PKR-IN-C16

Catalog No.S9668 Batch:S966802

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Technical Data

Formula

C13H8N4OS
Molecular Weight 268.29 CAS No. 608512-97-6
Solubility (25°C)* In vitro DMSO 14 mg/mL (52.18 mM)
Water Insoluble
Ethanol Insoluble
In vivo (Add solvents to the product individually and in order)
Clear solution
5%DMSO 40%PEG300 5%Tween80 50%ddH2O
0.35mg/ml Taking the 1 mL working solution as an example, add 50 μL of 7 mg/ml clarified DMSO stock solution to 400 μL of PEG300, mix evenly to clarify it; add 50 μL of Tween80 to the above system, mix evenly to clarify; then continue to add 500 μL of ddH2O to adjust the volume to 1 mL. The mixed solution should be used immediately for optimal results. 
Clear solution
5% DMSO 95% Corn oil
0.35mg/ml Taking the 1 mL working solution as an example, add 50 μL of 7 mg/ml clear DMSO stock solution to 950 μL of corn oil and mix evenly. The mixed solution should be used immediately for optimal results. 
* <1 mg/ml means slightly soluble or insoluble.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

Biological Activity

Description PKR-IN-C16 (imoxin, C16, Imidazolo-oxindole PKR inhibitor C16) is a specific inhibitor of RNA-dependent protein kinase (PKR, Protein Kinase R, EIF2AK2). PKR-IN-C16 prevents apoptosis and IL-1β production in an acute excitotoxic rat model with a neuroinflammatory component.
Targets
PKR [1] IL-1β [1]
In vitro

PKR-IN-C16 suppresses proliferation of HCC cells in a dose-dependent manner in vitro. Transcript levels of vascular endothelial growth factor-A and factor-B, platelet-derived growth factor-A and factor-B, fibroblast growth factor-2, epidermal growth factor, and hepatocyte growth factor, which are angiogenesis-related growth factors, are significantly decreased by PKR-IN-C16 in vitro. PKR-IN-C16 blockes tumor cell growth and angiogenesis via a decrease in mRNA levels of several growth factors.[2]
In vivo

Inflammation is induced by unilateral striatal injection of quinolinic acid (QA) in 10-week-old normotensive rats. The highest dose of C16 (600 μg/kg; C16-2) in QA rats reduces expression of the active catalytic domain of the PKR vs. that in vehicle-injected QA rats. A robust increase of IL-1b levels on the contralateral side of QA rats is prevented by C16-2 (97% inhibition). Macroscopic and microscopic observation of cerebral tissue revealed that tissue integrity is more preserved with C16-2 treatment than its vehicle in QA rats. Furthermore, C16-2 treatment decreases by 47% the neuronal loss and by 37% the number of positive cleaved caspase-3 neurons induced by QA injection. In conclusion, C16 prevents not only the PKR-induced neuronal loss but also the inflammatory response in this acute excitotoxic in vivo model, highlighting its promising neuroprotective properties to rescue acute brain lesions.[1]

Protocol (from reference)

Cell Assay:

[2]
  • Cell lines

    Huh7 cells

  • Concentrations

    500–3000 nM

  • Incubation Time

    120 min

  • Method

    In vitro cell viability is quantified with the MTS assay. Huh7 cells treated with several concentrations (500–3000  nM) of the PKR inhibitor are seeded in 96-well plates at 2 × 103 cells per well. At each time point, cells are treated with MTS reagent and incubated for 120 min. Absorbance at 450 nm is recorded. Cells treated with DMSO are used as controls. The wells are photographed under the microscope.
Animal Study:

[1]
  • Animal Models

    10-week-old male normotensive male Wistar rats

  • Dosages

    60 μg/kg, 600 μg/kg

  • Administration

    IP

Selleck's PKR-IN-C16 has been cited by 5 publications

Nucleus pulposus cells regulate macrophages in degenerated intervertebral discs via the integrated stress response-mediated CCL2/7-CCR2 signaling pathway [ Exp Mol Med, 2024, 56(2):408-421.] PubMed: 38316963
Sterile inflammation via TRPM8 RNA-dependent TLR3-NF-kB/IRF3 activation promotes antitumor immunity in prostate cancer [ EMBO J, 2024, 43(5):780-805.] PubMed: 38316991
GDF15 ameliorates sepsis-induced lung injury via AMPK-mediated inhibition of glycolysis in alveolar macrophage [ Respir Res, 2024, 25(1):201] PubMed: 38725041
Exploiting polypharmacology to dissect host kinases and kinase inhibitors that modulate endothelial barrier integrity [ Cell Chem Biol, 2021, S2451-9456(21)00303-2] PubMed: 34216546
PKR deficiency alleviates pulmonary hypertension via inducing inflammasome adaptor ASC inactivation [ Pulm Circ, 2021, 11(4):20458940211046156] PubMed: 34540200

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SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

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