Agmatine
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IUPAC name
1-(4-Aminobutyl)guanidine
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| Identifiers | |
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3D model (Jmol)
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| 3DMet | B00052 |
| ChEBI | |
| ChemSpider | |
| ECHA InfoCard | 100.005.626 |
| EC Number | 206-187-7 |
| KEGG | |
| MeSH | Agmatine |
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PubChem CID
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| Properties | |
| C5H14N4 | |
| Molar mass | 130.20 g·mol−1 |
| Density | 1.2 g/ml |
| Melting point | 102 °C (216 °F; 375 K) |
| Boiling point | 281 °C (538 °F; 554 K) |
| high | |
| log P | −1.423 |
| Basicity (pKb) | 0.52 |
| Hazards | |
| Flash point | 95.8 °C (204.4 °F; 368.9 K) |
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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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 (what is   ?) |
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| Infobox references | |
Agmatine, also known as (4-aminobutyl)guanidine, is an aminoguanidine that was discovered in 1910 by Albrecht Kossel. Agmatine is a chemical substance which is naturally created from the chemical arginine. Agmatine has been shown to exert modulatory action at multiple molecular targets, notably: neurotransmitter systems, ion channels, nitric oxide (NO) synthesis and polyamine metabolism and this provides bases for further research into potential applications.
Agmatine was discovered in 1910 by Albrecht Kossel. It took more than 100 years to find the exact functions of the chemical. The term stems from A- (for amino-) + g- (from guanidine) + -ma- (from ptomaine) + -in (German)/-ine (English) suffix with insertion of -t- apparently for euphony. A year after its discovery, it was found that Agmatine could increase blood flow in rabbits; however, the physiological relevance of these findings were questioned given the high concentrations (high μM range) required. In the 1920s, researchers in the diabetes clinic of Oskar Minkowski have shown that agmatine can exert mild hypoglycemic effects. In 1994, the discovery of endogenous agmatine synthesis in mammals occurred.
Agmatine biosynthesis by arginine decarboxylation is well-positioned to compete with the principal arginine-dependent pathways, namely: nitrogen metabolism (urea cycle), and polyamine and nitric oxide (NO) synthesis (see illustration 'Agmatine Metabolic Pathways'). Agmatine degradation occurs mainly by hydrolysis, catalyzed by agmatinase into urea and putrescine, the diamine precursor of polyamine biosynthesis. An alternative pathway, mainly in peripheral tissues, is by diamine oxidase-catalyzed oxidation into agmatine-aldehyde, which is in turn converted by aldehyde dehydrogenase into guanidinobutyrate and secreted by the kidneys.
Agmatine was found to exert modulatory actions directly and indirectly at multiple key molecular targets underlying cellular control mechanisms of cardinal importance in health and disease. It is considered capable of exerting its modulatory actions simultaneously at multiple targets. The following outline indicates the categories of control mechanisms and identifies their molecular targets:
Agmatine sulfate injection can increase food intake with carbohydrate preference in satiated, but not in hungry rats and this effect may be mediated by neuropeptide. However, supplementation in rat drinking water results in reductions in water intake and body weight gain. Also force feeding with agmatine leads to a reduction in body weight gain during rat development. Also, many fermented foods contain agmatine.
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