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- Satoh, A. et al. (2009) Bioorg. Med. Chem. Lett. 19, 5464.
- Yamasaki, T. et al. (2012) Eur. J. Nucl. Med. Mol. Imaging 39, 632.
- Alomone Labs FITM inhibits mGluR1-mediated Ca2+ mobilization in U2OS cells.Dose response of FITM (#F-200) normalized inhibition of human mGluR1-mediated, L-Glutamate-evoked Ca2+ mobilization. Cells were loaded with a calcium-sensitive dye, incubated with a range of FITM concentrations, and stimulated with 5 µM L-Glutamate (EC80). Changes in intracellular Ca2+ following stimulation were detected as changes in maximum relative fluorescence (RLU) using FLIPRTETRA™. IC50 was determined at 1.71 nM.
- Xie, L. et al. (2014) Int. J. Cancer 135, 1852.
- Leung, K. (2004-2013) Molecular Imaging and Contrast Agent Database (MICAD) National Center for Biotechnology Information (US).
- Zheng, G.Z. et al. (2005) J. Med. Chem. 48, 7374.
FITM is a potent and selective antagonist of mGluR1, displaying an IC50 value of 5.1 nM1 with little inhibition of mGluR2, mGluR5, and mGluR81,2.
Glutamate is the most abundant excitatory neurotransmitter in the central nervous system and it modulates activity of many types of synapses by activating in part metabotropic glutamate receptors (mGluRs), members of G-protein coupled receptors (GPCRs). These receptors are divided into three groups based on sequence homology with a total of eight subtypes, mGluR1 to mGluR8.
mGluR1 plays an important role in the central sensitization of pain and in a variety of functions with potential implications in neurological and psychiatric disorders2,3.
FITM (#F-200) is a highly pure, synthetic, and biologically active compound.
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