2. NF-κB Autophagy
  3. IKK NF-κB Autophagy
  4. IKKβ-IN-5

IKKβ-IN-5 is an orally active and selective IKKβ inhibitor with an IC50 of 7.5 nM. IKKβ-IN-5 directly inhibits IKKβ phosphorylation and attenuates NF κB mediated inflammatory and survival signals while promoting autophagy flux. IKKβ-IN-5 exhibits a 6-fold selectivity forIKKβ over the homologous kinase IKKα. IKKβ-IN-5 exerts robust antiproliferative effects through a dual mechanism involving G₂/M phase cell cycle arrest and autophagy activation, even under inflammatory stimulation in vitro. IKKβ-IN-5 demonstrates favorable pharmacokinetics and suppresses tumor growth in vivo. IKKβ-IN-5 can be used for colorectal cancer and potentially other inflammation driven malignancies research.

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IKKβ-IN-5

IKKβ-IN-5 Chemical Structure

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IKKβ-IN-5 Related Antibodies

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IKK-α IKK-β IKK IKKε TBK1

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NF-κB NF-κB1/p50 RelA/p65 RelB c-Rel

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Description

IKKβ-IN-5 is an orally active and selective IKKβ inhibitor with an IC50 of 7.5 nM. IKKβ-IN-5 directly inhibits IKKβ phosphorylation and attenuates NF κB mediated inflammatory and survival signals while promoting autophagy flux. IKKβ-IN-5 exhibits a 6-fold selectivity forIKKβ over the homologous kinase IKKα. IKKβ-IN-5 exerts robust antiproliferative effects through a dual mechanism involving G₂/M phase cell cycle arrest and autophagy activation, even under inflammatory stimulation in vitro. IKKβ-IN-5 demonstrates favorable pharmacokinetics and suppresses tumor growth in vivo. IKKβ-IN-5 can be used for colorectal cancer and potentially other inflammation driven malignancies research[1].

IC50 & Target[1]

IKK-β

7.5 nM (IC50)

In Vitro

IKKβ-IN-5 (compound LP46) (0-2 μM, 48 h) exhibits robust antiproliferative activity in RKO and HCT116 cells and low toxicity in NCM460 cells[1].
IKKβ-IN-5 (0.75-3.0 μM, 48 h) impacts protein expression of IKKβ phosphorylation and its downstream target IκBα by directly inhibiting the phosphorylation of IKKβ in RKO and HCT116 cells[1].
IKKβ-IN-5 (0.75-3.0 μM, 7 days) has long-term antiproliferative effects in RKO and HCT116 cells[1].
IKKβ-IN-5 (0.75-3.0 μM, 48 h) exerts the antiproliferative effects through a dual mechanism ( including inducing G2/M phase cell cycle arrest and activating autophagy) even in the presence of inflammatory stimuli, and has ability to block NF-κB pathway activation suppressing downstream inflammatory responses in RKO and HCT116 cells[1].
IKKβ-IN-5 (3 μM, 48 h) directly counteracts IKKβ-mediated pro-inflammatory and ant autophagy effects in IKKβ knockdown CRC cells or IKKβ overexpression CRC cells[1].

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

IKKβ-IN-5 Related Antibodies

Cell Viability Assay[1]

Cell Line: HCT116, RKO, and NCM460 cells
Concentration: 0, 0.4 0.8, 1.2, 1.6 and 2.0 μM
Incubation Time: 48 h
Result: Exhibited potent inhibitory activity, with IC50 values of 3.94 μM for RKO and 2.59 μM for HCT116.
Showed significantly lower toxicity in NCM460 cells, with an IC50 of 21.25 μM.

Western Blot Analysis[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 48 h
Result: Significantly reduced phosphorylation of both IKKβ and IκBα in a dose-dependent manner.
Induced greater inhibition of IKKβ phosphorylation.
Had no significant impact on either the expression or phosphorylation of TAK1 or MAP3K1.

Cell Proliferation Assay[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 7 days
Result: Observed Dose-dependent suppression of colony formation.
Demonstrated superior efficacy at the highest dose.

Cell Cycle Analysis[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 48 h
Result: Revealed a significant accumulation of RKO and HCT116 cells in the G2/M phase.

Cell Proliferation Assay[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 48 h
Result: Significantly inhibited DNA synthesis in both RKO and HCT116 cells.

Western Blot Analysis[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 48 h
Result: Dose-dependently increased expression levels of key autophagy-related markers, Beclin1 and LC3A/B both markers in RKO and HCT116 cells.
Enhanced expression of Beclin1 and LC3A/ B in these cells in RKO and HCT116 cells with TNF-α (HY-P1875).
Reduced p65 expression and inhibited its nuclear translocation in a dose-dependent manner.

RT-PCR[1]

Cell Line: RKO and HCT116 cells
Concentration: 0.75, 1.5, and 3 μM
Incubation Time: 48 h
Result: Significantly down regulated the expression of TNF-α, IL-6, and IL-1β in a dose dependent manner.

Western Blot Analysis[1]

Cell Line: IKKβ knockdown CRC cells or IKKβ overexpression CRC cells
Concentration: 3 μM
Incubation Time: 48 h
Result: Reduced the phosphorylation levels of both IκBα and p65, while concurrently increasing the expression of key autophagy markers, Beclin1 and LC3A/B and exhibited superior efficacy in inhibiting IKKβ phosphorylation and suppressing NF-κB signaling upon TNF-α stimulation in IKKβ knockdown cells.
Increased p-IκBα and p-p65 levels and reduced Beclin1 and LC3A/B expression upon TNF-α stimulation in overexpression of IKKβ cells.
Decreased NF-κB phosphorylation and restoration of autophagy-related protein levels, even under TNF-α stimulation and IKKβ-overexpressing conditions.

Cell Viability Assay[1]

Cell Line: HCT116, RKO, and NCM460 cells
Concentration: 0, 0.4 0.8, 1.2, 1.6 and 2.0 μM
Incubation Time: 48 h
Result: Exhibited potent inhibitory activity, with IC50 values of 3.94 μM for RKO and 2.59 μM for HCT116.
Showed significantly lower toxicity in NCM460 cells, with an IC50 of 21.25 μM.
Molecular Weight

417.48

Formula

C23H24FN7
SMILES

FC1=CN=C(N=C1C2=CC=C(C3=C2)C=NN3C)NC4=CC(N5CCN(CC5)C)=CC=C4
Shipping

Room temperature in continental US; may vary elsewhere.
Storage

Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
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IKKβ-IN-5 Related Classifications

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Help & FAQs
  • Do most proteins show cross-species activity?

    Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

Keywords:

IKKβ-IN-5IKKNF-κBAutophagyIκB kinaseI kappa B kinase Nuclear factor-κBNuclear factor-kappaBG?/M phase cell cycle colorectal cancerIKKβautophagyInhibitorinhibitorinhibit

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