Apigenin binds to IKK directly, inhibiting IKK kinase activity and suppressing NF-B/p65 activation in human prostate cancer cells far more efficiently than an IKK inhititor
Again, Codeage offers Liposomal Apigenin
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9505045/
2.7. NF-κB Signaling
Apigenin suppressed prostate cancer in TRAMP rats by interfering with NFκ-B activation in microgram dosages. Apigenin administration to TRAMP mice resulted in a significant reduction in prostate tumour sizes and the complete elimination of metastasis, which was linked to the suppression of DNA binding and NFκ-B activation. Furthermore, after apigenin feeding, NFκ-B-regulated gene products expression implicated in proliferation (COX-2 as well as cyclin D1), anti-apoptosis, and angiogenesis was downregulated [27].
Apigenin binds to IKK directly, inhibiting IKK kinase activity and suppressing NF-B/p65 activation in human prostate cancer cells far more efficiently than an IKK inhibitor. Apigenin was also shown to trigger cell cycle arrest in prostate cancer cells, similar to knocking down IKK. Moreover, the inhibition of cell proliferation, invasiveness and decrease in tumor growth by apigenin are mediated by its ability to suppress IKKα and downstream targets affecting NF-ĸB signaling pathways [26].
The interactions between apigenin and TRAIL in non-small cell lung cancer cells was determined. The synergistic effect between apigenin and TRAIL on the apoptosis of cancer cells was observed. In the meantime, apigenin suppressed NF-κB, ERK, and AKT activation. Furthermore, apigenin inhibited the prosurvival regulators NF-B, ERK and AKT, resulting in antitumor action in lung cancer cells stimulated by TRAIL [28].