Target intelligence / Profile preview

Histone acetyltransferase KAT6B (KAT6B)

Target
KAT6B
Molecular classification
Enzyme, Histone acetyltransferase, Histone modification, Epigenetic regulator
01

Overview

Histone acetyltransferase KAT6B (KAT6B) is an enzyme in the MYST family of lysine acetyltransferases that catalyzes the acetylation of lysine residues on histone proteins, particularly histone H3, thereby regulating gene activation and chromatin accessibility[1][2][3]. KAT6B forms stable complexes with other nuclear proteins, such as ING5, BRPF1, and KAT6A, and it plays a central role in the epigenetic control of gene expression during embryonic development, neurogenesis, and osteogenesis[2]. Germline loss-of-function or gain-of-function mutations in KAT6B are associated with rare congenital syndromes such as genitopatellar syndrome and the Say-Barber-Biesecker-Young-Simpson variant of Ohdo syndrome, characterized by skeletal, neurological, and genital abnormalities[1][2]. Somatic chromosomal rearrangements involving KAT6B are linked to acute myeloid leukemia, therapy-related myelodysplastic syndrome, and uterine leiomyoma, suggesting a role in tumorigenesis through dysregulation of histone acetylation and gene control[1][2]. No established drugs directly target KAT6B in the clinic, but it remains a putative therapeutic target in oncology and developmental disorders due to its critical role in chromatin modification and gene regulation.

Other names
Lysine acetyltransferase 6BMYST4MORFLysine (K) acetyltransferase 6B
02

Mechanism of action

Inhibition of KAT6B enzyme activity (for investigational agents); Disruption of histone acetylation and epigenetic gene regulation

03

Biological functions

Regulation of gene expressionChromatin remodelingCell differentiationCell cycle regulationNeurogenesisSkeletal developmentEmbryonic development
04

Disease associations

CancerIntellectual disability syndromes (e.g., Genitopatellar syndrome, Say-Barber-Biesecker-Young-Simpson syndrome)Growth retardationUterine leiomyoma (fibroids)
05

Safety considerations

Potential developmental toxicity from inhibition (due to essential role in embryonic and neural development)Risk of off-target effects on gene expression
06

Interacting drugs

No approved or widely reported small molecule inhibitors or drugs known to directly target KAT6B in current clinical use; investigational histone acetyltransferase inhibitors may interact but none are specifically indicated in major sources for KAT6B as a primary target.
07

Biomarkers

KAT6B mutation status (for congenital developmental disorders)KAT6B chromosomal rearrangement (in leukemia and some tumors)

Beyond the preview

Go deeper on Histone acetyltransferase KAT6B (KAT6B).

Explore the evidence, development activity, and competitive landscape with Gosset’s full data platform.

Drug pipeline

Full profile access

Explore the programs pursuing this target and their development progress.

  • Drug candidates
  • Developers
  • Development stage

Clinical trials

Full profile access

Follow the clinical studies evaluating therapies directed at this target.

  • Trial design
  • Status
  • Readouts

Competitive landscape

Full profile access

Compare approaches across drug candidates, modalities, and indications.

  • Programs
  • Modalities
  • Indications

Literature & evidence

Full profile access

Investigate the research and source evidence behind target biology and development.

  • Publications
  • Sources
  • Analysis

Patents

Full profile access

Explore patent activity around therapies and technologies addressing this target.

  • Patents
  • Assignees
  • Technologies

Research & analysis

Full profile access

Connect target biology, drug development, and emerging evidence in your research.

  • Biology
  • Development news
  • Analysis

Bring the full picture into focus.

See how Gosset can support your research on Histone acetyltransferase KAT6B (KAT6B).

Explore the full profile

Gosset Free

Get started with Gosset.

Enter your work email and we’ll be in touch with next steps.

Work email preferred.

Book a call