1. Cell Cycle/DNA Damage
    Autophagy
    Apoptosis
  2. PERK
    Autophagy
    Apoptosis
  3. ISRIB (trans-isomer)

ISRIB (trans-isomer) 

Cat. No.: HY-12495 Purity: 99.37%
Handling Instructions

ISRIB (trans-isomer) is a potent inhibitor of PERK with an IC50 of 5 nM.

For research use only. We do not sell to patients.

ISRIB (trans-isomer) Chemical Structure

ISRIB (trans-isomer) Chemical Structure

CAS No. : 1597403-47-8

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10 mM * 1 mL in DMSO USD 143 In-stock
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100 mg USD 780 In-stock
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Customer Review

Based on 5 publication(s) in Google Scholar

Top Publications Citing Use of Products

    ISRIB (trans-isomer) purchased from MCE. Usage Cited in: Oncogene. 2017 Nov 30;36(48):6738-6746.

    ISRIB reverses the expression of β-catenin. HCT116 cells are transfected and CT26.WT cells are infected for 48 and 72 h, respectively. The cells are treated with ISRIB (100 nM) for 24 h.
    • Biological Activity

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    Description

    ISRIB (trans-isomer) is a potent inhibitor of PERK with an IC50 of 5 nM.

    IC50 & Target[1]

    PERK

    5 nM (IC50)

    In Vitro

    Trans-ISRIB is 100-fold more potent (IC50=5 nM) than cis-ISRIB (IC50= 600 nM), indicating that the compound’s interaction with its cellular target is stereospecific. ISRIB reduces the viability of cells subjected to PERK-activation by chronic endoplasmic reticulum stress[1]. ISRIB substantially reverses the translational effects elicited by phosphorylation of eIF2α and induces no major changes in translation or mRNA levels in unstressed cells. eIF2α phosphorylation-induced stress granule (SG) formation is blocked by ISRIB[2].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    In Vivo

    ISRIB increases long-term memory in rodents. ISRIB-treated mice display significant enhancement in spatial and fear-associated learning. ISRIB displays a half-life in plasma of 8 hr and readily crossed the blood-brain barrier, quickly equilibrating with the central nervous system[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Molecular Weight

    451.34

    Formula

    C₂₂H₂₄Cl₂N₂O₄

    CAS No.

    1597403-47-8

    SMILES

    O=C(N[[email protected]@H]1CC[[email protected]@H](NC(COC2=CC=C(Cl)C=C2)=O)CC1)COC3=CC=C(Cl)C=C3

    Shipping

    Room temperature in continental US; may vary elsewhere.

    Storage
    Powder -20°C 3 years
    4°C 2 years
    In solvent -80°C 6 months
    -20°C 1 month
    Solvent & Solubility
    In Vitro: 

    DMSO : ≥ 38 mg/mL (84.19 mM)

    *"≥" means soluble, but saturation unknown.

    Preparing
    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 2.2156 mL 11.0781 mL 22.1562 mL
    5 mM 0.4431 mL 2.2156 mL 4.4312 mL
    10 mM 0.2216 mL 1.1078 mL 2.2156 mL
    *Please refer to the solubility information to select the appropriate solvent.
    References
    Cell Assay
    [1]

    U2OS cells are plated on 96-well plates and left to recover overnight. Cells are treated with either with 2 µg/ml tunicamycin or 100 nM thapsigargin in the presence or absence of 100 nM ISRIB or with ISRIB alone for the indicated and the level of eIF2α phosphorylation is determined[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [1]

    Mice: Intra-peritoneal (ip) route of administration is performed on 6-7 wk old female CD-1 mice. Animals receives a single, 5 mg/kg dose in groups of three mice/compound/route of administration. ISRIB is dissolved in DMSO then diluted 1:1 in Super-Refined PEG 400. Blood (80 μL) is collected from the saphenous vein at intervals post-dosing (20 min, 1 hr, 3 hr, 8 hr, 24 hr) in EDTA containing collection tubes and plasma is prepared for analysis. Compounds are detected by time-of-flight mass spectroscopy[1].

    MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References

    Purity: 99.37%

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    Keywords:

    ISRIB (trans-isomer)PERKAutophagyApoptosisProtein kinase R-like endoplasmic reticulum kinasePKR-like endoplasmic reticulum kinaseInhibitorinhibitorinhibit

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