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3D molecular structure with a yellow highlight on a blue background.
3D molecular structure with a yellow highlight on a blue background.

KAT6/7

Targeting epigenetic vulnerabilities through dual inhibition of KAT6 and KAT7 to drive synthetic lethality in cancer.

Targeting epigenetic drivers of cancer

Cancer is driven not only by genetic mutations, but also by dysregulation of epigenetic machinery that controls gene expression.1

KAT6 and KAT7 are lysine acetyltransferases that regulate how DNA is packaged and accessed. By opening chromatin structure, they enable activation of genes that promote tumor growth—and are often upregulated in cancer.2,3

Targeting either enzyme alone is often insufficient, as functional overlap enables tumor cells to compensate and survive.4,5

Diagram showing HDACs closing chromatin and HATs opening chromatin for gene expression. Diagram showing HDACs closing chromatin and HATs opening chromatin for gene expression.

Turning epigenetic redundancy into therapeutic vulnerability

IDEAYA is advancing a dual-inhibition strategy to convert this redundancy into a precision therapeutic opportunity. By simultaneously targeting KAT6 and KAT7, this approach with IDE574 creates a synthetic lethal state that disrupts tumor cell gene regulation and survival.4

A dual-targeting strategy designed to overcome resistance

Breaking redundancy

Inhibiting both KAT6
and KAT7 removes compensatory escape mechanisms5

Inducing synthetic lethality

Dual inhibition disables essential gene-expression pathways required for tumor survival6

Preventing adaptive resistance

Limits the emergence of resistant tumor cell populations7


This approach reflects IDEAYA’s precision medicine strategy, transforming biological redundancy into a targeted vulnerability to deliver deeper and more durable responses than single-agent therapies.