| Stereochemistry | ACHIRAL |
| Molecular Formula | C7H9N2O.I |
| Molecular Weight | 264.0636 |
| Optical Activity | NONE |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Charge | 0 |
SHOW SMILES / InChI
SMILES
[I-].C[N+]1=CC(=CC=C1)C(N)=O
InChI
InChIKey=IWEIZMCTGMHCRE-UHFFFAOYSA-N
InChI=1S/C7H8N2O.HI/c1-9-4-2-3-6(5-9)7(8)10;/h2-5H,1H3,(H-,8,10);1H
| Molecular Formula | HI |
| Molecular Weight | 127.91241 |
| Charge | 0 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
| Molecular Formula | C7H9N2O |
| Molecular Weight | 137.1592 |
| Charge | 1 |
| Count |
MOL RATIO
1 MOL RATIO (average) |
| Stereochemistry | ACHIRAL |
| Additional Stereochemistry | No |
| Defined Stereocenters | 0 / 0 |
| E/Z Centers | 0 |
| Optical Activity | NONE |
Trigonellamide (1-Methylnicotinamide) is a metabolite of nicotinamide and is produced primarily in the liver by nicotinamide N-methyltransferase. Trigonellamide may be an endogenous activator of prostacyclin (PGI2) production and thus may regulate thrombotic as well as inflammatory processes in the cardiovascular system. The mechanisms of action of Trigonellamide involve the activation of PGI2 release driven by cyclooxygenase 2 (COX-2). PGI2 releasing capacity of 1- Trigonellamide was shown to afford not only anti-thrombotic but also fibrinolytic, anti-inflammatory and gastroprotective effects. Interestingly, Trigonellamide did not directly either affect the activity of leucocytes or release PGI2 in the perfused rat hindquarters model. Still, Trigonellamide, due to its PGI2 releasing capacity, might serve as a hepatoprotective agent that protects against Concanavalin-A induced liver injury through the downregulation of interleukin-4 (IL-4) and tumor necrosis factor-α signalization (TNF-α). In addition to its anti-platelet, anti-thrombotic and anti-inflammatory activities, 1-MNA has also been shown to restore endothelial function in diabetic hyperglycemic rats, as well as to improve endothelial function in humans. PGI2 displays anti-metastatic activity, and the PGI2 releasing activity of Trigonellamide, the potential application of exogenous Trigonellamide to prevent metastatic cancer.
CNS Activity
Approval Year
Sourcing
PubMed
Patents
Sample Use Guides
30 mg 1-MNA (Trigonellamide ) or 90 mg 1-MNA (Trigonellamide ) three times daily for twelve weeks.
Route of Administration:
Oral
Primary cultures of granule neurons were prepared from cerebella of 7-day-old rats. The cells were used for experiments on the 6th to 8lh day in vitro (DIV). To verify the intrinsic neurotoxicity of MNA (Trigonellamide), on DIV 6 or 7 these substance was added directly to the cell growth medium and culturing was continued for 24 h under standard conditions. The acute neurotoxicity of D,L-homocysteine was induced at DIV 7 by replacing the BME growth medium with Locke 25 buffer containing aliquots of freshly prepared D,L-homocysteine alone or with MNA as required. After 30 min, the Locke medium was replaced with the original growth medium and the cultures continued for 24 h. In other experiments, MNA were present in the growth medium for 24 h before and after acute exposure to Hey. To examine sub-acute Hey neurotoxicity, this amino acid was applied at different concentrations directly to cultures for 24 h. In these experiments NAM or MNA, if present, were added 24 h before Hey.
