Deudextromethorphan (AVP-786) is a deuterated form of dextromethorphan/quinidine (AVP-923, Nuedexta). Deudextromethorphan, a glutamate-targeting agent, is an orally active N-methyl-D-aspartate (NMDA) receptor antagonist. Deudextromethorphan can be used for the research of Pseudo-Bulbar Affect, traumatic brain injury, behavioral disinhibition and agitation in AD[1][2][3].
Dalzanemdor (SAGE-718) is a N-methyl-D-aspartate (NMDA) receptor positive allosteric modulator[1].
L-Homocysteic acid (L-HCA) is an endogenous excitatory amino acid that acts as a NMDA receptor agonist (EC50: 14 μM). L-Homocysteic acid is neurotoxic, and can be used in the research of neurological disorders[1][2][3].
TAK-653, an AMPA receptor potentiator with minimal agonistic activity, produces an antidepressant-like effect with a favorable safety profile in rats.
DNQX (FG 9041) disodium salt, a quinoxaline derivative, is a selective, potent competitive non-NMDA glutamate receptor antagonist (IC50s = 0.5, 2 and 40 μM for AMPA, kainate and NMDA receptors, respectively)[1].
GYKI 52466 dihydrochloride is a potent, selective, orally active and non-competitive kainate- and AMPA-activated currents antagonist with IC50s of 7.5 μM and 11 μM, respectively. GYKI 52466 dihydrochloride is inactive against N-methyl-D-aspartate (NMDA) or γ-aminobutyric acid responses. GYKI 52466 dihydrochloride ia a muscle relaxant and anticonvulsant agent, and has good blood brain barrier permeability[1][2].
L-Glutamic acid-13C2 is the 13C labeled L-Glutamic acid[1]. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals[2].
Midafotel (SDZ-EAA 494) is a potent and comprtitive NMDA antagonist with an ED50 value of 39 nM. Midafotel causes intense stereotyped behaviors. Midafotel shows neuroprotective effects[1][2][3].
Glycine is an inhibitory neurotransmitter in the CNS and also acts as a co-agonist along with glutamate, facilitating an excitatory potential at the glutaminergic N-methyl-D-aspartic acid (NMDA) receptors.
Neboglamine (CR-2249, XY-2401) hydrochloride is an orally active NMDA receptor glycine site positive modulator that can be used in schizophrenia research[1].
GNE 0723 is a brain permeable positive allosteric modulator of NMDAR, with an EC50 of 21 nM for GluN2A, 7.4 and 6.2 μM for GluN2C and GluN2D, respectively.
L-Glutamic acid-13C5,15N is the 13C- and 15N-labeled L-Glutamic acid. L-Glutamic acid acts as an excitatory transmitter and an agonist at all subtypes of glutamate receptors (metabotropic, kainate, NMDA, and AMPA). L-Glutamic acid shows a direct activating effect on the release of DA from dopaminergic terminals.
Ro 25-6981 Maleate is a potent and selective activity-dependent blocker of NMDA receptors containing the NR2B subunit. IC50 values are 0.009 and 52 μM for cloned receptor subunit combinations NR1C/NR2B and NR1C/NR2A respectively.IC50 value: 9 nM [1]Target: NMDA receptor subtype of NR1C & NR2Bin vitro: Ro 25-6981 inhibited 3H-MK-801 binding to rat forebrain membranes in a biphasic manner with IC50 values of 0.003 microM and 149 microM for high- (about 60%) and low-affinity sites, respectively. NMDA receptor subtypes expressed in Xenopus oocytes were blocked with IC50 values of 0.009 microM and 52 microM for the subunit combinations NR1C & NR2B and NR1C & NR2A, respectively, which indicated a >5000-fold selectivity [1]. Increasing the concentration of spermidine did not change the efficacy of RO 25-6981 and minimally changed the IC(50) value. Epsilon1Q336R receptors were more inhibited by ifenprodil and RO 25-9681 than wildtype epsilon1 receptors in ligand binding assays but not in functional assays [2].in vivo: Intrathecal injection of Ro 25-6981 significantly enhanced the paw withdrawal mechanical threshold and paw withdrawal thermal latency after the operation. Significant change has been observed after intrathecal injection of 800.0 μg of Ro 25-6981 and at 2h after operation in the oblique pull test degree and BBB rating score. Pretreatment of Ro 25-6981 decreased the high level expression of NR2B with tyrosine phosphorylation in spinal dorsal horn of the rat model after the operation [3].
Selurampanel (BGG 492) is an orally active and competitive AMPA receptor antagonist with an IC50 of 190 nM. Selurampanel has reasonable blood-brain barrier penetration. Selurampanel can be used for epilepsy research[1][2].
(S)-Willardiine is a potent agonist of AMPA/kainate receptors with EC50 of 44.8 uM.IC50 value: 44.8 uM(EC50) [1]Target: AMPA/kainate receptor agonistin vitro: The (S)- but not (R)-isomers of willardiine and 5-bromowillardiine were potent agonists, producing rapidly but incompletely desensitizing responses [1]. At a concentration of 1.8 mM, Ca2+ inhibited the currents induced by 100 microM willardiine by approximately 50% [2].in vivo: In newborn mice (P5, histopathology at P10), local injection of the AMPA receptor agonist S-bromo-willardiine at day 5 after birth induced cortical damage and white matter damage, which was reduced in a dose-dependent manner by the AMPA receptor antagonists [3].
CIQ is a subunit-selective potentiator of NMDA receptors containing the NR2C or NR2D subunit. IC50 value: 2.7 μM (EC50, for NR2C) and 2.8 μM (EC50, NR2D)Target: NMDA receptorCIQ increases channel opening frequency of recombinant NR2Cor NR2D containing receptors by two-fold (EC50 = 2.7 and 2.8 μM, respectively), with no effect on NR2A or NR2B subtypes. CIQ does not alter the EC50 values for glutamate or glycine on channel opening. CIQ increases channel opening efficiency and enhances NMDA receptor responses. CIQ reduces associated behaviours in schizophrenia models and potentially enhances dopamine release in Parkinson's disease models.
Mibampator (LY451395) is a potent and highly selective potentiator of the AMPA receptors.
Neu2000 is an uncompetitive N-methyl-D-aspartate (NMDA) receptor antagonist.
(R)-(+)-HA-966 ((+)-HA-966) is a partial agonist/antagonist of glycine site of the N-methyl-D-aspartate (NMDA) receptor complex. (R)-(+)-HA-966 selectively blocks the activation of the mesolimbic dopamine system by amphetamine[1][2]. (R)-(+)-HA-966 can cross the blood-brain barrier and has the potential for neuropathic and acute pain[3].
Lanicemine (AZD6765) is a low-trapping NMDA channel blocker with a binding (Ki) of 0.56-2.1 μM[1].
NYX-2925 is a Novel NMDA Receptor-Specific Spirocyclic-β-Lactam That Modulates Synaptic Plasticity Processes Associated with Learning and Memory.
IC87201, an inhibitor of PSD95-nNOS protein-protein interactions, suppresses NMDAR-dependent NO and cGMP formation.
Org 26576 is a AMPA receptor positive allosteric modulator.
CFM-2 is a selective non-competitive AMPAR antagonist.IC50 value:Target: AMPAR antagonistin vitro: AMPA antagonists GYKI 52466 and CFM-2 inhibit the extracellular signal regulated kinase (ERK1/2) pathway, CFM-2 reduced phosphorylation of cAMP-responsive element binding protein (CREB), suppressed expression of cyclin D1, upregulated the cell cycle regulators and tumor suppressor proteins p21 and p53 and decreased number of lung adenocarcinoma cells in G2 and S phases of the cell cycle.in vivo: Pretreatment with CFM-2 delayed the progression of seizure rank during repeated administration of pentylentetrazole. At the end of the period of repeated pentylentetrazole treatment (6 weeks) the mean seizure score was 0 in vehicle treated controls, 4.3 in animals treated with vehicle + pentylentetrazole, 2.2 in rats treated chronically with CFM-2 (20 micromol kg(-1) i.p.) + pentylentetrazole and 1.0 in rats treated repeatedly with CFM-2 (50 micromol kg(-1) i.p.) + pentylenetetrazole. CFM-2 was also able to antagonize the long-term increase in sensitivity of the convulsant effects of GABA function inhibitors in pentylentetrazole-kindled animals [1]. CFM-2 has been proven to possess anticonvulsant activity in various models of seizures [2]. Intrathecal application of two selective non-competitive AMPAR antagonists, CFM-2 (25 and 50 microg) and GYKI 52466 (50 microg), significantly attenuated mechanical and thermal hypersensitivities on the ipsilateral hind paw at 2 and 24 h post-CFA injection. Neither CFM-2 nor GYKI 52466 affected the contralateral basal responses to thermal and mechanical stimuli [4].
Ro 8-4304 hydrochloride is a potent NMDA receptor antagonist. Ro 8-4304 hydrochloride is a NR2B selective, non-competitive, voltage-independent antagonist[1].
Coluracetam(MKC-231) is a new choline uptake enhancer.IC50 value:Target:in vitro: MKC-231 (10(-10)-10(-6) moll) significantly increased high affinity choline uptake (HACU) when it was incubated with the hippocampal synaptosomes of ethylcholine mustard aziridinium ion (AF64A) treated rats, but not of normal rats. MKC-231 did not affect the AChE activity, [3H]- quinuclidinyl benzilate binding, and [3H]-pirenzepine binding [1].in vivo: Oral administration of MKC-231 (1-10 mg/kg) significantly improved the learning deficits in the Morris' water maze of AF64A-treated rats, but it did not produce any significant side effects, like tremor, salivation or hypothermia, which were observed in rats treated with high doses of tacrine [1]. In acute behavioral experiments, MKC-231 and THA had no significant effect on AF64A-induced memory deficits at any doses tested (0.3, 1.0 and 3.0 mg/kg), whereas Dup 996, at a dose of 1.0 mg/kg, significantly improved memory deficits. In chronic experiments, MKC-231 improved memory deficit at all doses tested (0.3, 1.0, or 3.0 mg/kg p.o., once daily for 11 days) and Dup 996 did so only at a dose of 3.0 mg/kg, whereas THA did not improve memory deficit at any doses tested [2].
Indole-2-carboxylic acid is a strong inhibitor of lipid peroxidation. Indole-2-carboxylic acid (I2CA) specifically and competitively inhibits the potentiation by glycine of NMDA-gated current[1][2].
Deudextromethorphan (AVP-786) hydrobromide hydrate is a deuterated form of dextromethorphan/quinidine (AVP-923, Nuedexta). Deudextromethorphan hydrobromide hydrate, a glutamate-targeting agent, is an orally active N-methyl-D-aspartate (NMDA) receptor antagonist. Deudextromethorphan hydrobromide hydrate can be used for the research of Pseudo-Bulbar Affect, traumatic brain injury, behavioral disinhibition and agitation in AD[1][2][3].
Lanicemine (AZD6765) dihydrochloride is a low-trapping NMDA channel blocker (Ki of 0.56-2.1 μM for NMDA receptor; IC50s of 4-7 μM and 6.4 μM in CHO and Xenopus oocyte cells, respectively). Antidepressant effects[1].
Nevadistinel (NYX-458; NYX-3054) is a positive allosteric modulator of N-methyl-D-aspartate (NMDA) receptor. Nevadistinel can be used to inhibit cognitive impairment associated with neurodegenerative diseases, such as mild cognitive impairment, mild Alzheimer's disease, Parkinson's disease, Lewy body disease[1].