(S)-3-Hydroxyphenylglycine

(S)-3-Hydroxyphenylglycine ((S)-3HPG) (98-1000 μM; 45 min) acts as a moderate agonist with an EC₅₀ of 98 μM at metabotropic glutamate receptors linked to phosphoinositide hydrolysis in postnatal days 6-8 rat pup cerebral cortical slices, and does not antagonize ACPD-stimulated phosphoinositide hydrolysis in this system^[1].
(S)-3-Hydroxyphenylglycine (1 mM; 20 min) acts as a weak agonist for mGluR1-expressing CHO cells with an EC₅₀ of 1 mM^[2].
(S)-3-Hydroxyphenylglycine (0.1-1 mM) acts as a weak partial antagonist for mGluR1-expressing CHO cells, inhibiting L-glutamate-induced IP formation by 15% at 0.1 mM and 25% at 1 mM^[2].
(S)-3-Hydroxyphenylglycine (10-200 μM; 5-7 min) reversibly attenuates NMDA receptor-gated whole-cell currents in primary cultured mouse cortical neurons via activation of mGluR1/5, through a G protein-dependent mechanism independent of intracellular Ca²⁺, cAMP, or protein kinase signaling^[3].
(S)-3-Hydroxyphenylglycine (300 μM) attenuates NMDA-induced intracellular Ca²⁺ accumulation in primary cultured mouse cortical neurons^[3].
(S)-3-Hydroxyphenylglycine (20-100 μM; 2-5 min) suppresses NMDA receptor single-channel activity in excised outside-out membrane patches from primary cultured mouse cortical neurons via a G protein-dependent, mGluR1/5-mediated mechanism that does not alter channel conductance or open time^[3].

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