyl phosphate is slightly soluble (in water) and a moderately acidic compound (based on its pKa). 3-phospho-d-glyceroyl phosphate can be found in a number of food items such as tamarind, narrowleaf cattail, mustard spinach, and cereals and cereal products, which makes 3-phospho-d-glyceroyl phosphate a potential biomarker for the consumption of these food products. 3-phospho-d-glyceroyl phosphate exists in E.coli (prokaryote) and yeast (eukaryote).
Potassium
Potassium is an essential electrolyte. Potassium balance is crucial for regulating the excitability of nerves and muscles and so critical for regulating contractility of cardiac muscle. Although the most important changes seen in the presence of deranged potassium are cardiac, smooth muscle is also affected with increasing muscle weakness, a feature of both hyperkalaemia and hypokalaemia. Physiologically, it exists as an ion in the body. Potassium (K+) is a positively charged electrolyte, cation, which is present throughout the body in both intracellular and extracellular fluids. The majority of body potassium, >90\\%, are intracellular. It moves freely from intracellular fluid (ICF) to extracellular fluid (ECF) and vice versa when adenosine triphosphate increases the permeability of the cell membrane. It is mainly replaced inside or outside the cells by another cation, sodium (Na+). The movement of potassium into or out of the cells is linked to certain body hormones and also to certain physiological states. Standard laboratory tests measure ECF potassium. Potassium enters the body rapidly during food ingestion. Insulin is produced when a meal is eaten; this causes the temporary movement of potassium from ECF to ICF. Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from hyperkalaemia, this mechanism can be manipulated beneficially by administering high concentration (50\\%) intravenous glucose. Insulin can be added to the glucose, but glucose alone will stimulate insulin production and cause movement of potassium from ECF to ICF. The stimulation of alpha receptors causes increased movement of potassium from ICF to ECF. A noradrenaline infusion can elevate serum potassium levels. An adrenaline infusion, or elevated adrenaline levels, can lower serum potassium levels. Metabolic acidosis causes a rise in extracellular potassium levels. In this situation, excess of hydrogen ions (H+) are exchanged for intracellular potassium ions, probably as a result of the cellular response to a falling blood pH. Metabolic alkalosis causes the opposite effect, with potassium moving into the cells. (PMID: 17883675) [HMDB]. Potassium is found in many foods, some of which are half-highbush blueberry, liquor, grouper, and squashberry. Potassium is an essential electrolyte. Potassium balance is crucial for regulating the excitability of nerves and muscles and so critical for regulating contractility of cardiac muscle. Although the most important changes seen in the presence of deranged potassium are cardiac, smooth muscle is also affected with increasing muscle weakness, a feature of both hyperkalaemia and hypokalaemia. Physiologically, it exists as an ion in the body. Potassium (K+) is a positively charged electrolyte, cation, which is present throughout the body in both intracellular and extracellular fluids. The majority of body potassium, >90\\%, are intracellular. It moves freely from intracellular fluid (ICF) to extracellular fluid (ECF) and vice versa when adenosine triphosphate increases the permeability of the cell membrane. It is mainly replaced inside or outside the cells by another cation, sodium (Na+). The movement of potassium into or out of the cells is linked to certain body hormones and also to certain physiological states. Standard laboratory tests measure ECF potassium. Potassium enters the body rapidly during food ingestion. Insulin is produced when a meal is eaten; this causes the temporary movement of potassium from ECF to ICF. Over the ensuing hours, the kidneys excrete the ingested potassium and homeostasis is returned. In the critically ill patient, suffering from hyperkalaemia, this mechanism can be manipulated beneficially by administering high concentration (50\\%) intravenous glucose. Insulin can be added to the glucose, but glucose alone will stimulate insulin production and cause movement of potassium from ECF to ICF. The stimulation of alpha receptors causes increased movement of potassium from ICF to ECF. A noradrenaline infusion can elevate serum potassium levels. An adrenaline infusion, or elevated adrenaline levels, can lower serum potassium levels. Metabolic acidosis causes a rise in extracellular potassium levels. In this situation, excess of hydrogen ions (H+) are exchanged for intracellular potassium ions, probably as a result of the cellular response to a falling blood pH. Metabolic alkalosis causes the opposite effect, with potassium moving into the cells. (PMID: 17883675).
Oleoyl-CoA
Oleoyl-CoA is a substrate for Acyl-CoA desaturase and Protein FAM34A. [HMDB]. Oleoyl-CoA is found in many foods, some of which are cardoon, fruits, hyssop, and rice. Oleoyl-CoA is a substrate for Acyl-CoA desaturase and Protein FAM34A.
Tungsten
Tungsten is a transition metal found, along with chromium, molybdenum and seaborgium, in Group VI of the Periodic Table of elements. Since its discovery in the last quarter of 18th century, tungsten-based products have been in use in a wide range of applications stretching from daily household necessities to highly specialized components of modern science and technology. As new applications and uses are discovered continuously, interest on and demand for tungsten, already an essential commodity, are projected to increase steadily in the years to come. Unavoidably, as is the case with other natural materials and/or non-renewable resources, increased demand and use of tungsten will spawn (a) increased interactions with other materials and/or non-sustainable practices, (b) a greater number of possible entry points into the natural and human environment and (c) a higher probability of deliberate or accidental releases. Currently, the existing knowledge base does not provide clear information about the behavior of tungsten-based products in the environment. The toxicological profile of tungsten, including possible effects on living organisms and exposure pathways, remains rather sketchy, narrow and fragmentary. Regulation of tungsten, both in terms of environmental and occupational safety and health, is at present limited in comparison with other metals. This pattern of environmental obscurity has been unequivocally disrupted by the events of Fallon, Nevada and the possible implication of tungsten to an acute lymphocytic leukemia (ALL) cluster. Tungsten is now the focus of scrutiny as it currently occupies the top of to do lists of various regulatory, health and environmental agencies. The occurrence of a childhood leukemia cluster in Fallon, Nevada prompted a wide investigation that involved several local, state and federal agencies led by the Centers of Disease Control (CDC). In essence, the objective of this investigation was to assess whether environmental causes were responsible for the cluster. The 16 reported leukemia cases within the time frame of 1997-2001, were well above the average for Nevada (3.0 cases/100,000 children/5 years). Several possible causes were proposed, such as jet fuel (JP-8) from a nearby military base or from a JP-8 pipeline running through the city, high levels of arsenic and other metals in the drinking water supplies, industrial pollution from a local tungsten smelting facility, and agrochemical contamination resulting from agricultural pesticide/fungicide use. Although the exact causes of leukemia are not well known, genetic and/or environmental factors may trigger the disease including ionizing and electromagnetic radiation, infectious and chemical agents. Physiologically, it exists as an ion in the body.(PMID: 16343746). Tungsten is a chemical element with the chemical symbol W and atomic number 74. Tungsten is the only metal from the third transition series that is known to occur in biomolecules, where it is used in a few species of bacteria. It is the heaviest element known to be used by any living organism. Tungsten interferes with molybdenum and copper metabolism, and is somewhat toxic to animal life. [Wikipedia]. Tungsten is found in many foods, some of which are orange bell pepper, black walnut, parsnip, and eggplant.
Diadenosine tetraphosphate
Diadenosine tetraphosphate (AP4A) is a diadenosine polyphosphate. Diadenosine polyphosphates (APnAs, n=3-6) are a family of endogenous vasoactive purine dinucleotides which have been isolated from thrombocytes. APnAs have been demonstrated to be involved in the control of vascular tone as well as the growth of vascular smooth muscle cells and hence, possibly, in atherogenesis. APnAs isolated substances are Ap3A, Ap4A, Ap5A, and Ap6A. APnAs are naturally occurring substances that facilitate tear secretion; they are released from the corneal epithelium, they stimulate tear production and therefore they may be considered as physiological modulators of tear secretion. The APnAs were discovered in the mid-sixties in the course of studies on aminoacyl-tRNA synthetases (aaRS). APnAs have emerged as intracellular and extracellular signalling molecules implicated in the maintenance and regulation of vital cellular functions and become considered as second messengers. Great variety of physiological and pathological effects in mammalian cells was found to be associated with alterations of APnAs. APnAs are polyphosphated nucleotidic substances which are found in the CNS and are known to be released in a calcium-dependent manner from storage vesicles in brain synaptosomes. AP5A is a specific adenylate kinase inhibitor in the hippocampus, decreasing the rate of decomposition of ADP and the formation of ATP; a pathway that influences the availability of purines in the central nervous system. AP4A is the only APnA that can induce a considerable increase in [Ca2+] in endothelial cells, indicating that its vasoactive effects are comparable to the known effects of arginine vasopressin, Angiotensin II, and ATP. AP4A is a ubiquitous ApnA is a signal molecule for DNA replication in mammalian cells. AP4A is a primer for oligoadenylate synthesis catalyzed by interferon-inducible 2-5A synthetase. AP4A is an avid inhibitor of eosinophil-derived neurotoxin (EDN). EDN is a catalytically proficient member of the pancreatic ribonuclease superfamily secreted along with other eosinophil granule proteins during innate host defense responses and various eosinophil-related inflammatory and allergic diseases. The ribonucleolytic activity of EDN is central to its antiviral and neurotoxic activities and possibly to other facets of its biological activity. (PMID: 11212966, 12738682, 11810214, 9607303, 8922753, 9187362, 16401072, 9694344, 9351706, 1953194). Diadenosine tetraphosphate (AP4A) is a diadenosine polyphosphate. Diadenosine polyphosphates (APnAs, n=3-6) are a family of endogenous vasoactive purine dinucleotides which have been isolated from thrombocytes. APnAs have been demonstrated to be involved in the control of vascular tone as well as the growth of vascular smooth muscle cells and hence, possibly, in atherogenesis. APnAs isolated substances are Ap3A, Ap4A, Ap5A, and Ap6A. APnAs are naturally occurring substances that facilitate tear secretion; they are released from the corneal epithelium, they stimulate tear production and therefore they may be considered as physiological modulators of tear secretion. The APnAs were discovered in the mid-sixties in the course of studies on aminoacyl-tRNA synthetases (aaRS). APnAs have emerged as intracellular and extracellular signalling molecules implicated in the maintenance and regulation of vital cellular functions and become considered as second messengers. Great variety of physiological and pathological effects in mammalian cells was found to be associated with alterations of APnAs. APnAs are polyphosphated nucleotidic substances which are found in the CNS and are known to be released in a calcium-dependent manner from storage vesicles in brain synaptosomes. AP5A is a specific adenylate kinase inhibitor in the hippocampus, decreasing the rate of decomposition of ADP and the formation of ATP; a pathway that influences the availability of purines in the central nervous system. D006401 - Hematologic Agents > D010975 - Platelet Aggregation Inhibitors
Perillyl aldehyde
(s)-perillaldehyde, also known as P-mentha-1,8-dien-7-al, is a member of the class of compounds known as menthane monoterpenoids. Menthane monoterpenoids are monoterpenoids with a structure based on the o-, m-, or p-menthane backbone. P-menthane consists of the cyclohexane ring with a methyl group and a (2-methyl)-propyl group at the 1 and 4 ring position, respectively. The o- and m- menthanes are much rarer, and presumably arise by alkyl migration of p-menthanes. Thus, (s)-perillaldehyde is considered to be an isoprenoid lipid molecule (s)-perillaldehyde is practically insoluble (in water) and an extremely weak basic (essentially neutral) compound (based on its pKa). (s)-perillaldehyde is a cherry, fat, and fatty tasting compound found in herbs and spices, which makes (s)-perillaldehyde a potential biomarker for the consumption of this food product (s)-perillaldehyde can be found primarily in saliva. Perillaldehyde, or perilla aldehyde, is a natural organic compound found most abundantly in the perennial herb perilla, but also in a wide variety of other plants and essential oils. It is a monoterpenoid containing an aldehyde functional group.
Propylene glycol
Propylene glycol (CAS: 57-55-6), also known as 1,2-propanediol, is an organic compound (a diol alcohol), usually a tasteless, odourless, and colourless clear oily liquid that is hygroscopic and miscible with water, acetone, and chloroform. It is manufactured by the hydration of propylene oxide. Propylene glycol is used as a solvent for intravenous, oral, and topical pharmaceutical preparations It is generally considered safe. However, in large doses, it can be toxic, especially if given over a short period of time. Intravenous lorazepam contains the largest amount of propylene glycol of commonly used drugs. In adults with normal liver and kidney function, the terminal half-life of propylene glycol ranges from 1.4 to 3.3 hours. Propylene glycol is metabolized by the liver to form lactate, acetate, and pyruvate. The nonmetabolized drug is excreted in the urine mainly as the glucuronide conjugate, approximately 12 to 45 percent is excreted unchanged in urine. Renal clearance decreases as the dose administered increases (390 ml/minute/173 m2 at a dose of 5 g/day but only 144 ml/minute/173 m2 at a dose of 21 g/day). These data suggest that renal clearance declines at higher propylene glycol doses because of the saturation of proximal tubular secretion of the drug. As an acceptable level of propylene glycol has not been defined, the clinical implication of a propylene glycol level is unclear. The World Health Organization (WHO) recommends a maximum consumption of 25 mg/kg/day (1.8 g/day for a 75 kg male) of propylene glycol when used as a food additive, but this limit does not address its use as a drug solvent. No maximum dose is recommended in the literature for intravenous therapy with propylene glycol. Intoxication occurs at much higher doses than the WHO dose limit and is exclusive to pharmacologic exposure. Propylene glycol toxicity includes the development of serum hyperosmolality, lactic acidosis, and kidney failure. It has been suggested that proximal tubular necrosis is the cause of acute kidney injury from propylene glycol. Along these lines, proximal tubular cell injury occurs in cultured human cells exposed to propylene glycol. Acute tubular necrosis was described with propylene glycol toxicity in a case of concomitant administration of intravenous lorazepam and trimethoprim sulfamethoxazole. Propylene glycol induced intoxication can also mimic sepsis or systemic inflammatory response syndrome (SIRS). Patients suspected of having sepsis with negative cultures should be evaluated for propylene glycol toxicity if they have been exposed to high dose lorazepam or other medications containing this solvent (PMID:17555487). Propylene glycol is an anticaking agent, antioxidant, dough strengthener, emulsifier, flavouring agent, formulation aid, humectant, solvent, preservative, stabiliser, hog/poultry scald agent, and surface active agent. It is found in foods such as roasted sesame seeds, oats, truffle and other mushrooms. (R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1]. (R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1].
Adenosine tetraphosphate
Adenosine 5 tetraphosphate, Ap4, is a natural nucleotide present in many biological systems. This nucleotide has been found as a constituent of the nucleotide pool present in the aqueous humor of a number of mammals and appears to act as a regulator of intraocular pressure (PMID: 14600249). AP4 may also play a significant role in the physiological regulation of vascular tone (PMID: 8599250). The plasma concentration of AP4 is in the nanomolar range. Technically adenosine tetraphosphate is condensation product of adenosine with tetraphosphoric acid at the 5 position. Acetyl coenzyme A (CoA) synthetase (EC 6.2.1.1) catalyzes the synthesis of adenosine 5-tetraphosphate (P4A) and adenosine 5-pentaphosphate (p5A) from ATP and tri- or tetrapolyphosphate (P3 or P4). [HMDB] Adenosine 5 tetraphosphate, Ap4, is a natural nucleotide present in many biological systems. This nucleotide has been found as a constituent of the nucleotide pool present in the aqueous humor of a number of mammals and appears to act as a regulator of intraocular pressure (PMID: 14600249). AP4 may also play a significant role in the physiological regulation of vascular tone (PMID: 8599250). The plasma concentration of AP4 is in the nanomolar range. Technically adenosine tetraphosphate is condensation product of adenosine with tetraphosphoric acid at the 5 position. Acetyl coenzyme A (CoA) synthetase (EC 6.2.1.1) catalyzes the synthesis of adenosine 5-tetraphosphate (P4A) and adenosine 5-pentaphosphate (p5A) from ATP and tri- or tetrapolyphosphate (P3 or P4).
Octreolin
H - Systemic hormonal preparations, excl. sex hormones and insulins > H01 - Pituitary and hypothalamic hormones and analogues > H01C - Hypothalamic hormones > H01CB - Somatostatin and analogues D005765 - Gastrointestinal Agents D000970 - Antineoplastic Agents Octreotide (SMS 201-995) is a somatostatin receptor agonist and synthetic octapeptide endogenous somatostatin analogue. Octreotide (SMS 201-995) can bind to the somatostatin receptor and mainly subtypes 2, 3, and 5, increases Gi activity, and reduces intracellular cAMP production. Octreotide (SMS 201-995) has antitumor activity, mediates apoptosis and may also be used in disease studies in acromegaly[1][2].
Thiamylal
Thiamylal is only found in individuals that have used or taken this drug. It is a barbiturate that is administered intravenously for the production of complete anesthesia of short duration, for the induction of general anesthesia, or for inducing a hypnotic state. (From Martindale, The Extra Pharmacopoeia, 30th ed, p919)Thiamylal binds at a distinct binding site associated with a Cl- ionopore at the GABAA receptor, increasing the duration of time for which the Cl- ionopore is open. The post-synaptic inhibitory effect of GABA in the thalamus is, therefore, prolonged. D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D006993 - Hypnotics and Sedatives D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D000777 - Anesthetics C78272 - Agent Affecting Nervous System > C29756 - Sedative and Hypnotic > C67084 - Barbiturate D018377 - Neurotransmitter Agents > D018682 - GABA Agents > D018757 - GABA Modulators C78272 - Agent Affecting Nervous System > C245 - Anesthetic Agent
Entacapone
Entacapone is an inhibitor drug of catechol O-methyltransferase, which catalyzes the reaction between catechol and S-adenosyl-L-methionine to produce guaiacol and S-adenosyl-L-homocysteine. [HMDB] Entacapone is an inhibitor drug of catechol O-methyltransferase, which catalyzes the reaction between catechol and S-adenosyl-L-methionine to produce guaiacol and S-adenosyl-L-homocysteine. D002491 - Central Nervous System Agents > D018726 - Anti-Dyskinesia Agents > D000978 - Antiparkinson Agents D004791 - Enzyme Inhibitors > D065098 - Catechol O-Methyltransferase Inhibitors N - Nervous system > N04 - Anti-parkinson drugs > N04B - Dopaminergic agents C78272 - Agent Affecting Nervous System > C38149 - Antiparkinsonian Agent
Methylprednisolone acetate
C147908 - Hormone Therapy Agent > C548 - Therapeutic Hormone > C1636 - Therapeutic Steroid Hormone C308 - Immunotherapeutic Agent > C574 - Immunosuppressant > C211 - Therapeutic Corticosteroid D000893 - Anti-Inflammatory Agents
Cytarabine
Cytarabine, or cytosine arabinoside, a pyrimidine nucleoside analog, is found in mushrooms. Cytarabine is isolated from the mushroom Xerocomus nigromaculatus of unknown palatability. Cytarabine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute myelogenous leukemia and meningeal leukemia. Cytarabine is an antimetabolite antineoplastic agent that inhibits the synthesis of DNA. Its actions are specific for the S phase of the cell cycle to stop normal cell development and division. Cytarabine is metabolized intracellularly into its active triphosphate form (cytosine arabinoside triphosphate). This metabolite then damages DNA by multiple mechanisms, including the inhibition of alpha-DNA polymerase, inhibition of DNA repair through an effect on beta-DNA polymerase, and incorporation into DNA. The latter mechanism is probably the most important. Cytotoxicity is highly specific for the S phase of the cell cycle. Cytarabine is a chemotherapy agent used mainly in the treatment of hematological malignancies such as acute myeloid leukemia (AML) and non-Hodgkin lymphoma. It is also known as ara C. Cytosine arabinoside is an antimetabolic agent with the chemical name of 1 -arabinofuranosylcytosine. Its mode of action is due to its rapid conversion into cytosine arabinoside triphosphate, which damages DNA when the cell cycle holds in the S phase (synthesis of DNA). Rapidly dividing cells, which require DNA replication for mitosis, are therefore most affected. Cytosine arabinoside also inhibits both DNA and RNA polymerases and nucleotide reductase enzymes needed for DNA synthesis L - Antineoplastic and immunomodulating agents > L01 - Antineoplastic agents > L01B - Antimetabolites > L01BC - Pyrimidine analogues C274 - Antineoplastic Agent > C186664 - Cytotoxic Chemotherapeutic Agent > C272 - Antimetabolite D007155 - Immunologic Factors > D007166 - Immunosuppressive Agents D000890 - Anti-Infective Agents > D000998 - Antiviral Agents D009676 - Noxae > D000963 - Antimetabolites COVID info from COVID-19 Disease Map D000970 - Antineoplastic Agents KEIO_ID C119; [MS2] KO008896 KEIO_ID C119 Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS Cytarabine, a nucleoside analog, causes S phase cell cycle arrest and inhibits DNA polymerase. Cytarabine inhibits DNA synthesis with an IC50 of 16 nM. Cytarabine has antiviral effects against HSV. Cytarabine shows anti-orthopoxvirus activity. Cytarabine, a nucleoside analog, causes S phase cell cycle arrest and inhibits DNA polymerase. Cytarabine inhibits DNA synthesis with an IC50 of 16 nM. Cytarabine has antiviral effects against HSV. Cytarabine shows anti-orthopoxvirus activity.
Dexmedetomidine
Dexmedetomidine is only found in individuals that have used or taken this drug. It is an agonist of receptors, adrenergic alpha-2 that is used in veterinary medicine for its analgesic and sedative properties. It is the racemate of dexmedetomidine. [PubChem]Dexmedetomidine is a specific and selective alpha-2 adrenoceptor agonist. By binding to the presynaptic alpha-2 adrenoceptors, it inhibits the release if norepinephrine, therefore, terminate the propagation of pain signals. Activation of the postsynaptic alpha-2 adrenoceptors inhibits the sympathetic activity decreases blood pressure and heart rate. D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D006993 - Hypnotics and Sedatives C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D000322 - Adrenergic Agonists COVID info from clinicaltrial, clinicaltrials, clinical trial, clinical trials D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents N - Nervous system > N05 - Psycholeptics > N05C - Hypnotics and sedatives D002491 - Central Nervous System Agents > D000700 - Analgesics Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS Dexmedetomidine ((+)-Medetomidine) is a potent, selective and orally active agonist of α2-adrenoceptor, with a Ki of 1.08 nM. Dexmedetomidine shows 1620-fold selectivity against α1-adrenoceptor. Dexmedetomidine exhibits anxiolysis, sedation, and modest analgesia effects[1][2][3]. Medetomidine is an orally active α2-adrenoceptor agonist (Ki: 1.08 nM). Medetomidine has sedative and analgesic effects. Medetomidine can cause peripheral vasoconstriction through the activation of α2 adrenoceptors on blood vessels[1][2][3][4].
5-Hydroxyflavone
5-Hydroxyflavone, a flavonoid ligand, shows no cytotoxic activity against MCF-7, FaDU, MDA-MB-435S, U87, RPE-1, and HEK293 cells[1]. 5-Hydroxyflavone, a flavonoid ligand, shows no cytotoxic activity against MCF-7, FaDU, MDA-MB-435S, U87, RPE-1, and HEK293 cells[1].
Octreotide
Octreotide is only found in individuals that have used or taken this drug. It is the acetate salt of a cyclic octapeptide. It is a long-acting octapeptide with pharmacologic properties mimicking those of the natural hormone somatostatin.Octreotide binds to somatostatin receptors. These receptors are coupled via pertussis toxin sensitive G proteins which lead to inhibition of adenylyl cyclase. Octreotide binding to these receptors also stimulates phosphotyrosine phosphatase and activation of the Na(+)/H(+) exchanger via pertussis toxin insensitive G proteins. H - Systemic hormonal preparations, excl. sex hormones and insulins > H01 - Pituitary and hypothalamic hormones and analogues > H01C - Hypothalamic hormones > H01CB - Somatostatin and analogues D005765 - Gastrointestinal Agents D000970 - Antineoplastic Agents Octreotide (SMS 201-995) is a somatostatin receptor agonist and synthetic octapeptide endogenous somatostatin analogue. Octreotide (SMS 201-995) can bind to the somatostatin receptor and mainly subtypes 2, 3, and 5, increases Gi activity, and reduces intracellular cAMP production. Octreotide (SMS 201-995) has antitumor activity, mediates apoptosis and may also be used in disease studies in acromegaly[1][2].
levomedetomidine
D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D006993 - Hypnotics and Sedatives C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D000322 - Adrenergic Agonists D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D002491 - Central Nervous System Agents > D000700 - Analgesics Medetomidine is an orally active α2-adrenoceptor agonist (Ki: 1.08 nM). Medetomidine has sedative and analgesic effects. Medetomidine can cause peripheral vasoconstriction through the activation of α2 adrenoceptors on blood vessels[1][2][3][4].
decanoyl-CoA
Decanoyl-coa, also known as 10:0-coa or decanoyl-coenzyme a, is a member of the class of compounds known as 2,3,4-saturated fatty acyl coas. 2,3,4-saturated fatty acyl coas are acyl-CoAs carrying a 2,3,4-saturated fatty acyl chain. Thus, decanoyl-coa is considered to be a fatty ester lipid molecule. Decanoyl-coa is slightly soluble (in water) and an extremely strong acidic compound (based on its pKa). Decanoyl-coa can be synthesized from decanoic acid and coenzyme A. Decanoyl-coa can also be synthesized into 3-oxodecanoyl-CoA. Decanoyl-coa can be found in a number of food items such as swede, triticale, ohelo berry, and moth bean, which makes decanoyl-coa a potential biomarker for the consumption of these food products. Decanoyl-coa may be a unique S.cerevisiae (yeast) metabolite.
Decanoyl-CoA (n-C10:0CoA)
Decanoyl CoA is a human liver acyl-CoA ester. It is selected to determine apparent kinetic constants for human liver acyl-CoA due to its relevance to the human diseases with cellular accumulation of this esters, especially to metabolic defects in the acyl-CoA dehydrogenation steps of the branched-chain amino acids, lysine, 5-hydroxy lysine, tryptophan, and fatty acid oxidation pathways. It is concluded that the substrate concentration is decisive for the glycine conjugate formation and that the occurrence in urine of acylglycines reflects an intramitochondrial accumulation of the corresponding acyl-CoA ester. (PMID: 3707752) [HMDB] Decanoyl CoA is a human liver acyl-CoA ester. It is selected to determine apparent kinetic constants for human liver acyl-CoA due to its relevance to the human diseases with cellular accumulation of this esters, especially to metabolic defects in the acyl-CoA dehydrogenation steps of the branched-chain amino acids, lysine, 5-hydroxy lysine, tryptophan, and fatty acid oxidation pathways. It is concluded that the substrate concentration is decisive for the glycine conjugate formation and that the occurrence in urine of acylglycines reflects an intramitochondrial accumulation of the corresponding acyl-CoA ester. (PMID: 3707752). COVID info from COVID-19 Disease Map Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Repaglinide
C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C98079 - Meglitinide Antidiabetic Agent A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins D007004 - Hypoglycemic Agents CONFIDENCE standard compound; INTERNAL_ID 2189 CONFIDENCE standard compound; EAWAG_UCHEM_ID 3349
fosinopril
C - Cardiovascular system > C09 - Agents acting on the renin-angiotensin system > C09A - Ace inhibitors, plain > C09AA - Ace inhibitors, plain D004791 - Enzyme Inhibitors > D011480 - Protease Inhibitors > D000806 - Angiotensin-Converting Enzyme Inhibitors D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents CONFIDENCE standard compound; INTERNAL_ID 2247
Nateglinide
C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C98079 - Meglitinide Antidiabetic Agent A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins D007004 - Hypoglycemic Agents CONFIDENCE standard compound; EAWAG_UCHEM_ID 3289
Protopine
Annotation level-1 D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D009294 - Narcotics D018377 - Neurotransmitter Agents > D018494 - Histamine Agents > D006633 - Histamine Antagonists relative retention time with respect to 9-anthracene Carboxylic Acid is 0.601 D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents D006401 - Hematologic Agents > D010975 - Platelet Aggregation Inhibitors D002491 - Central Nervous System Agents > D000700 - Analgesics relative retention time with respect to 9-anthracene Carboxylic Acid is 0.596 IPB_RECORD: 1441; CONFIDENCE confident structure Protopine (Corydinine), an isoquinoline alkaloid, is a specific reversible and competitive inhibitor of acetylcholinesterase. Protopine exhibits anti-inflammation, anti-microbial, anti-angiogenic and anti-tumour activity[1][2]. Protopine (Corydinine), an isoquinoline alkaloid, is a specific reversible and competitive inhibitor of acetylcholinesterase. Protopine exhibits anti-inflammation, anti-microbial, anti-angiogenic and anti-tumour activity[1][2].
R-Phycoerythrin
This record is a MS2 spectrum. Link to the MS spectrum is added in the following comment field.; [MS] MCH00018; Profile spectrum of this record is given as a JPEG file.; [Profile] MCH00020.jpg The metal-free red phycobilin pigment in a conjugated chromoprotein of red algae. It functions as a light-absorbing substance together with chlorophylls. This record is a MS2 spectrum. Link to the MS spectrum is added in the following comment field.; [MS] MCH00018; Profile spectrum of this record is given as a JPEG file.; [Profile] MCH00019.jpg Profile spectrum of this record is given as a JPEG file.; [Profile] MCH00018.jpg
betaxolol
C - Cardiovascular system > C07 - Beta blocking agents > C07A - Beta blocking agents > C07AB - Beta blocking agents, selective S - Sensory organs > S01 - Ophthalmologicals > S01E - Antiglaucoma preparations and miotics > S01ED - Beta blocking agents C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C72900 - Adrenergic Antagonist D018373 - Peripheral Nervous System Agents > D001337 - Autonomic Agents > D013565 - Sympatholytics D018377 - Neurotransmitter Agents > D018663 - Adrenergic Agents > D018674 - Adrenergic Antagonists D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents Betaxolol is a selective beta1 adrenergic receptor blocker that can be used for the research of hypertension and glaucoma.
Ergonovine
A monocarboxylic acid amide that is lysergamide in which one of the hydrogens attached to the amide nitrogen is substituted by a 1-hydroxypropan-2-yl group (S-configuration). An ergot alkaloid that has a particularly powerful action on the uterus, its maleate (and formerly tartrate) salt is used in the active management of the third stage of labour, and to prevent or treat postpartum of postabortal haemorrhage caused by uterine atony: by maintaining uterine contraction and tone, blood vessels in the uterine wall are compressed and blood flow reduced. G - Genito urinary system and sex hormones > G02 - Other gynecologicals > G02A - Uterotonics > G02AB - Ergot alkaloids C78272 - Agent Affecting Nervous System > C29747 - Adrenergic Agent > C87053 - Adrenergic Agonist C78272 - Agent Affecting Nervous System > C66884 - Dopamine Agonist D012102 - Reproductive Control Agents > D010120 - Oxytocics CONFIDENCE Claviceps purpurea sclerotia relative retention time with respect to 9-anthracene Carboxylic Acid is 0.382 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.380 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.373 relative retention time with respect to 9-anthracene Carboxylic Acid is 0.375
glimepiride
A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent D007155 - Immunologic Factors > D007166 - Immunosuppressive Agents D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D007004 - Hypoglycemic Agents CONFIDENCE standard compound; INTERNAL_ID 2355 CONFIDENCE standard compound; INTERNAL_ID 8512
Dofetilide
C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BD - Antiarrhythmics, class iii C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D026902 - Potassium Channel Blockers D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
NICORANDIL
C - Cardiovascular system > C01 - Cardiac therapy > C01D - Vasodilators used in cardiac diseases COVID info from clinicaltrial, clinicaltrials, clinical trial, clinical trials C78274 - Agent Affecting Cardiovascular System > C29707 - Vasodilating Agent D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents D018977 - Micronutrients > D014815 - Vitamins Same as: D01810 Corona-virus Coronavirus SARS-CoV-2 COVID-19 SARS-CoV COVID19 SARS2 SARS
Entacapone
D002491 - Central Nervous System Agents > D018726 - Anti-Dyskinesia Agents > D000978 - Antiparkinson Agents D004791 - Enzyme Inhibitors > D065098 - Catechol O-Methyltransferase Inhibitors N - Nervous system > N04 - Anti-parkinson drugs > N04B - Dopaminergic agents C78272 - Agent Affecting Nervous System > C38149 - Antiparkinsonian Agent
diazoxide
V - Various > V03 - All other therapeutic products > V03A - All other therapeutic products > V03AH - Drugs for treatment of hypoglycemia C - Cardiovascular system > C02 - Antihypertensives > C02D - Arteriolar smooth muscle, agents acting on > C02DA - Thiazide derivatives C78274 - Agent Affecting Cardiovascular System > C29707 - Vasodilating Agent D002317 - Cardiovascular Agents > D000959 - Antihypertensive Agents D002317 - Cardiovascular Agents > D014665 - Vasodilator Agents
nalbuphine
D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D009294 - Narcotics D002492 - Central Nervous System Depressants > D009294 - Narcotics > D053610 - Opiate Alkaloids N - Nervous system > N02 - Analgesics > N02A - Opioids > N02AF - Morphinan derivatives D018373 - Peripheral Nervous System Agents > D018689 - Sensory System Agents C78272 - Agent Affecting Nervous System > C67413 - Opioid Receptor Agonist D002491 - Central Nervous System Agents > D000700 - Analgesics
flecainide
C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BC - Antiarrhythmics, class ic D002317 - Cardiovascular Agents > D026941 - Sodium Channel Blockers > D061567 - Voltage-Gated Sodium Channel Blockers C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
disopyramide
C - Cardiovascular system > C01 - Cardiac therapy > C01B - Antiarrhythmics, class i and iii > C01BA - Antiarrhythmics, class ia D002317 - Cardiovascular Agents > D026941 - Sodium Channel Blockers > D061567 - Voltage-Gated Sodium Channel Blockers C78274 - Agent Affecting Cardiovascular System > C47793 - Antiarrhythmic Agent D002317 - Cardiovascular Agents > D000889 - Anti-Arrhythmia Agents D049990 - Membrane Transport Modulators C93038 - Cation Channel Blocker
glyburide
A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent D007004 - Hypoglycemic Agents Glibenclamide (Glyburide) is an orally active ATP-sensitive K+ channel (KATP) inhibitor and can be used for the research of diabetes and obesity[1]. Glibenclamide inhibits P-glycoprotein. Glibenclamide directly binds and blocks the SUR1 subunits of KATP and inhibits the cystic fibrosis transmembrane conductance regulator protein (CFTR)[3]. Glibenclamide interferes with mitochondrial bioenergetics by inducing changes on membrane ion permeability[4]. Glibenclamide can induce autophagy[5].
tolbutamide
A - Alimentary tract and metabolism > A10 - Drugs used in diabetes > A10B - Blood glucose lowering drugs, excl. insulins > A10BB - Sulfonylureas C78276 - Agent Affecting Digestive System or Metabolism > C29711 - Anti-diabetic Agent > C97936 - Sulfonylurea Antidiabetic Agent V - Various > V04 - Diagnostic agents > V04C - Other diagnostic agents > V04CA - Tests for diabetes An N-sulfonylurea that consists of 1-butylurea having a tosyl group attached at the 3-position. D007004 - Hypoglycemic Agents
oleoyl-CoA
An octadecenoyl-CoA that results from the formal condensation of the thiol group of coenzyme A with the carboxy group of oleic acid.
CoA 18:1
CoA 10:0
(R)-(−)-Propylene glycerol
(R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1]. (R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1].
XS-89
D020011 - Protective Agents > D002316 - Cardiotonic Agents > D002301 - Cardiac Glycosides D020011 - Protective Agents > D002316 - Cardiotonic Agents > D013328 - Strophanthins Strophanthidin is a naturally available cardiac glycoside[1]. Strophanthidin 0.1 and 1 nmol/L increases and 1~100 μmol/L inhibits the Na+/K+-ATPase activities, but Strophanthidin 10 and 100 nmol/L does not affect Na+/K+-ATPase activities in cardiac sarcolemmal[2]. Strophanthidin increases both diastolic and systolic intracellular Ca2+ concentration[3]. Strophanthidin is a naturally available cardiac glycoside[1]. Strophanthidin 0.1 and 1 nmol/L increases and 1~100 μmol/L inhibits the Na+/K+-ATPase activities, but Strophanthidin 10 and 100 nmol/L does not affect Na+/K+-ATPase activities in cardiac sarcolemmal[2]. Strophanthidin increases both diastolic and systolic intracellular Ca2+ concentration[3].
Sulphur Black 1
D010575 - Pesticides > D005659 - Fungicides, Industrial > D004140 - Dinitrophenols A dinitrophenol having the nitro groups at the 2- and 4-positions. D004791 - Enzyme Inhibitors > D014475 - Uncoupling Agents D004396 - Coloring Agents
Nandrolone decanoate
D006730 - Hormones, Hormone Substitutes, and Hormone Antagonists > D006728 - Hormones > D045930 - Anabolic Agents C147908 - Hormone Therapy Agent > C548 - Therapeutic Hormone > C1636 - Therapeutic Steroid Hormone D050071 - Bone Density Conservation Agents
thiamylal
D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D006993 - Hypnotics and Sedatives D002491 - Central Nervous System Agents > D002492 - Central Nervous System Depressants > D000777 - Anesthetics C78272 - Agent Affecting Nervous System > C29756 - Sedative and Hypnotic > C67084 - Barbiturate D018377 - Neurotransmitter Agents > D018682 - GABA Agents > D018757 - GABA Modulators C78272 - Agent Affecting Nervous System > C245 - Anesthetic Agent
R-1,2-PROPANEDIOL
(R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1]. (R)-(-)-1,2-Propanediol is a (R)-enantiomer of 1,2-Propanediol that produced from glucose in Escherichia coli expressing NADH-linked glycerol dehydrogenase genes[1].
Diadenosine tetraphosphate
A diadenosyl tetraphosphate compound having the two 5-adenosyl residues attached at the P(1)- and P(4)-positions. D006401 - Hematologic Agents > D010975 - Platelet Aggregation Inhibitors
decanoyl-CoA
A medium-chain fatty acyl-CoA that results from the formal condensation of the thiol group of coenzyme A with the carboxy group of decanoic acid.
Glyceric acid 1,3-biphosphate
1,3-Bisphosphoglycerate. CAS Common Chemistry. CAS, a division of the American Chemical Society, n.d. https://commonchemistry.cas.org/detail?cas_rn=1981-49-3 (retrieved 2024-10-16) (CAS RN: 1981-49-3). Licensed under the Attribution-Noncommercial 4.0 International License (CC BY-NC 4.0).
