Aminooxyacetic acid (hemihydrochloride)

Aminooxyacetic acid (Carboxymethoxylamine) hemihydrochloride is a malate-aspartate shuttle (MAS) inhibitor which also inhibits the GABA degradating enzyme GABA-T. IC50 & Target: MAS^[1], GABA-T^[2] In Vitro: Aminooxyacetic acid hemihydrochloride (AOAA) dose-dependently decreases the survival of C6 glioma cells. Aminooxyacetic acid hemihydrochloride treatment produces a significant increase in the percentage of the cells arrested in the stage of G0/G1, as well as a significant decrease in the percentage of the cells at S phase and G2/M phase. Aminooxyacetic acid hemihydrochloride treatment leads to an obvious decrease in the number of the cells in the phase of cell division. Aminooxyacetic acid hemihydrochloride significantly increases the percentage of the cells in both early-stage apoptosis and necrosis. Treatment of the cells with 1 mM or 5 mM Aminooxyacetic acid hemihydrochloride leads to decreased levels of aging of the cells^[1]. Glutamine-dependent cell lines show greater inhibition of cell growth by Aminooxyacetic acid hemihydrochloride (AOA) compare with cells that are less glutamine dependent^[3]. In Vivo: The accumulation of GABA in cerebellum and whole brain is initially very rapid, being significantly increased already 5 min after the injection of Aminooxyacetic acid hemihydrochloride (AOAA). The rapid initial accumulation becomes gradually slower and maximal levels (400 to 600 % of the control levels) are reached 2 to 6 h after Aminooxyacetic acid hemihydrochloride. Still 24 h after Aminooxyacetic acid hemihydrochloride the GABA levels are elevated by about 250%. From 2 to 6 h after Aminooxyacetic acid hemihydrochloride the convulsions are completely blocked. Twenty four hours after Aminooxyacetic acid hemihydrochloride the convulsions are almost identical to the controls^[2].