Magnesium Oxaloacetate is an inhibitor of the amebicidal activity of activated murine macrophages, helping the parasite to survive within the mouse large intestine and increasing the survival of C. elegans exposed to H2O2.
Piperazine (2HCl) is gamma-aminobutyric acid (GABA) agonists and its major effects appear to be on the central nervous system. Piperazine was the anthelmintic with the greatest number of reports of toxicoses and suspected toxicoses in cats. Piperazine neurotoxicity in cats and dogs usually was manifested by muscle tremors, ataxia, and/or behavioral disturbances within 24 hours after estimated daily dose(s) between 20 and 110 mg/kg[1]. For di-substituted derivatives, ciprofloxacin was selected and hybrids were synthesized via substitution at piperazinyl-N4. The reaction of piperazinyl-NH of ciprofloxacin with selected drugs resulted in pronounced growth inhibition of standard as well as resistant bacterial strains[2]. The parent piperazine 6 was found to exhibit a reasonable activity toward the HeLa and MDA MB 231 tumor cell lines (IC50= 9.2 and 8.4 μΜ, respectively)[3]. Piperazine adipate (10 mM) causes mortality of A. galli and H. gallinae after a maximum of 30 min exposure, inhibits malate oxidation by 78%, and inhibits aldolase activity in both parasites. Piperazine adipate (10 mM) also inhibits cholinesterase activity by 96% in Ascaridia galli (A. galli) and 93% in Heterakis gallinae (H. gallinae). Piperazine adipate inhibits oxaloacetate reduction by 26% and 55% in A. galli and H. gallinae, resepctively[4].
Aspulvinone H is a natural inhibitor of glutamic oxaloacetate transaminase 1 (GOT1), suppressing glutamine metabolism, making PDAC cells sensitive to oxidative stress and inhibiting cell proliferation, exhibiting potent in vivo antitumor activity in an SW1990-cell-induced xenograft model.
Clofibric acid-d4 is intended for use as an internal standard for the quantification of clofibric acid by GC- or LC-MS. Clofibric acid is a peroxisome proliferator-activated receptor α (PPARα) agonist (EC50 = 50 µM in a transactivation assay) and the active metabolite of clofibrate. It is formed from clofibrate by tissue and serum esterases. Dietary administration of clofibric acid (0.067-0.22%) reduces serum cholesterol, phospholipid, and triglyceride levels in rats. It decreases glutamate oxaloacetate transaminase (GOT) levels and increases glutamate pyruvate transaminase (GPT) and lactate dehydrogenase (LDH) levels, markers of xenobiotic stress, in the plasma of carp (C. carpio) when administered in tank water at a concentration of 10 µg/L. Clofibric acid has been found in wastewater effluent.
(-)-Hydroxycitric acid (HCA) can inhibit fat synthesis and reduces food intake, the primary mechanism of action of HCA appears to be related to its ability to act as a competitive inhibitor of the enzyme ATP-citrate lyase, which catalyzes the conversion of citrate and coenzyme A to oxaloacetate and acetyl coenzyme A (acetyl-CoA), primary building blocks of fatty acid and cholesterol synthesis.