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Results for "

Long-term potentiation

" in MedChemExpress (MCE) Product Catalog:

26

Inhibitors & Agonists

3

Peptides

5

Natural
Products

1

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0403

    Apoptosis Inflammation/Immunology
    2,3,4',5-Tetrahydroxystilbene 2-O-β-D-glucoside (TSG) is an active product that can be extracted from Polygonum multiflorum Thunb. TSG has anti-inflammatory, antioxidative, anti-atherosclerotic, anti-apoptotic, and free radical scavenging activities, TSG is also indicated to facilitate long-term potentiation and learning and memory in both normal and pathological conditions .
    2,3,4',5-Tetrahydroxystilbene 2-O-β-D-glucoside
  • HY-Y0378

    (R)-Leucine

    Endogenous Metabolite Neurological Disease
    D-Leucine is a more potent anti-seizure agent than L-leucine. D-leucine potently terminates seizures even after the onset of seizure activity. D-leucine, but not L-leucine, reduces long-term potentiation but had no effect on basal synaptic transmission in vitro .
    D-Leucine
  • HY-P10235

    Amylin Receptor Neurological Disease
    Cyclic AC253 is an antagonist for amylin receptor, with IC50 of 0.3 μM. Cyclic AC253 exhibits neuroprotective efficacy against Aβ toxicity and abrogates Aβ-induced impairment of hippocampal long-term potentiation. Cyclic AC253 penetrate blood-brain barrier (BBB) .
    Cyclic AC253
  • HY-Y0378S

    (R)-Leucine-d10

    Isotope-Labeled Compounds Endogenous Metabolite Neurological Disease
    D-Leucine-d10 is the deuterium labeled D-Leucine. D-Leucine is a more potent anti-seizure agent than L-leucine. D-leucine potently terminates seizures even after the onset of seizure activity. D-leucine, but not L-leucine, reduces long-term potentiation but had no effect on basal synaptic transmission in vitro .
    D-Leucine-d10
  • HY-116673

    Histone Acetyltransferase Neurological Disease
    TTK21 is an activator of the histone acetyltransferases CBP/p300. TTK21 passes the blood–brain barrier, induces no toxicity, and reaches different parts of the brain when conjugated to glucose-based carbon nanosphere (CSP). TTK21 has beneficial implications for the brain functions of neurogenesis and long-term memory .CSP-TTK21 can ameliorate Aβ-impaired long-term potentiation (LTP). CSP-TTK21 may enhance the transcription of genes that promote synaptic health and cognitive function . CSP-TTK21 is orally effective and leads to improvements in motor functions, histone acetylation dynamics in a spinal injury rat model .
    TTK21
  • HY-103570

    mGluR Neurological Disease
    MCPG is a carboxylic phenyl glycine. MCPG can block metabotropic glutamate receptor (mGluR)(HY-15129) and has antagonistic activity of mGluR subtype. MCPG can be used to study the induction and maintenance of long-term potentiation (LTP) .
    MCPG sodium
  • HY-120386

    iGluR Neurological Disease
    LY382884 is a selective antagonist for GluR5 kainate receptor. LY382884 prevents the induction of NMDA receptor independent long-term potentiation (LTP) .
    LY382884
  • HY-176550

    Sodium Channel Neurological Disease
    ASIC1a antagonist-1 (Compound 5b) is an orthosteric noncompetitive Acid sensing ion channels 1a (ASIC1a) antagonist with an IC50 of 27 nM (pH 6.7). ASIC1a antagonist-1 shifts pH dependence of ASIC1a activation and inhibits its maximal evoked response. ASIC1a antagonist-1 completely inhibits long-term potentiation (LTP) induction in CA3-CA1 pathway. ASIC1a antagonist-1 can be used for brain diseases and pathologies research .
    ASIC1a antagonist-1
  • HY-111129

    Adenosine Receptor Neurological Disease
    CP-66713 is a selective adenosine A2 receptor antagonist, with Ki of 22 nM. CP-66713 inhibits induction of long-term potentiation of evoked synaptic potentials. CP-66713 can be used in the study of neurological diseases .
    CP-66713
  • HY-148250

    iGluR Neurological Disease
    TP-050 is a potent, orally active and selective NMDAR agonist with an EC50 value of 0.51 µM and 9.6 µM for GluN2A and GluN2D, respecticely. TP-050 can cross the blood-brain barrier (BBB). TP-050 induces hippocampal long-term (LPT) potentiation enhancemen and enhances neuronal signal transmission .
    TP-050
  • HY-Y0378R

    (R)-Leucine (Standard)

    Reference Standards Endogenous Metabolite Neurological Disease
    D-Leucine (Standard) is the analytical standard of D-Leucine. This product is intended for research and analytical applications. D-Leucine is a more potent anti-seizure agent than L-leucine. D-leucine potently terminates seizures even after the onset of seizure activity. D-leucine, but not L-leucine, reduces long-term potentiation but had no effect on basal synaptic transmission in vitro .
    D-Leucine (Standard)
  • HY-155687

    Phosphodiesterase (PDE) Neurological Disease
    PDE5-IN-10 (compound 4b) is a potent PDE5 inhibitor with an IC50 of 20 nM. PDE5-IN-10 improves in vitro microsomal stability (t1/2 = 44.6 min) as well as excellent efficacy in restoring long-term potentiation. PDE5-IN-10 can be used for Alzheimer’s disease (AD) research .
    PDE5-IN-10
  • HY-N2922

    Amyloid-β NF-κB Neurological Disease Inflammation/Immunology
    β-Amyrin shows effectively counteract amyloid β (Aβ)-induced impairment of long-term potentiation (LTP). β-Amyrin is a promising candidate for Alzheimer's disease (AD) research. β-Amyrin exhibits anti-inflammatory effects, protective activity against pulmonary fibrosis, and notable antibacterial capabilities. β-Amyrin is an orally active natural triterpenoid compound .
    β-Amyrin
  • HY-N2922R

    Reference Standards Amyloid-β Neurological Disease
    β-Amyrin shows effectively counteract amyloid β (Aβ)-induced impairment of long-term potentiation (LTP). β-Amyrin is a promising candidate for Alzheimer's disease (AD) research. β-Amyrin exhibits anti-inflammatory effects, protective activity against pulmonary fibrosis, and notable antibacterial capabilities. β-Amyrin is an orally active natural triterpenoid compound .
    β-Amyrin (Standard)
  • HY-171844

    iGluR Neurological Disease
    CX1739 is a low impact enhancer of AMPA-glutamate receptors (AMPARs). CX1739 enhances long-term potentiation dose-dependently in mouse model. CX1739 also abrogates amphetamine-induced locomotor activity. CX1739 rapidly reverses opioid-induced respiratory depression. CX1739 can be studied in research for dementia, neuropsychiatric disorders, and severe complication of opiate-induced suppression of endogenous inspiratory breathing rhythms .
    CX1739
  • 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-121299

    mCPBG

    5-HT Receptor Neurological Disease
    m-Chlorophenylbiguanide (mCPBG) is a potent high-affinity agonist of the 5-HT3 receptor, exhibiting an inhibitory effect on long-term potentiation (LTP) in the mossy fiber-CA3 system. mCPBG attenuates the magnitude of LTP at concentrations of 0.3-1 microM, demonstrating its role in modulating synaptic plasticity. Additionally, the impact of mCPBG on LTP is reversible by the GABAA receptor antagonist bicuculline, indicating a connection between its action and GABAergic neurotransmission.
    m-Chlorophenylbiguanide
  • HY-P3688

    Aβ (1-38); Aβ38

    Amyloid-β Neurological Disease
    β-Amyloid (1-38) (Aβ (1-38)) is a β-Amyloid (Aβ) peptide. β-Amyloid (1-38) interferes with the conversion of Aβ(1-42) to a β-sheet-rich aggregate. β-Amyloid (1-38) reverses the negative impact of Aβ(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an Aβ(1-42) phenotype in Caenorhabditis elegans .
    β-Amyloid (1-38)
  • HY-P3688A

    Aβ (1-38) TFA; Aβ38 TFA

    Amyloid-β Neurological Disease
    β-Amyloid (1-38) (Aβ (1-38)) TFA is a β-Amyloid (Aβ) peptide. β-Amyloid (1-38) TFA interferes with the conversion of Aβ(1-42) to a β-sheet-rich aggregate. β-Amyloid (1-38)TFA reverses the negative impact of Aβ(1-42) on long-term potentiation in acute hippocampal slices and on membrane conductance in primary neurons, and mitigates an Aβ(1-42) phenotype in Caenorhabditis elegans .
    β-Amyloid (1-38) TFA
  • HY-100617A

    (RS)-4-Carboxyphenylglycine

    mGluR Others
    (RS)-4CPG ((RS)-4-Carboxyphenylglycine) is a type I metabotropic glutamate receptor antagonist with activity in blocking LTP induction. In mice lacking IP3R1, (RS)-4CPG (500μM) nearly blocked long-term potentiation (LTP) induced by type I metabotropic glutamate receptor activation, with LTP of 117.6±1.7% (n = 8) in IP3R1(-/-) mice and 116.9±1.8% (n = 5) in IP3R1(+/+) mice.
    (RS)-4CPG
  • HY-156104

    PROTACs CaMK Neurological Disease
    CaMKIIα-PHOTAC is a photochemically targeted chimera (PHOTAC) targeting Ca2+/calmodulin-dependent protein kinase II α (CaMKIIα). Molecules such as PHOTAC can catalyze the ubiquitination and degradation of target proteins through the endogenous proteasome under specific wavelengths of light. CaMKIIα-PHOTAC reduces synaptic function under light conditions, and it attenuates the intensity of evoked field excitatory postsynaptic potentials in the mouse hippocampus in response to physiological stimuli. CaMKIIα-PHOTAC plays a critical role in maintaining long-term potentiation and memory capacity in subcellular dendritic domains .
    CaMKIIα-PHOTAC
  • HY-16728A

    GLYX-13 acetate

    iGluR Neurological Disease
    Rapastinel acetate (GLYX-13 acetate) is an N-methyl-D-aspartate (NMDA) receptor modulator with long-acting antidepressant activity. Rapastinel acetate exerts its antidepressant effects by enhancing long-term potentiation (LTP) of synaptic transmission. Rapastinel acetate transiently enhances NMDAR-mediated currents in pyramidal neurons in the hippocampus and medial prefrontal cortex by binding to unique sites on the NMDAR complex. Rapastinel acetate significantly enhanced NMDAR-mediated currents at a concentration of 1 μmol/l and significantly reduced the currents at a concentration of 10 μmol/l. The mechanism of action of Rapastinel acetate is related to the reduction of affinity to intracellular calcium inactivation sites, which provides a theoretical basis for enhancing conductance mediated by NMDAR .
    Rapastinel acetate
  • HY-107111

    mAChR Neurological Disease
    GSK1034702 is an orally active and allosteric agonist of M1 mAChR (pEC50=8.1) that can cross the blood-brain barrier. GSK1034702 activates the Gq/11 protein-mediated signaling pathway, enhancing neuronal firing and long-term potentiation (LTP) in the CA1 region of the hippocampus. GSK1034702 can modulate hippocampal function, improve memory encoding in the nicotine withdrawal cognitive dysfunction model, and show pro-cognitive effects in rodents. GSK1034702 can be used for the study of the mechanisms of cognitive impairment diseases such as Alzheimer's disease, and has certain peripheral M receptor activation-related side effects (such as gastrointestinal reactions) .
    GSK1034702
  • HY-107111A

    Cholinesterase (ChE) mAChR Neurological Disease
    GSK1034702 hydrochloride is an orally active and allosteric agonist of M1 mAChR (pEC50=8.1) that can cross the blood-brain barrier. GSK1034702 hydrochloride activates the Gq/11 protein-mediated signaling pathway, enhancing neuronal firing and long-term potentiation (LTP) in the CA1 region of the hippocampus. GSK1034702 hydrochloride can modulate hippocampal function, improve memory encoding in the nicotine withdrawal cognitive dysfunction model, and show pro-cognitive effects in rodents. GSK1034702 hydrochloride can be used for the study of the mechanisms of cognitive impairment diseases such as Alzheimer's disease, and has certain peripheral M receptor activation-related side effects (such as gastrointestinal reactions) .
    GSK1034702 hydrochloride
  • HY-116143

    MAGL Metabolic Disease
    SAR127303 is an orally active, selective, competitive monoacylglycerol lipase (MAGL) covalent inhibitor with IC50s of 3.8 nM and 29 nM for mouse and human MAGL, respectively. SAR127303 potently elevates hippocampal levels of 2-AG in mice. SAR127303 decreased long term potentiation (LTP) of CA1 synaptic transmission and acetylcholine release in the hippocampus. SAR127303 produces antinociceptive effects in assays of inflammatory and visceral pain. SAR127303 slows down epileptogenesis .
    MAGL-IN-12
  • HY-107601

    ACET

    iGluR Neurological Disease
    UBP316 (ACET) is a highly potent and selective kainate receptor GluK1 (GluR5) antagonist, with a Kb value of 1.4 nM. UBP316 is effective at blocking the depression of both field excitatory postsynaptic potentials (fEPSPs) and monosynaptically-evoked GABAergic transmission induced by ATPA, a GluK1 selective agonist .
    UBP316

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