L-Mimosine - CAS 500-44-7
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Not Intended for Therapeutic Use. For research use only.
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L-Mimosine is a non-protein amino acid, and acts as an iron chelator.It is a toxic non-protein free amino acid otherwise chemically similar to tyrosine.
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1.Bone substitute materials supplemented with prolyl hydroxylase inhibitors decrease osteoclastogenesis in vitro.
Vinzenz P1,2, Schröckmair S1,2, Gruber R1,2,3, Agis H2,4. J Biomed Mater Res B Appl Biomater. 2015 Aug;103(6):1198-203. doi: 10.1002/jbm.b.33295. Epub 2014 Oct 14.
BACKGROUND AND OBJECTIVE: Inhibition of prolyl hydroxylases stimulates bone regeneration. Consequently, bone substitute materials were developed that release prolyl hydroxylase inhibitors. However, the impact of prolyl hydroxylase inhibitors released from these carriers on osteoclastogenesis is not clear. We therefore assessed the effect of bone substitute materials that release prolyl hydroxylase inhibitors on osteoclastogenesis.
2.Effects of mimosine on Wolbachia in mosquito cells: cell cycle suppression reduces bacterial abundance.
Fallon AM1. In Vitro Cell Dev Biol Anim. 2015 Oct;51(9):958-63. doi: 10.1007/s11626-015-9918-7. Epub 2015 May 28.
The plant allelochemical L-mimosine (β-[N-(3-hydroxy-4-pyridone)]-α-aminopropionic acid; leucenol) resembles the nonessential amino acid, tyrosine. Because the obligate intracellular alphaproteobacterium, Wolbachia pipientis, metabolizes amino acids derived from host cells, the effects of mimosine on infected and uninfected mosquito cells were investigated. The EC50 for mimosine was 6-7 μM with Aedes albopictus C7-10 and C/wStr cell lines, and was not influenced by infection status. Mosquito cells responded to concentrations of mimosine substantially lower than those used to synchronize the mammalian cell cycle; at concentrations of 30-35 μM, mimosine reversibly arrested the mosquito cell cycle at the G1/S boundary and inhibited growth of Wolbachia strain wStr. Although lower concentrations of mimosine slightly increased wStr abundance, concentrations that suppressed the cell cycle reduced Wolbachia levels.
3.Release kinetics of prolyl hydroxylase inhibitors from collagen barrier membranes.
Hamid O1, Pensch M1, Agis H2. J Biomater Appl. 2015 Mar;29(8):1059-67. doi: 10.1177/0885328214556158. Epub 2014 Oct 17.
Collagen barrier membranes are used in guided tissue regeneration to support healing. This strategy, however, relies on the healing capacity of the tissue. Pharmacological inhibitors of prolyl hydroxylases can support regeneration by enhancing angiogenesis and are therefore a promising tool for periodontology. Here we evaluate the release kinetics of the prolyl hydroxylase inhibitors dimethyloxalylglycine and L-mimosine from collagen barrier membranes. Dimethyloxalylglycine and L-mimosine were lyophilized onto the collagen barrier membranes. The morphology of the collagen barrier membranes was analysed using scanning electron microscopy. The release of prolyl hydroxylase inhibitors was assessed by colorimetric and spectroscopic methods. Their ability to induce a cellular response was assessed in bioassays with gingival and periodontal ligament fibroblasts based on vascular endothelial growth factor production, proliferation, and metabolic activity of the cells.
4.Effects of Prolyl Hydroxylase Inhibitor L-mimosine on Dental Pulp in the Presence of Advanced Glycation End Products.
Müller HD1, Cvikl B2, Janjić K3, Nürnberger S4, Moritz A3, Gruber R5, Agis H6. J Endod. 2015 Nov;41(11):1852-61. doi: 10.1016/j.joen.2015.08.002. Epub 2015 Sep 26.
INTRODUCTION: Proangiogenic prolyl hydroxylase (PHD) inhibitors represent a novel approach to stimulate tissue regeneration. Diabetes mellitus involves the accumulation of advanced glycation end products (AGEs). Here we evaluated the impact of AGEs on the response of human pulp tissue to the PHD inhibitor L-mimosine (L-MIM) in monolayer cultures of dental pulp-derived cells (DPCs) and tooth slice organ cultures.
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CAS 500-44-7 L-Mimosine

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