Parsanathan, Rajesh et al. published new experimental results with the assistance of cas: 329-89-5

6-Aminonicotinamide (cas:329-89-5)Name: 6-Aminonicotinamide induces apoptosis in tumor cells. It is clinically used in disseminated neoplastic disease. It also acts as 6-phosphogluconate dehydrogenase inhibitor. It aids in the treatment of psoriasis. It is used as cancer chemotherapeutic drug in animals.

Name: 6-Aminonicotinamide《L-Cysteine in vitro can restore cellular glutathione and inhibits the expression of cell adhesion molecules in G6PD-deficient monocytes》 was published in 2018. The authors were Parsanathan, Rajesh;Jain, Sushil K., and the article was included in《Amino Acids》. The author mentioned the following in the article:

L-Cysteine is a precursor of glutathione (GSH), a potent physiol. antioxidant. Excess glucose-6-phosphate dehydrogenase (G6PD) deficiency in African Americans and low levels of L-cysteine diet in Hispanics can contributes to GSH deficiency and oxidative stress. Oxidative stress and monocyte adhesion was considered to be an initial event in the progression of vascular dysfunction and atherosclerosis. However, no previous study has investigated the contribution of GSH/G6PD deficiency to the expression of monocyte adhesion mols. Using human U937 monocytes, this study examined the effect of GSH/G6PD deficiency and L-cysteine supplementation on monocyte adhesion mols. G6PD/GSH deficiency induced by either siRNA or inhibitors (6AN/BSO, resp.) significantly (p < 0.005) increased the levels of cell adhesion mols. (ICAM-1, VCAM-1, SELL, ITGB1 and 2); NADPH oxidase (NOX), reactive oxygen species (ROS) and MCP-1 were upregulated, and decreases in levels of GSH, and nitric oxide were observed The expression of ICAM-1 and VCAM-1 mRNA levels increased in high glucose, MCP-1 or TNF-α-treated G6PD-deficient compared to G6PD-normal cells. L-Cysteine treatment significantly (p < 0.005) increased G6PD activity and levels of GSH, and decreased NOX, ROS, and adhesion mols. Thus, GSH/G6PD deficiency increases susceptibility to monocyte adhesion processes, whereas L-cysteine supplementation can restore cellular GSH/G6PD and attenuates NOX activity and expression of cell adhesion mols. The experimental procedure involved many compounds, such as 6-Aminonicotinamide (cas: 329-89-5) .

6-Aminonicotinamide (cas:329-89-5)Name: 6-Aminonicotinamide induces apoptosis in tumor cells. It is clinically used in disseminated neoplastic disease. It also acts as 6-phosphogluconate dehydrogenase inhibitor. It aids in the treatment of psoriasis. It is used as cancer chemotherapeutic drug in animals.

Reference:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics