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Results for "

decay

" in MedChemExpress (MCE) Product Catalog:

17

Inhibitors & Agonists

1

Fluorescent Dye

1

Peptides

1

Natural
Products

4

Recombinant Proteins

1

Antibodies

1

Oligonucleotides

Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-W012642

    DNA Stain Others
    2-Aminopurine, a fluorescent analog of guanosine and adenosine, is a widely used fluorescence-decay-based probe of DNA structure. When 2-Aminopurine is inserted in anoligonucleotide, its fluorescence is highly quenched by stacking with the natural bases. 2-Aminopurine has been used to probe nucleic acid structure and dynamics .
    2-Aminopurine
  • HY-161111

    Others Cancer
    KVS0001 is a potent inhibitor of SMG1 and nonsense mediated decay (NMD) that has anti-tumor activity .
    KVS0001
  • HY-111374
    NMDI14
    3 Publications Verification

    Others Cancer
    NMDI14 is a nonsense mediated RNA decay (NMD) inhibitor. NMDI14 disrupts the SMG7-UPF1 interactions and inhibits NMD.
    NMDI14
  • HY-B2053

    Bacterial Infection
    Tolclofos-methyl is a broad-spectrum aromatic hydrocarbon fungicide that is used as a see treatment for protection against soil-borne and seed borne fungal pathogens that caused seed decay and seedling blights.
    Tolclofos-methyl
  • HY-153475

    IRE1 Cancer
    IRE1α kinase-IN-9 (compound 2) is a potent IRE-1α inhibitor,exhibits an average IC50 value of <0.1 μM. IRE1α kinase-IN-9 can be used for research in diseases associated with the unfolded protein response or with regulated IRE1-dependent decay (RIDD) .
    IRE1α kinase-IN-9
  • HY-153474

    IRE1 Others
    IRE1α kinase-IN-8, a benzoheterocyclecarboxaldehyde derivative, is a potent IRE-1α inhibitor. IRE1α kinase-IN-8 can be used for research in diseases associated with the unfolded protein response or with regulated IRE1-dependent decay (RIDD) .
    IRE1α kinase-IN-8
  • HY-167695

    Others Others
    Propiosyringone is derived from the breakdown of Eucalyptus globulus wood by wood-decaying fungi.
    Propiosyringone
  • HY-118202

    (-)-Methoxyverapamil

    Others Cardiovascular Disease
    (-)-Gallopamil exerts a selective modulation of the fast voltage-dependent inactivation. (-)-Gallopamil inhibits efficiently Cav1.2 constructs formed by β-subunits (promoting fast voltage-dependent inactivation). (-)-Gallopamil also accelerates the voltage-dependent phase of ICa decay (as well as the voltage-dependent decay of Ba 2+ currents). (-)-Gallopamil is promising for research of antiarrhythmics .
    (-)-Gallopamil
  • HY-118202A

    (-)-Methoxyverapamil hydrochloride

    Others Cardiovascular Disease
    (-)-Gallopamil (hydrochloride) exerts a selective modulation of the fast voltage-dependent inactivation. (-)-Gallopamil (hydrochloride) inhibits efficiently Cav1.2 constructs formed by β-subunits (promoting fast voltage-dependent inactivation). (-)-Gallopamil (hydrochloride) also accelerates the voltage-dependent phase of ICa decay (as well as the voltage-dependent decay of Ba 2+ currents). (-)-Gallopamil (hydrochloride) is promising for research of antiarrhythmics .
    (-)-Gallopamil hydrochloride
  • HY-103501

    GABA Receptor Neurological Disease
    SB-205384 is a GABAA receptor modulator. The primary effect of SB-205384 on GABAA-activated currents is a prolonged response decay half-life upon removal of the agonist .
    SB-205384
  • HY-138100

    (+)-Hyalodendrin

    Fungal Infection
    Hyalodendrin ((+)-Hyalodendrin) is a fungal growth inhibitor with inhibitory activity against wood decay fungi. Hyalodendrin has low phytotoxicity, with an acute toxicity (LD50) of 75 mg/kg in mice .
    Hyalodendrin
  • HY-100686

    GABA Receptor Neurological Disease
    U93631 is a GABAA receptor ligand of novel chemical structure with IC50 of 100 nM,and has been shown to induce a rapid, time-dependent decay of GABA-induced whole-cell Cl-currents in recombinant GABAA receptors.
    U93631
  • HY-145422

    IRE1 Apoptosis Others
    KIRA9 is a potent IRE1 inhibitor (IC50=4.8 μM in INS-1 cells). KIRA9 is able to fully engage the ATP-binding site of IRE1α. KIRA9 can block ER-localized mRNA decay and apoptosis .
    KIRA9
  • HY-126429

    Sodium Channel Neurological Disease
    Nav1.1 activator 1 (compound 4), a highly potent Nav1.1 activator with BBB penetration, increases decay time constant τ of Nav1.1 currents at 0.03 μM along with significant selectivity against Nav1.2, Nav1.5, and Nav1.6 .
    Nav1.1 activator 1
  • HY-101513
    eIF4A3-IN-1
    3 Publications Verification

    Eukaryotic Initiation Factor (eIF) Cancer
    eIF4A3-IN-1 (compound 53a) is a selective eukaryotic initiation factor 4A3 (eIF4A3) inhibitor (IC50=0.26 μM; Kd=0.043 μM), which binds to a non-ATP binding site of eIF4A3 and shows significant cellular nonsense-mediated RNA decay (NMD) inhibition at 10 and 3 μM and can be as a probe for further study of eIF4A3, the exon junction complex (EJC), and NMD .
    eIF4A3-IN-1
  • HY-150090
    SRI-41315
    1 Publications Verification

    CFTR Inflammation/Immunology
    SRI-41315 induces a prolonged pause at stop codons and suppresses PTCs (premature termination codons) associated with cystic fibrosis in immortalized and primary human bronchial epithelial cells, restoring CFTR (cystic fibrosis transmembrane conductance regulator) expression and function. SRI-41315 suppresses PTCs by reducing the abundance of the termination factor eRF1. SRI-41315 also potentiates aminoglycoside-mediated readthrough, leading to synergistic increases in CFTR activity .
    SRI-41315
  • HY-121143

    Cholinesterase (ChE) Neurological Disease
    Bis-Q is an acetylcholine (ACh) agonist that targets voltage-clamped muscle fibers of the fish Xenomystus nigris. Bis-Q exists in two forms: cis-Bis-Q (non-agonist) and trans-Bis-Q (agonist). Photoisomerization converts cis-Bis-Q to trans-Bis-Q, which induces agonist-induced currents. Channels activated by trans-Bis-Q and ACh have similar conductances and open times. Flashes increase the ratio of trans-Bis-Q to cis-Bis-Q until light equilibrium is reached. Further flashes transiently increase agonist-induced currents, indicating binding of trans-Bis-Q to desensitized receptors. Higher concentrations of cis-Bis-Q produce larger agonist-induced currents that decay exponentially. .
    Bis-Q

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