2-Aminoimidazole

2-Aminoimidazole is a potent antibiofilm agent that can be used as an adjuvant to antimicrobial. 2-aminoimidazoles disrupts the ability of bacteria to protect themselves by inhibiting biofilm formation and genetically-encoded antibiotic resistance traits. 2-Aminoimidazole is also a weak noncompetitive inhibitor of human arginase I with a K_i of 3.6 mM^[1][2][3]. IC50 & Target:bacteria^[1]
Ki: 3.6 mM (human arginase I)^[3] In Vitro:The 2-aminoimidazole analogs 2AI-1 (100 µM, 30 min) is able to cross both A. baumannii cell membranes and enter the cytoplasm, confirmed by confocal microscopy. ^[1].
The 2-aminoimidazole analogs 2AI-1 can specificly target to BfmR, a response regulator that is the master controller of biofilm formation, dertermined by pull-down assays and binding assays. ^[1].
The 2-aminoimidazole analogs imi-AAC-5 (50 µM - 100 µM) displays a significant biofilm reduction in most biofilm models, as dertermined by crystal violet staining^[2].
The 2-aminoimidazole analogs imi-AAC-5 (25 µM - 50 µM) displays a low planktonic inhibition in most biofilm models. imi-AAC-5 doesn’ affect planktonic growth in biofilm models where biofilm inhibition is observed at 50 µM and doesn’ affect planktonic growth in any of the biofilm models at 25 µM^[2].
The 2-aminoimidazole analogs imi-AAC-5 (25 µM - 50 µM) shows a reduction of the number of metabolically active cells in 3 out of 6 biofilm models each at 50 µM and only 1 out of 6 reduction at 25 µM, based on the resazurin viability assay^[2].
The 2-aminoimidazole analogs imi-AAC-5 (25 µM - 50 µM) shows antagonistic effects in 2 out of 6 models at 50 µM combined with 50 µM tannic acid, while shows antagonistic effects in 1 out of 6 model at 25 µM combined with 25 µM tannic acid^[2].
2-Aminoimidazole is a weak noncompetitive inhibitor of human arginase I with K_i = 3.6 mM. In contrast, its analogs A1P is a competitive inhibitor with K_i = 4 μM, but A1P has low micromolar affinity with K_d = 2 μM^[3].
In Vivo:The 2-aminoimidazole analogs A1P (80 μg/g, Nebulization, Once in total) can reduce airways hyperresponsiveness to methacholine in an acute (3-week) ovalbumin (OVA)-sensitization and -challenge murine model^[3].