Aminoguanidinium Bicarbonate

• CAT Number: R019158
• CAS Number: 2582-30-1
• Molecular Formula: C2H8N4O3
• Molecular Weight: 136.11
• Purity: ≥95%
• Storage: Store at +4 °C
• Related CAS: 79-17-4
• IUPAC Name: 2-aminoguanidine;carbonic acid
• InChI: InChI=1S/CH6N4.CH2O3/c2-1(3)5-4;2-1(3)4/h4H2,(H4,2,3,5);(H2,2,3,4)
• InChIKey: OTXHZHQQWQTQMW-UHFFFAOYSA-N
• SMILES: C(=NN)(N)N.C(=O)(O)O

Aminoguanidinium bicarbonate（Cat No.:R019158）, is a chemical compound with applications in both biological and chemical fields. This organic salt contains aminoguanidine, a compound often utilized for its potential role in pharmaceutical research and drug development due to its ability to react with carbonyl compounds in a process known as the “Aminoguanidine Reaction.” This reaction has relevance in the study of advanced glycation end products (AGEs), which are implicated in various health conditions. Aminoguanidinium bicarbonate’s unique properties make it a valuable tool in scientific investigations aimed at understanding biochemical processes and developing therapeutic interventions.

Reference

1. Chromosoma. 1982;84(4):571-83. doi: 10.1007/BF00292856.Spermine and aminoguanidine protect cells from chromosome aberrations induced by adenovirus during the G2 phase of the cell cycle.Bellett AJ, Waldron-Stevens LK, Braithwaite AW, Cheetham BF.

 

Adenovirus uncouples DNA replication from polyamine biosynthesis and causes chromosome aberrations in rodent cells. Addition of polyamines protected infected cells from this chromosome damage. Spermine was the only individual polyamine which protected. The diamine oxidase inhibitor aminoguanidine also protected. Neither compound detectably reduced synthesis of viral early proteins. The protective effects of spermine and aminoguanidine were not additive. Maximal protection was obtained when the compounds were added 4.5 h before mitosis, but significant protection was observed up to 1.25 h before mitosis. This suggests that the compounds act in G2. In vitro, spermine bound strongly to DNA and protected it from mild endonuclease attack, but aminoguanidine did neither. We propose that viral infection causes a deficiency in spermine during a critical period G2, possibly accompanied by an increase in endonuclease activity. The resulting chromosome damage can be prevented by adding exogenous spermine, or by inhibiting the oxidative degradation of endogenous spermine.


2.Chem Biol Interact. 1978 Jul;22(1):91-8. doi: 10.1016/0009-2797(78)90152-7.Reversal by aminoguanidine of the inhibition of proliferation of human fibroblasts by spermidine and spermine.Gahl WA, Pitot HC.

 

The inhibitory effect of the polyamines, spermidine and spermine, on the proliferation of human fibroblasts in culture was found to be reversed by the addition of aminoguanidine (AM), a specific and highly effective inhibitor of diamine oxidase (DAO) present in fetal calf serum (FCS). Aminoguanidine itself in concentration as high as 10(-3) M exhibited no effect upon cell proliferation nor did putrescine at similar concentrations. However, at higher concentrations of putrescine, cell proliferation was inhibited and this inhibition was unaffected by the addition of mM concentrations of AM. These studies support earlier hypotheses on the mechanisms of the toxic effects of polyamines on cell proliferation and establish further that the diamine oxidase-catalyzed metabolism of spermine and spermidine is necessary for their toxic effects in cell culture.