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BZAD-01 is a potent, selective and orally active inhibitor of NMDA NR2B subunit, with a Ki of 72 nM. BZAD-01 can improve postural asymmetry as well as Apomorphine-induced rotation .
Sepimostat (FUT-187 free base) exhibits neuroprotective activity via NR2B N-methyl-D-aspartate receptor antagonism at the Ifenprodil-binding site of the NR2B subunit. Sepimostat inhibits the Ifenprodil binding with a Ki value of 27.7 µM .
Tat-HA-NR2B9 contains a fragment of the cellmembrane transduction domain of HIV-1 Tat, a influenza virus hemagglutinin (HA) epitope-tag, and the C-terminal 9 amino acids of NR2B (NR2B9c). Tat-HA-NR2B9 reduces infarct size and improves neurological functions in ischemia-induced cerebral injury in the rats
Onfasprodil is negative allosteric modulator of NR2B. Onfasprodil in combination with GABA receptor regulator has the potential for the research of Alzheimer's disease (extracted from patent CN111481543A) .
Sepimostat dimethanesulfonate (FUT-187) 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 .
Ro 04-5595 is a selective antagonist with specific activity against the NR2B subunit of the NMDA receptor. Ro 04-5595 exhibits favorable pharmacokinetic properties in in vitro and in vivo studies, with rapid uptake and clearance. Ro 04-5595 exhibits strong binding in NR2B receptor-enriched regions and low binding in the cerebellum. Ro 04-5595 is able to effectively inhibit specific binding, showing high affinity for the NR2B receptor and a clear ranking of binding affinity with a variety of other compounds .
NMDA-IN-1 is a potent and NR2B-selective NMDA antagonist with Ki of 0.85 nM; NR2B Ca2+ influx IC50 is 9.7 nM; no activities on NR2A, NR2C, NR2D, hERG-channel and α1-adrenergic receptor.
Tat-NR2B9c (Tat-NR2Bct; NA-1) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c also inhibits?neuronal nitric oxide synthase (nNOS)/PSD-95?interaction, and possesses neuroprotective efficacy [2] .
Ro 8-4304 hydrochloride is a potent NMDA receptor antagonist. Ro 8-4304 hydrochloride is a NR2B selective, non-competitive, voltage-independent antagonist .
Tat-NR2B9c TFA (Tat-NR2Bct TFA) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c TFA disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c TFA also inhibits neuronal nitric oxide synthase (nNOS)/PSD-95 interaction, and possesses neuroprotective efficacy .
(Rac)-NMDAR antagonist 1 is the racemate of NMDAR antagonist 1. NMDAR antagonist 1 is a potent and orally bioavailable NR2B-selective NMDAR antagonist .
Radiprodil (RGH-896) is an orally active and selective NMDA NR2B antagonist. A potential therapeutic agent in treatment of neuropathic pain and possibly other chronic pain conditions .
Ifenprodil tartrate is a typical noncompetitive NMDA receptor antagonist. Ifenprodil tartrate exerts high affinity at NR1A/NR2B receptors (IC50=0.34 μM) over 400-fold than at NR1A/NR2A receptors (IC50=146 μM) . Ifenprodil tartrate inhibits GIRK (Kir3), reduces inward currents through the basal GIRK activity. Ifenprodil tartrate has the potential to be a cerebral vasodilator [2].
NMDA receptor antagonist 2 is a potent and orally active NR2B subtype-selective NMDA antagonist with an IC50 and a Ki of 1.0 nM and 0.88 nM, respectively. NMDA receptor antagonist 2 is used for the study of neuropathic pain and Parkinson’s disease .
Nelonemdaz (Salfaprodil) potassium is an NR2B-selective and uncompetitive antagonist of N-methyl-D-aspartate (NMDA). Nelonemdaz potassium is also a free radical scavenger. Nelonemdaz potassium has excellent neuroprotection against NMDA- and free radical-induced cell death [2].
Ro 25-6981 is a potent, selective and activity-dependent NR2B subunit specific NMDA receptor antagonist. Ro 25-6981 shows anticonvulsant and anti-parkinsonian activity. Ro 25-6981 has the potential for the research of parkinson's disease (PD) [2] .
Nelonemdaz (Salfaprodil free base) is an NR2B-selective and uncompetitive antagonist of N-methyl-D-aspartate (NMDA). Nelonemdaz is also a free radical scavenger. Nelonemdaz has excellent neuroprotection against NMDA- and free radical-induced cell death [2].
Ro 25-6981 hydrochloride is a potent, selective and activity-dependent NR2B subunit specific NMDA receptor antagonist. Ro 25-6981 hydrochloride shows anticonvulsant and anti-parkinsonian activity. Ro 25-6981 hydrochloride has the potential for the research of parkinson's disease (PD) [2] .
Ro 25-6981 Maleate is a potent, selective and activity-dependent NR2B subunit specific NMDA receptor antagonist. Ro 25-6981 Maleat shows anticonvulsant and anti-parkinsonian activity. Ro 25-6981 Maleate has the potential for the research of parkinson's disease (PD) [2] .
HSD17B13-IN-7 (compound 1), a fluorophenol-containing compound, is a potent HSD17B13 inhibitor with IC50s of 0.18 μM and 0.25 μM β-estradiol and Leukotriene B4 as substrates, respectively. HSD17B13-IN-7 is a potent N-methyl-D-aspartate (NMDA) NR2B receptor antagonist. HSD17B13-IN-7 has the potential for non-alcoholic fatty liver disease research .
QNZ46 is a NR2C/NR2D-selective NMDA receptor non-competitive antagonist (IC50 values are 3, 6, 229, and >300, >300 μM for NR2D, NR2C, NR2A, NR2B, and GluR1, respectively).
Tat-NR2BAA TFA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA TFA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95 .
Tat-NR2BAA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95 [2].
threo Ifenprodil hemitartrate is a σ receptor agonist, with Kis of 59.1 and 2 nM for σ1 and σ2 receptors, respectively. threo Ifenprodil hemitartrate is also a NR2B subunit-selective NMDA receptor antagonist (IC50=0.22 μM). threo Ifenprodil hemitartrate is a hERG potassium channel inhibitor, with an IC 50 of 88 nM, showing antiarrhythmic activity [2] .
BMT-108908 is a negative allosteric modulator with selective activity on the NR2B subtype of the NMDA receptor. BMT-108908 has been shown to damage cognition in research, affecting cognitive functions in multiple areas. BMT-108908 failed to show a significant impact on the γ wave power of the EEG in the experiment, but it had a significant inhibitory and enhancement effect on the β wave and δ wave power. The effects of BMT-108908 differ from those of other NMDA receptor channel blockers such as ketamine and lanimol .
Tat-NR2B9c (Tat-NR2Bct; NA-1) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c also inhibits?neuronal nitric oxide synthase (nNOS)/PSD-95?interaction, and possesses neuroprotective efficacy [2] .
Tat-NR2B9c TFA (Tat-NR2Bct TFA) is a postsynaptic density-95 (PSD-95) inhibitor, with EC50 values of 6.7 nM and 670 nM for PSD-95d2 (PSD-95 PDZ domain 2) and PSD-95d1, respectively. Tat-NR2B9c TFA disrupts the PSD-95/NMDAR interaction, inhibiting NR2A and NR2B binding to PSD-95 with IC50 values of 0.5 μM and 8 μM, respectively. Tat-NR2B9c TFA also inhibits neuronal nitric oxide synthase (nNOS)/PSD-95 interaction, and possesses neuroprotective efficacy .
Tat-NR2BAA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95 [2].
Tat-HA-NR2B9 contains a fragment of the cellmembrane transduction domain of HIV-1 Tat, a influenza virus hemagglutinin (HA) epitope-tag, and the C-terminal 9 amino acids of NR2B (NR2B9c). Tat-HA-NR2B9 reduces infarct size and improves neurological functions in ischemia-induced cerebral injury in the rats
Tat-NR2BAA TFA is the control peptide of Tat-NR2B9c (HY-P0117), inactive. The sequence of Tat-NR2BAA TFA is similar to Tat-NR2B9c, but it has a double-point mutation in the COOH terminal tSXV motif, making it incapable of binding PSD-95. Tat-NR2B9c is a membrane-permeant peptide and disrupts PSD-95/NMDAR binding, correlate with uncoupling NR2B- and/or NR2A-type NMDARs from PSD-95 .
Ifenprodil tartrate is a typical noncompetitive NMDA receptor antagonist. Ifenprodil tartrate exerts high affinity at NR1A/NR2B receptors (IC50=0.34 μM) over 400-fold than at NR1A/NR2A receptors (IC50=146 μM) . Ifenprodil tartrate inhibits GIRK (Kir3), reduces inward currents through the basal GIRK activity. Ifenprodil tartrate has the potential to be a cerebral vasodilator [2].
CoREST Antibody (YA1813) is a rabbit-derived non-conjugated IgG antibody (Clone NO.: YA1813), targeting CoREST, with a predicted molecular weight of 53 kDa (observed band size: 66 kDa). CoREST Antibody (YA1813) can be used for WB, IHC-P, ICC/IF experiment in human, mouse, rat background.
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