1. NF-κB
  2. NF-κB
  3. SN50


Cat. No.: HY-P0151
Handling Instructions

SN50 is a cell permeable inhibitor of NF-κB translocation.

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

SN50 Chemical Structure

SN50 Chemical Structure

CAS No. : 213546-53-3

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1 mg USD 108 In-stock
Estimated Time of Arrival: December 31
5 mg USD 432 In-stock
Estimated Time of Arrival: December 31
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Customer Review

Based on 16 publication(s) in Google Scholar

Top Publications Citing Use of Products

    SN50 purchased from MCE. Usage Cited in: Inflammation. 2019 Feb;42(1):319-330.

    The protein expression of iNOS and COX-2 in TNF-α stimulated RAW264.7 cells with selectively co-cultured with SN50 and SiGDF11, as determined by western blot.

    SN50 purchased from MCE. Usage Cited in: Mol Cell Endocrinol. 2019 Nov.

    HUVECs are treated with HG (30 mM), IL-1β (10 ng/mL) and/or SN50 (50 μg/mL), an NF-κB inhibitor. After treatment for 48 h, the protein levels of NF-κB p65 and p-NF-κB p65 in the nucleus of HUVECs were determined using Western blotting. Histone H3 was used for normalization.

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    SN50 is a cell permeable inhibitor of NF-κB translocation.

    IC50 & Target[1]



    In Vitro

    Pretreatment with SN50 results in a significant reduction in amount of PI-positive cells at 12, 24, and 48 h time-point post TBI compared with vehicle-treated groups[1]. Topical SN50 suppresses nuclear factor-κB activation in local cells and reduces the incidence of epithelial defects/ulceration in healing corneas. Myofibroblast generation, macrophage invasion, activity of matrix metalloproteinases, basement membrane destruction, and expression of cytokines are all decreased in treated corneas compared with controls[2]. Treating the human gastric cancer cells SGC7901 with SN50 could significantly enhance the effects of LY294002 on inducing cell death after 24 h[3]. SN50 can inhibit translocation of NF-kB and production of inflammatory cytokines that are implicated in lipopolysaccharide (LPS)-induced lung injury[4].

    In Vivo

    Treatment with SN50 accelerates the recovery of motor functional outcome from 1st to 4th day. Animals subjected to SN50 pretreatment demonstrate a significant decrease in the visuospatial learning latencies relative to the control group at 7 and 8 days post-TBI. Pretreatment with SN50 results in a significant reduction of NF-κB p65 protein levels from 6 to 48 h post-TBI and TNF-a protein levels from 12 to 48 h post-TBI[1].

    Molecular Weight




    CAS No.




    Sequence Shortening





    Room temperature in continental US; may vary elsewhere.

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

    H2O : ≥ 50 mg/mL (17.98 mM)

    *"≥" means soluble, but saturation unknown.

    Stock Solutions
    Concentration Solvent Mass 1 mg 5 mg 10 mg
    1 mM 0.3595 mL 1.7976 mL 3.5952 mL
    5 mM 0.0719 mL 0.3595 mL 0.7190 mL
    10 mM 0.0360 mL 0.1798 mL 0.3595 mL
    *Please refer to the solubility information to select the appropriate solvent.
    Cell Assay

    SN50 is diluted in distilled sterilization water to create a stock solution. The final concentration of the SN50 solution used is 18 µM. Cell viability is assessed with MTT assay. To determine the effects of SN50 on enhancing the role of LY294002 on SGC7901 cells, cells are plated into 96-well microplates (7×1000 cells/well) and cultured for 24 h. Then LY294002 (50 µM), SN50 (18 µM) and LY294002+SN50 are added to the culture medium and cell viability is assessed with MTT 24 h after drug treatment[3].

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

    Animal Administration

    Mice: SN50 is prepared in saline (total volume: 1 μL, concentration: 0.1 μg/μL). SN50 is administered into the ipsilateral cerebral ventricle 10 min before TBI. After TBI, the bone flap is replaced, the scalp incision is sutured, and then mice are allowed to awaken and returned to their cages. Mice are killed at 1, 6, 12, 24, 48, and 72 h after operation. Loss of plasmalemma integrity is evaluated by intraperitoneal injection of PI 1 h before killing the animal[1].

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

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    SN50SN 50SN-50NF-κBNuclear factor-κBNuclear factor-kappaBInhibitorinhibitorinhibit

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