Investigational Drug Details
| Drug ID: | D401 |
| Drug Name: | N,N-dimethylarginine |
| Synonyms: | |
| Type: | small molecule |
| DrugBank ID: | DB01686 |
| DrugBank Description: | Asymmetric dimethylarginine (ADMA) is a naturally occurring chemical found in blood plasma. It is a metabolic by-product of continual protein modification processes in the cytoplasm of all human cells which is closely related to L-arginine, a conditionally-essential amino acid. ADMA interferes with L-arginine in the production of nitric oxide, a key chemical to endothelial and hence cardiovascular health. |
| PubChem ID: | 123831 |
| CasNo: | 30315-93-6 |
| Repositioning for NAFLD: | Yes |
| SMILES: | N[C@@H](CCC\N=C(/N)N(C)C)C(O)=O |
| Structure: |
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| InChiKey: | YDGMGEXADBMOMJ-LURJTMIESA-N |
| Molecular Weight: | 202.2541 |
| DrugBank Targets: | Nitric oxide synthase, inducible; Nitric oxide synthase, endothelial |
| DrugBank MoA: | |
| DrugBank Pharmacology: | Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, is formed by methylation of arginine residues in proteins and released after proteolysis. In this reaction, S-adenosylmethionine is methyldonor and S-adenosylhomocysteine the demethylated product. ADMA and homocysteine are thus biochemically linked. Both plasma homocysteine and ADMA concentrations are increased in patients with renal dysfunction, probably as a result of an impairment in their metabolic, but not urinary, clearance. Hyperhomocysteinemia has been associated with an increased risk of cardiovascular disease in end-stage renal disease, especially in patients without malnutrition and inflammation. Also, plasma ADMA levels have been associated with cardiovascular disease in renal failure patients. Both homocysteine and ADMA are thought to mediate their adverse vascular effects by impairing endothelial, nitric oxide-dependent function resulting in decreased vasodilatation, increased smooth muscle cell proliferation, platelet dysfunction and increased monocyte adhesion. |
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