DFMTI

DFMTI abolishes the Tobacco Mosaic Virus (TMV) resistance phenotype of Nicotiana benthamiana overexpressing NbAS-B by inhibiting glutamate production required for the activation of the Salicylic acid (HY-B0167) pathway^[1].
DFMTI (MK5435) (incubated for 5 min) potently inhibits human mGluR1a-mediated intracellular Ca²⁺ mobilization in CHO cells, with an IC₅₀ of 4.3 nM, and exhibits low activity against human mGluR5^[2].
DFMTI (10 μM) displaces specific [¹⁸F]MK-1312 binding in rhesus monkey and human brain slices, and effectively determines the non-displaceable binding of [¹⁸F]MK-1312 in rhesus monkey and human cerebellar homogenates, confirming that it interacts specifically with mGluR1 in these tissues^[2].
DFMTI (compound 3) potently inhibits glutamate-induced calcium mobilization in TREx293 cells, with IC₅₀ values of 8 nM, 31 nM, 21 nM, and 14 nM in cells expressing rmGlu1 WT, hmGlu1 WT, rmGlu1 V757L, and hmGlu1 L757V, respectively; the potency differs by approximately 4-fold between human and rat wild-type receptors^[3].
DFMTI acts as a non-competitive allosteric antagonist against rmGlu1 WT, rmGlu1 V757L, hmGlu1 WT, and hmGlu1 L757V, with subtle variations in its potency depending on the amino acid at position 757^[3].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.