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Results for "

glutamate release

" in MedChemExpress (MCE) Product Catalog:

45

Inhibitors & Agonists

8

Peptides

5

Natural
Products

18

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-W276106
    KM02894

    		Others Cancer
    KM02894 is an inhibitor of glutamate release. Cancer cells release high levels of glutamate, which disrupts normal bone turnover and may lead to cancer-induced bone pain. KM02894 can be used for cancer related research .
    KM02894
  • HY-147512
    CB1/2 agonist 1

    		Cannabinoid Receptor Inflammation/Immunology
    CB1/2 agonist 1 is a potent and cross the blood-brain barrier CB1/2 agonist with EC50s of 56.15, 11.63 nM for CB1R and CB2R, respectively. CB1/2 agonist 1 reduces glutamate release and LPS-induced activation of microglial cells. CB1/2 agonist 1 shows anti-inflammatory and antinociceptive effects. CB1/2 agonist 1 has the potential for the research of multiple sclerosis .
    CB1/2 agonist 1
  • HY-131885
    RuBi-Glutamate hexafluorophosphate sodium

    		Others Neurological Disease
    RuBi-Glutamate hexafluorophosphate sodium is a novel cage glutamate compound based on ruthenium photochemistry. RuBi-Glutamate hexafluorophosphate sodium can be excited at visible wavelengths and release glutamate after single or two-photon excitation. It has high quantum efficiency and can be used at low concentrations, partially avoiding the blocking of GABA energy transmission by other cage compounds. Two-photon release of RuBi-Glutamate hexafluorophosphate sodium has high spatial resolution and produces a physiodynamic excitatory response in a single dendritic spine .
    RuBi-Glutamate hexafluorophosphate sodium
  • HY-153691
    BTB01303

    		Others Others
    BTB01303 is a (glutamate release) inhibitor. Cancer cells release high levels of (glutamate), which disrupts normal bone turnover and may lead to cancer-induced bone pain. BTB01303 has the potential to improve cancer-induced bone pain .
    BTB01303
  • HY-W037817
    Dimethyl L-glutamate

    Dimethyl glutamate

    		 Potassium Channel Bacterial Infection Metabolic Disease
    Dimethyl L-glutamate (Dimethyl glutamate), a membrane-permeable analog of Glutamate, can stimulate insulin release induced by Glucose. Dimethyl L-glutamate suppresses the KATP channel activities. Dimethyl L-glutamate inhibits E. gracilis growth and causes abnormal cell division. Dimethyl L-glutamate can be used in the research of diabetes, glucose transport, phosphorylation, and further metabolism .
    Dimethyl L-glutamate
  • HY-107520A
    MNI-caged-L-glutamate TFA

    		Others
    MNI-caged-L-glutamate TFA is a reagent capable of rapidly and efficiently releasing neuroactive amino acids .
    MNI-caged-L-glutamate TFA
  • HY-132219
    N,N-Dipropyldopamine hydrobromide

    		Others Cancer
    N. N-dipropyrldopamine is a potent inhibitor of glutamate release and has anticancer activity. The increase of glutamate secretion leads to cancer-induced bone pain (CIBP). N. N-dipropyrldopamine plays an analgesic role in CIBP .
    N,N-Dipropyldopamine hydrobromide
  • HY-100802
    Homoquinolinic acid

    		iGluR Neurological Disease
    Homoquinolinic acid is a non endogenous agonist of NMDAR2 receptor .
    Homoquinolinic acid
  • HY-P0188
    ω-Conotoxin MVIIC

    ω-Conotoxin MVIIC is a N- and P/Q-type Ca 2+ channel blocker, significantly suppresses the 11-keto-βboswellic acid-mediated inhibition of glutamate release .
    ω-Conotoxin MVIIC
  • HY-P0188A
    ω-Conotoxin MVIIC TFA

    		Calcium Channel Neurological Disease
    ω-Conotoxin MVIIC TFA is a N- and P/Q-type Ca 2+ channel blocker, significantly suppresses the 11-keto-βboswellic acid-mediated inhibition of glutamate release .
    ω-Conotoxin MVIIC TFA
  • HY-P3089
    Dendrotoxin K

    		Potassium Channel Others
    Dendrotoxin K is a Kv1.1 channel blocker. Dendrotoxin K determines glutamate release in CA3 neurons in a time-dependent manner through the control of the presynaptic spike waveform .
    Dendrotoxin K
  • HY-N10772
    Albanin A

    		Calcium Channel Calmodulin Adenylate Cyclase Neurological Disease Inflammation/Immunology
    Albanin A, a flavonoid, suppresses glutamate release by decreasing Ca 2+/calmodulin/adenylate Cyclase 1 (AC1) activation in synaptosomes and exerts neuroprotective effect in vivo. Albanin A has anti-inflflammatory activity .
    Albanin A
  • HY-P3089A
    Dendrotoxin K TFA

    		Potassium Channel Others
    Dendrotoxin K TFA is a Kv1.1 channel blocker. Dendrotoxin K TFA determines glutamate release in CA3 neurons in a time-dependent manner through the control of the presynaptic spike waveform .
    Dendrotoxin K TFA
  • HY-108335
    Sipatrigine

    619C89; BW 619C89

    		 Sodium Channel Calcium Channel Neurological Disease
    Sipatrigine (619C89), a neuroprotective agent, is a glutamate release inhibitor, voltage-dependent sodium channel and calcium channel inhibitor, penetrating the central nervous system. Has the potential in the study for focal cerebral ischemia and stroke .
    Sipatrigine
  • HY-100403
    Ro 67-7476
    Maximum Cited Publications
    6 Publications Verification

    		 mGluR Cancer
    Ro 67-7476 is a potent positive allosteric modulator of mGluR1 and potentiates glutamate-induced calcium release in HEK293 cells expressing rat mGluR1a with an EC50 of 60.1 nM . Ro 67-7476 is a potent P-ERK1/2 agonist and activates ERK1/2 phosphorylation in the absence of exogenously added glutamate (EC50=163.3 nM) .
    Ro 67-7476
  • HY-B0495A
    Lamotrigine hydrate

    LTG hydrate; BW430C hydrate

    		 Sodium Channel Autophagy Neurological Disease
    Lamotrigine hydrate is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine hydrate selectively blocks voltage-gated Na + channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine hydrate can be used for the research of epilepsy, focal seizure, et al .
    Lamotrigine hydrate
  • HY-B0495
    Lamotrigine
    Maximum Cited Publications
    6 Publications Verification

    LTG; BW430C

    		 Sodium Channel Autophagy Neurological Disease
    Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na + channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al .
    Lamotrigine
  • HY-14608S
    L-Glutamic acid-13C

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid- 13C is the 13C-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.
    L-Glutamic acid-13C
  • HY-14608S7
    L-Glutamic acid-d5

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid-d5 is the deuterium 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.
    L-Glutamic acid-d5
  • HY-14608S8
    L-Glutamic acid-d3

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid-d3 is the deuterium 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.
    L-Glutamic acid-d3
  • HY-14608S5
    L-Glutamic acid-13C5

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid- 13C5 is the 13C-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.
    L-Glutamic acid-13C5
  • HY-14608S2
    L-Glutamic acid-15N

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid- 15N is the 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[1].
    L-Glutamic acid-15N
  • HY-14608
    L-Glutamic acid
    3 Publications Verification

    		 Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid is an excitatory amino acid neurotransmitter that acts as an agonist for all subtypes of glutamate receptors (metabolic rhodophylline, NMDA, and AMPA). L-Glutamic acid has an agonist effect on the release of DA from dopaminergic nerve endings. L-Glutamic acid can be used in the study of neurological diseases .
    L-Glutamic acid
  • HY-14608S1
    L-Glutamic acid-1-13C

    		Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid-1- 13C is the 13C-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.
    L-Glutamic acid-1-13C
  • HY-14608S6
    L-Glutamic acid-5-13C

    		Isotope-Labeled Compounds Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid-5- 13C is the 13C-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.
    L-Glutamic acid-5-13C
  • HY-110032
    Lamotrigine isethionate

    LTG isethionate; BW430C isethionate

    		 Sodium Channel Autophagy Neurological Disease Cancer
    Lamotrigine (BW430C) isethionate is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine isethionate selectively blocks voltage-gated Na + channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine isethionate can be used for the research of epilepsy, focal seizure, et al .
    Lamotrigine isethionate
  • HY-N6776
    Penitrem A

    		Potassium Channel Neurological Disease Cancer
    Penitrem A is an indole diterpene neurotoxic alkaloid produced by Penicillium, acts as a selective BK channel antagonist with antiproliferative and anti-invasive activities against multiple malignancies. Penitrem A increases the spontaneous release of endogenous glutamate, gamma-aminobutyric acid (GABA) and aspartate from cerebrocortical synaptosomes, and induces tremorgenic syndromes in animals .
    Penitrem A
  • HY-14608A
    L-Glutamic acid monosodium salt
    3 Publications Verification

    		 iGluR Apoptosis Ferroptosis Endogenous Metabolite Neurological Disease
    L-Glutamic acid monosodium salt is an excitatory amino acid neurotransmitter that acts as an agonist for all subtypes of glutamate receptors (metabolic rhodophylline, NMDA, and AMPA). L-Glutamic acid monosodium salt has an agonist effect on the release of DA from dopaminergic nerve endings. L-Glutamic acid monosodium salt can be used in the study of neurological diseases .
    L-Glutamic acid monosodium salt
  • HY-14608S3
    L-Glutamic acid-13C5,15N

    		Isotope-Labeled Compounds Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    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.
    L-Glutamic acid-13C5,15N
  • HY-14608S9
    L-Glutamic acid-15N,d5

    		Isotope-Labeled Compounds Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid- 15N,d5 is the deuterium 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.
    L-Glutamic acid-15N,d5
  • HY-14608S10
    L-Glutamic acid-13C2

    		Apoptosis iGluR Ferroptosis Endogenous Metabolite Neurological Disease
    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].
    L-Glutamic acid-13C2
  • HY-N9404
    6-Benzoylheteratisine

    		Sodium Channel Neurological Disease
    6-Benzoylheteratisine is an Aconitum alkaloid with potential neuroprotective activity. 6-Benzoylheteratisine can antagonize tetrodotoxin, inhibit the increase of [Na +]i, [Ca 2+]i and glutamate release, and block sodium channels. 6-Benzoylheteratisine has an inhibitory effect on the neuronal activity underlying epileptiform burst discharge .
    6-Benzoylheteratisine
  • HY-14608S4
    L-Glutamic acid-13C5,15N,d5

    		Isotope-Labeled Compounds Endogenous Metabolite iGluR Ferroptosis Apoptosis Neurological Disease
    L-Glutamic acid- 13C5, 15N,d5 is the deuterium, 13C-, and 15-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.
    L-Glutamic acid-13C5,15N,d5
  • HY-B0495S4
    Lamotrigine-13C3

    LTG-13C3; BW430C-13C3

    		 Sodium Channel Autophagy Neurological Disease
    Lamotrigine- 13C3 is the 13C-labeled Lamotrigine. Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na+ channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al[1][2].
    Lamotrigine-13C3
  • HY-B0495S5
    Lamotrigine-d3

    LTG-d3; BW430C-d3

    		 Autophagy Sodium Channel
    Lamotrigine-d3 is the deuterium labeled Lamotrigine[1]. Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na+ channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al[2][3].
    Lamotrigine-d3
  • HY-B0495S1
    Lamotrigine-13C,d3

    LTG-13C,d3; BW430C-13C,d3

    		 Isotope-Labeled Compounds Sodium Channel Autophagy Neurological Disease
    Lamotrigine- 13C,d3 is the 13C- and deuterium labeled Lamotrigine. Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na+ channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al[1][2].
    Lamotrigine-13C,d3
  • HY-B0495S
    Lamotrigine-13C3,d3

    LTG-13C3,d3; BW430C-13C3,d3

    		 Sodium Channel Autophagy Neurological Disease
    Lamotrigine- 13C3,d3 is the 13C-labeled Lamotrigine. Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na+ channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al[1][2].
    Lamotrigine-13C3,d3
  • HY-120511
    KNT-127

    		Opioid Receptor Neurological Disease
    KNT-127 is a potent and selective δ-opioid receptor agonist effective by systemic administration. KNT-127 shows selectivity for the δ-receptor (Ki 0f 21.3, 0.16, 153 nM for opioid μ-, δ-, and κ-receptors, respectively). KNT-127 increases the release of dopamine and L-glutamate in the striatum, nucleus accumbens and median pre-frontal cortex. Antidepressant-like effects .
    KNT-127
  • HY-B0495S3
    Lamotrigine-13C2,15N

    		Autophagy Sodium Channel
    Lamotrigine-13C2,15N is the 13C and 15N labeled Lamotrigine[1]. Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na+ channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy, focal seizure, et al[2][3].
    Lamotrigine-13C2,15N
  • HY-B0495S6
    Lamotrigine-13C2,15N2,d3

    LTG-13C2,15N2,d3; BW430C-13C2,15N2,d3

    		 Autophagy Sodium Channel Isotope-Labeled Compounds Neurological Disease Cancer
    Lamotrigine- 13C2, 15N2,d3 is 15N and deuterated labeled Lamotrigine (HY-B0495). Lamotrigine (BW430C) is a potent and orally active anticonvulsant or antiepileptic agent. Lamotrigine selectively blocks voltage-gated Na + channels, stabilizing presynaptic neuronal membranes and inhibiting glutamate release. Lamotrigine can be used for the research of epilepsy,?focal seizure, et al .
    Lamotrigine-13C2,15N2,d3
  • HY-70057
    Safinamide
    2 Publications Verification

    FCE 26743; EMD 1195686

    		 Monoamine Oxidase Neurological Disease
    Safinamide is a potent, selective, and reversible monoamine oxidase B (MAO-B) inhibitor (IC50=0.098 µM) over MAO-A (IC50=580 µM) . Safinamide also blocks sodium channels and modulates glutamate (Glu) release, showing a greater affinity at depolarized (IC50=8 µM) than at resting (IC50=262 µM) potentials. Safinamide has neuroprotective and neurorescuing effects and can be used for the study of parkinson disease, ischemia stroke etc.al .
    Safinamide
  • HY-P1080
    ω-Agatoxin IVA

    		Calcium Channel Neurological Disease
    ω-Agatoxin IVA is a potent, selective P/Q type Ca 2+ (Cav2.1) channel blocker with IC50s of 2 nM and 90 nM for P-type and Q-type Ca 2+ channels, respectively. ω-Agatoxin IVA (IC50, 30-225 nM) inhibits glutamate exocytosis and calcium influx elicited by high potassium. ω-Agatoxin IVA also blocks the high potassium-induced release of serotonin and norepinephrine. ω-Agatoxin IVA has no effect on L-type or N-type calcium channels .
    ω-Agatoxin IVA
  • HY-70057A
    Safinamide mesylate
    2 Publications Verification

    FCE 26743 mesylate; EMD 1195686 mesylate

    		 Monoamine Oxidase Cardiovascular Disease Neurological Disease
    Safinamide (FCE 26743; EMD 1195686) mesylate is a potent, selective, and reversible monoamine oxidase B (MAO-B) inhibitor (IC50=0.098 µM) over MAO-A (IC50=580 nM) . Safinamide mesylate also blocks sodium channels and modulates glutamate (Glu) release, showing a greater affinity at depolarized (IC50=8 µM) than at resting (IC50=262 µM) potentials. Safinamide mesylate has neuroprotective and neurorescuing effects and can be used for the study of parkinson disease, ischemia stroke et.al .
    Safinamide mesylate
  • HY-P1080A
    ω-Agatoxin IVA TFA

    		Calcium Channel Neurological Disease
    ω-Agatoxin IVA TFA is a potent, selective P/Q type Ca 2+ (Cav2.1) channel blocker with IC50s of 2 nM and 90 nM for P-type and Q-type Ca 2+ channels, respectively. ω-Agatoxin IVA TFA (IC50, 30-225 nM) inhibits glutamate exocytosis and calcium influx elicited by high potassium. ω-Agatoxin IVA TFA also blocks the high potassium-induced release of serotonin and norepinephrine. ω-Agatoxin IVA TFA has no effect on L-type or N-type calcium channels .
    ω-Agatoxin IVA TFA
  • HY-70057S1
    Safinamide-d4-1

    FCE 26743-d4-1; EMD 1195686-d4-1

    		 Isotope-Labeled Compounds Monoamine Oxidase Neurological Disease
    Safinamide-d4-1 is deuterium labeled Safinamide. Safinamide is a potent, selective, and reversible monoamine oxidase B (MAO-B) inhibitor (IC50=0.098 µM) over MAO-A (IC50=580 µM)[1]. Safinamide also blocks sodium channels and modulates glutamate (Glu) release, showing a greater affinity at depolarized (IC50=8 µM) than at resting (IC50=262 µM) potentials. Safinamide has neuroprotective and neurorescuing effects and can be used for the study of parkinson disease, ischemia stroke etc.al[2][3].
    Safinamide-d4-1

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