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Results for "

glutamatergic

" in MedChemExpress (MCE) Product Catalog:

12

Inhibitors & Agonists

1

Biochemical Assay Reagents

2

Peptides

3

Natural
Products

2

Isotope-Labeled Compounds

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-45609

    iGluR Endogenous Metabolite Neurological Disease
    L-Cysteine S-sulfate sodium hydrate is a potent N-methyl-d-aspartate (NMDA) glutamatergic receptors agonist. L-Cysteine S-sulfate sodium hydrate is the substrate for cystine lyase, it can be used in mass spectrometry operations .
    L-Cysteine S-sulfate sodium hydrate
  • HY-19411

    nAChR Neurological Disease
    SSR180711 hydrochloride is an orally active, selective and reversible α7 acetylcholine nicotinic receptor (n-AChRs) partial agonist. SSR180711 hydrochloride can act on rat α7 n-AChR (Ki=22 nM; IC50=30 nM) and human α7 n-AChR (Ki=14 nM; IC50=18 nM). SSR180711 hydrochloride increases glutamatergic neurotransmission, ACh release and long-term potentiation (LTP) in the hippocampus .
    SSR180711 hydrochloride
  • HY-17030

    Calcium N-acetylhomotaurinate

    GABA Receptor Neurological Disease
    Acamprosate calcium(Campral EC) is a GABA receptor agonist and modulator of glutamatergic systems; reduces alcohol consumption in animal models of alcohol addiction.
    Acamprosate calcium
  • HY-17030S

    GABA Receptor Neurological Disease
    Acamprosate-d3 (calcium) is the deuterium labeled Acamprosate calcium. Acamprosate calcium is a GABA receptor agonist and modulator of glutamatergic systems[1][2].
    Acamprosate-d3 calcium
  • HY-P2259
    TAT-GluA2 3Y
    1 Publications Verification

    iGluR Neurological Disease
    TAT-GluA2 3Y, an interference peptide, blocks long-term depression (LTD) at glutamatergic synapses by disrupting the endocytosis of AMPAR. TAT-GluA2 3Y can alleviate Pentobarbital-induced spatial memory deficits and synaptic depression .
    TAT-GluA2 3Y
  • HY-113084

    iGluR Endogenous Metabolite Neurological Disease
    L-Cysteine S-sulfate is a potent N-methyl-d-aspartate (NMDA) glutamatergic receptor agonist. L-Cysteine S-sulfate is the substrate for cystine lyase, and can be used in mass spectrometry operations .
    L-Cysteine S-sulfate
  • HY-110233S

    GABA Receptor Neurological Disease
    Acamprosate-d6 (calcium) is the deuterium labeled Acamprosate calcium. Acamprosate calcium (Campral EC) is a GABA receptor agonist and modulator of glutamatergic systems[1].
    Acamprosate-d6 calcium
  • HY-100616A

    trans-1-Aminocyclobutane-1,3-dicarboxylic acid

    iGluR Neurological Disease
    trans-ACBD (trans-1-Aminocyclobutane-1,3-dicarboxylic acid) is a very potent and selective NMDA receptor agonist that modulates glutamatergic neurotransmission .
    trans-ACBD
  • HY-123272

    5-HT Receptor Neurological Disease
    E6801 is a 5-HT6 receptor agonist that improves recognition memory by jointly modulating cholinergic and glutamatergic neurotransmission. E6801 can be used in studies of dementia, depression, obesity, epilepsy, etc .
    E6801
  • HY-100787

    iGluR Endogenous Metabolite Neurological Disease
    L-Cysteine S-sulfate sodium is a potent N-methyl-d-aspartate (NMDA) glutamatergic receptors agonist. L-Cysteine S-sulfate sodium hydrate is the substrate for cystine lyase, it can be used in mass spectrometry operations .
    L-Cysteine S-sulfate sodium
  • HY-133195

    Fenazoxine

    Others Neurological Disease
    Nefopam (Fenazoxine) is an orally active, non-opioid and non-steroidal centrally acting analgesic agent. Nefopam blocks voltage-sensitive sodium channels (IC50=27 μM) and modulates glutamatergic transmission in rodents. Nefopam can be used in studies of neuropathic pain, anticonvulsant, as well as the prevention of postoperative shivering and hiccups .
    Nefopam
  • HY-118275

    Cholinesterase (ChE) Neurological Disease
    FK960 is a potential anti-dementia agent that reverses the reduction in cerebral blood flow (rCBF) caused by sensory stimulation by enhancing cholinergic neurotransmission. In macaque experiments, physostigmine (AChE inhibitor; HY-N6608) was able to completely eliminate the rCBF in the sensory cortex increased by vibrotactile stimulation. FK960 (1-1000 μg/kg) can restore the eliminated rCBF response, and the action time can last for 1 hour. However, FK960 cannot restore the rCBF response eliminated by HA-966 (NMDA modulator; HY-100822), indicating that its function is not dependent on non-glutamatergic neurotransmission.
    FK960

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