1. NF-κB
  2. IKK

IKK 16 

Cat. No.: HY-13687 Purity: 99.78%
Data Sheet SDS Handling Instructions

IKK 16 is a selective IκB kinase (IKK) inhibitor for IKK-2, IKK complex and IKK-1 with IC50s of 40 nM, 70 nM and 200 nM, respectively.

For research use only. We do not sell to patients.
IKK 16 Chemical Structure

IKK 16 Chemical Structure

CAS No. : 873225-46-8

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Free Sample (0.5-1 mg)   Apply now  
10 mM * 1 mL in DMSO USD 191 In-stock
10 mg USD 174 In-stock
50 mg USD 714 In-stock
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    IKK 16 purchased from MCE. Usage Cited in: Respir Res. 2017 Sep 20;18(1):174.

    BECs are pretreated with specific STAT6 inhibitor (AS1517499) or a selective IκB kinase inhibitor (IKK 16) for half an hour, then treated for 24 h in the presence or absence of 20 ng/mL IL-4. Immunofluorescence staining of MUC5AC protein is performed according to the Methods.

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    Description

    IKK 16 is a selective IκB kinase (IKK) inhibitor for IKK-2, IKK complex and IKK-1 with IC50s of 40 nM, 70 nM and 200 nM, respectively.

    IC50 & Target

    IC50: 40 nM (IKK-2), 70 nM (IKK complex), 200 nM (IKK-1)[1]

    In Vitro

    IKK 16 is a potent inhibitor of IKK2 with IC50 value of 40 nM[1]. IKK 16 increases the expression of Nrf2 but it has no effect on TGF-β1-induced endothelial-mesenchymal transition (EndMT). IKK-16 has the ability to enhance the expression of IκBα and Nrf2. IKK 16 (10 μmol/mL) has the ability to enhance the expression of IκBα and Nrf2 but it has no effect on Smad7 expression. In addition, the AT-RvD1 can also enhance the expression of IκBα[2].

    In Vivo

    IKK 16 also demonstrates significant in vivo activity in an acute model of cytokine release. Both routes of administration of IKK 16 (30 mg/kg, sc) or orally (30 mg/kg, p.o) at the indicated dose results in a significant inhibition of 86% (sc) and 75% (p.o.).IKK 16(10 mg/kg, sc) is also active in the thioglycollate-induced peritonitis model in the mouse. The maximal inhibition of neutrophil extravasation in this model is about 50%[1]. Treatment of septic mice with IKK 16 (1 mg/kg body weight i.v.) results in a significantly increased degree of phosphorylation (P<0.05) of serine residues on Akt and eNOS in the liver[3].

    References
    Preparing Stock Solutions
    Concentration Volume Mass 1 mg 5 mg 10 mg
    1 mM 2.0677 mL 10.3385 mL 20.6770 mL
    5 mM 0.4135 mL 2.0677 mL 4.1354 mL
    10 mM 0.2068 mL 1.0338 mL 2.0677 mL
    Please refer to the solubility information to select the appropriate solvent.
    Cell Assay
    [2]

    IKK 16 is prepared in DMSO and stored, and then diluted with appropriate medium before use[2].

    Human umbilical vein vascular endothelial cells line (HUVECs) are cultured in DMEM supplemented with 10% fetal bovine serum, streptomycin, and penicillin. The cells is grown at 37°C in a humidified 5% CO2 atmosphere. Cells are pretreated with IKK 16 (10 μmol/mL) for 1 hr. The cells are then cultured with TGF-β1 (20 ng/mL) and AT-RvD1 (20 ng/mL). After incubation, the gene expressions of Nrf2 and Smad7 are determined by RT-PCR. The protein expression of Nrf2 and IκBα are determined by Western blot[2]. MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Administration
    [3][1]

    IKK 16 is prepared in DMSO and diluted with saline or PBS.

    Rats and Mice[1]
    IKK 16 is tested in two animal models. First, its efficacy to inhibit TNFα release into plasma upon LPS-challenge in the rat is determined. IKK 16 is dosed sc (30 mg/kg) or orally (30 mg/kg) 1 h prior to the LPS-challenge. Four hours after the challenge, plasma is collected and the systemic TNFα levels are analyzed using a commercially available ELISA kit. Both routes of administration of IKK 16 at the indicated dose results in a significant inhibition of 86% (sc) and 75% (p.o.). In a second experiment, IKK 16 is also active in the thioglycollate-induced peritonitis model in the mouse. The maximal inhibition of neutrophil extravasation in this model is about 50% at a dose of 10 mg/kg sc.
    Mice[3]
    Two-month-old male C57BL/6 mice receive LPS (9 mg/kg body weight) and PepG (3 mg/kg body weight) in 0.9% saline (5 mL/kg body weight) intraperitoneally. Sham mice are not subjected to LPS/PepG, but are otherwise treated the same way. At 1 hour after LPS/PepG co-administration, mice are treated either with IKK 16 (1 mg/kg body weight i.v.) or vehicle (5 mL/kg body weight 10% DMSO i.v.). At 24 hours the experiment is terminated and organ and blood samples are collected for quantification of organ dysfunction and/or injury. Mice are randomly allocated into four different groups: (1) sham+vehicle (n=10); (2) sham+IKK 16 (n=3); (3) LPS/PepG+vehicle (n=9); (4) LPS/PepG+IKK 16 (n=10). MCE has not independently confirmed the accuracy of these methods. They are for reference only.

    References
    Molecular Weight

    483.63

    Formula

    C₂₈H₂₉N₅OS

    CAS No.

    873225-46-8

    Storage
    Powder -20°C 3 years
      4°C 2 years
    In solvent -80°C 6 months
      -20°C 1 month
    Shipping

    Room temperature in continental US; may vary elsewhere

    Solvent & Solubility

    DMSO: ≥ 27 mg/mL

    * "<1 mg/mL" means slightly soluble or insoluble. "≥" means soluble, but saturation unknown.

    Purity: 99.78%

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    IKK 16
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