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| Names | |
|---|---|
| IUPAC name N-[4-({[(6Ξ)-2-Amino-4-oxo-1,4,5,6,7,8-hexahydropteridin-6-yl]methyl}amino)benzoyl]-L-glutamic acid | |
| Systematic IUPAC name (2S)-2-[4-({[(6Ξ)-2-Amino-4-oxo-1,4,5,6,7,8-hexahydropteridin-6-yl]methyl}amino)benzamido]pentanedioic acid | |
| Identifiers | |
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3D model (JSmol) | |
| 101189 | |
| ChEBI | |
| ChemSpider |
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| DrugBank |
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| KEGG |
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| MeSH | 5,6,7,8-tetrahydrofolic+acid |
| UNII | |
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| Properties | |
| C19H23N7O6 | |
| Molar mass | 445.43 g/mol |
| Melting point | 250 °C (482 °F; 523 K) |
| 0.27 g/L | |
| Acidity (pKa) | 3.51 |
Except where otherwise noted, data are given for materials in theirstandard state (at 25 °C [77 °F], 100 kPa). | |
Tetrahydrofolic acid (THFA), ortetrahydrofolate, is afolic acid derivative.
In humans, tetrahydrofolic acid is produced fromdihydrofolic acid bydihydrofolate reductase. This reaction is inhibited bymethotrexate.[1] It is converted into5,10-methylenetetrahydrofolate byserine hydroxymethyltransferase.
Many bacteria produce tetrahydrofolic acid viadihydropteroate.[citation needed] Humans lack the enzymes to do this, thus molecules that shut down these enzymes are effective antibacterial compounds. For example,sulfonamide antibiotics competitively binds the active site ofdihydropteroate synthetase, ecluding the binding of the dihydropteroate precuror,4-aminobenzoic acid (PABA).
Tetrahydrofolic acid is acofactor in many reactions, especially in the synthesis (or anabolism) ofamino acids andnucleic acids. In addition, it serves as a carrier molecule for single-carbon moieties, that is, groups containing one carbon atom e.g.methyl,methylene,methenyl,formyl, or formimino. When combined with one such single-carbon moiety as in10-formyltetrahydrofolate, it acts as a donor of a group with one carbon atom. Tetrahydrofolate gets this extra carbon atom by sequesteringformaldehyde produced in other processes. These single-carbon moieties are important in the formation of precursors for DNA synthesis. A shortage in tetrahydrofolic acid (FH4) can causemegaloblastic anemia.[2][3][4]
Methotrexate acts on dihydrofolate reductase, likepyrimethamine ortrimethoprim, as an inhibitor and thus reduces the amount of tetrahydrofolate made. This may result in megaloblastic anemia.
Tetrahydrofolic acid is involved in the conversion offormiminoglutamic acid toglutamic acid; this may reduce the amount ofhistidine available for decarboxylation and protein synthesis, and hence the urinary histamine and formiminoglutamic acid may be decreased.[5]
