ifenprodil

Ifenprodil (RC61-91) is an inhibitor of the NMDA receptor, specifically of GluN1 (glycine-binding NMDA receptor subunit 1) and GluN2B (glutamate-binding NMDA receptor subunit 2) subunits. Additionally, Ifenprodil inhibits GIRK channels and interacts with alpha1 adrenergic, serotonin, and sigma receptors.

Ifenprodil is a selective NMDA receptor (glutamate) antagonist.

Ifenprodil glucuronide, a derivative of Ifenprodil, is a vasodilator and an inhibitor of platelet aggregation. In contrast to Ifenprodil, Ifenprodil glucuronide does not affect platelet aggregation nor arterial contraction.

σ receptor agonist and NR2B subunit-selective NMDA receptor antagonist

Ifenprodil hemitartrate is a NMDA receptor antagonist, acting at the polyamine site. Also anα-adrenergic vasodilator.σ2ligand displaying about 3-fold selectivity overσ1sites.

Arcaine sulfate is a NMDA antagonist.

Sepimostat exhibits neuroprotective activity via NR2B N-methyl-D-aspartate receptor antagonism at the Ifenprodil-binding site of the NR2B subunit. Sepimostat dimethanesulfonate inhibits the Ifenprodil binding with a Ki value of 27.7 μM.

WMS-1405 is a derivative of ifenprodil. As a potent NR2B-selective NMDA receptor antagonist, it exhibits a Ki value of 5.4 nM. Synthesized through a central building block approach, WMS-1405 displays high NR2B affinity due to the specific distance between its basic nitrogen atom and phenyl residue. WMS-1405 has the potential to serve as an NMDA antagonist for excitotoxicity treatment.

Sepimostat dimethanesulfonate (FUT-187), a chemical compound, demonstrates neuroprotective properties by antagonizing NR2B N-methyl-D-aspartate receptors at the NR2B subunit's Ifenprodil-binding site. This compound effectively inhibits Ifenprodil binding, exhibiting a Ki value of 27.7 μM[1].

Ro 04-5595 is a selective antagonist of NMDA receptors NR2B subunits. Ro 04-5595 had an EC 50 of 186 ± 32 nmol L. Ro 04-5595 was predicted to bind the EVT-101 binding site, not the ifenprodil-binding site. Specific binding, defined with a new NR2B-specific antagonist Ro 04-5595 at 10 microM was fully inhibited by several compounds with the following rank order of affinities--Ro 25-6981 > CP-101,606 > Ro 04-5595 = ifenprodil >> eliprodil > haloperidol > spermine > spermidine > MgCl2 > CaCl2--and partially inhibited by competitive glutamate recognition site antagonists. Complementary high-resolution autoradiographic images using [3H]Ro04-5595 demonstrated strong binding in NR2B receptor-rich regions and low binding in cerebellum where NR2B concentration is low.

EVT-101 is a GluN2B antagonist, binding at the same GluN1 GluN2B dimer interface as ifenprodil but adopting a remarkably different binding mode involving a distinct subcavity and receptor interactions.