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04/20/2026

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04/08/2026

The lunasin peptide stands out as the only biological agent in nature known to specifically inhibit histone H3 lysine 14 acetylation (H3K14ac). This unique property could have important implications for therapeutic applications, given how critical histone modifications are to gene regulation. If you would like to discuss further or explore potential opportunities, please let me know.

The lunasin peptide is the only biological agent in nature to specifically inhibit histone H3 lysine 14 acetylation (H3K14ac).

Here are the research studies on the epigenetic biomarker, H3K14ac, its associated histone acetyltransferase enzyme, KAT7/HBO1, and their involvement in aging and chronic disease development.

1) Review article
H3K14: A histone site closely related to diseases
https://pmc.ncbi.nlm.nih.gov/articles/PMC12374959/

2) Cellular Senescence (Cellular Aging)
A genome-wide CRISPR-based screen identifies KAT7 as a driver of cellular senescence
https://www.science.org/doi/10.1126/scitranslmed.abd2655

3) Alzheimer’s disease and neuroinflammation
Epigenetic control of microglial mitochondrial immunity by KAT7 drives Alzheimer’s disease pathogenesis
https://www.biorxiv.org/content/10.64898/2026.02.19.706884v1

4) Cardiovascular disease and inflammation
Increased acetylation of H3K14 in the genomic regions that encode trained immunity enzymes in lysophosphatidylcholine-activated human aortic endothelial cells – Novel qualification markers for chronic disease risk factors and conditional DAMPs
https://www.sciencedirect.com/science/article/pii/S2213231719303866

Kat7 contributes to ponatinib-induced hypertension by promoting endothelial senescence and inflammatory responses through activating NF-KappaB signaling pathway
https://journals.lww.com/jhypertension/fulltext/2025/05000/kat7_contributes_to_ponatinib_induced_hypertension.14.aspx

5) Breast Cancer
A chemical toolbox for the study of bromodomains and epigenetic signaling
https://www.nature.com/articles/s41467-019-09672-2

6) Colorectal Cancer
Targeting KAT7 inhibits the progression of colorectal cancer
https://www.thno.org/v15p1478.htm

7) Ovarian Cancer
HBO1 determines epithelial-mesenchymal transition and promotes immunotherapy resistance in ovarian cancer cells
https://link.springer.com/article/10.1007/s13402-025-01055-8

8) Leukemia
KAT7 is a genetic vulnerability of acute myeloid leukemias driven by MLL rearrangements
https://www.nature.com/articles/s41375-020-1001-z

HBO1 is required for the maintenance of leukemia stem cells
https://www.nature.com/articles/s41586-019-1835-6

Histone acetylation by HBO1 (KAT7) activates Wnt/B-catenin signaling to promote leukemogenesis in B-cell acute lymphoblastic leukemia
https://www.nature.com/articles/s41419-023-06019-0

9) Prostate Cancer
BAZ2A-mediated repression via H3K14ac-marked enhancer promotes prostate cancer stem cells
https://link.springer.com/article/10.15252/embr.202153014

03/24/2026

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03/23/2026

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03/11/2026

For more info about lunasin: https://wealththrunutrition.com/lunasin/

KAT7 drives Alzheimer’s disease pathogenesis

KAT7 (also known as HBO1) is a histone acetyltransferase that selectively acetylates the fourteenth lysine residue (H3K14) from the N-terminus of histone H3.

A new study from Johns Hopkins School of Medicine has identified KAT7 as a key epigenetic driver of Alzheimer’s disease (AD) by promoting pathogenic microglial activation.
(https://www.biorxiv.org/content/10.64898/2026.02.19.706884v1).

KAT7 and H3K14ac levels are significantly increased in microglia from AD mouse models and human AD brains.

Elevated KAT7 and H3K14ac in microglia increase expression of Cmpk2, enhancing mitochondrial DNA (mtDNA) release that activates innate immunity signaling (cGAS-STING and NLRP3) , and turning microglia into a pro-inflammatory, pathogenic state that leads to chronic neuroinflammation.

Inhibition of KAT7 and H3K14ac reduces this neuroinflammation, decreases amyloid-β burden, and improves cognitive function in Alzheimer's disease models.

This study identifies microglia-driven neuroinflammation as an alternative causal mechanism for Alzheimer's disease, challenging the traditional amyloid hypothesis. Furthermore, it highlights KAT7 and the inhibition of H3K14ac as potential therapeutic targets for intervention.

The lunasin peptide is the only naturally occurring biological agent that inhibits H3K14ac, acting not through KAT7 inactivation but by binding directly to the H3K14 substrate and preventing its acetylation.