Epigenetics

Epigenetics research delves into the molecular mechanisms that control gene expression and cellular traits without altering the underlying DNA sequence. One crucial aspect of this field is the role of small molecules, which act as powerful regulators of epigenetic modifications. These small compounds, typically comprising a few dozen to a few hundred atoms, have emerged as essential tools in understanding and manipulating the epigenome.

  • DNA Methylation Inhibitors: Small molecules like 5-azacytidine and 5-aza-2'-deoxycytidine are DNA methyltransferase inhibitors. They block the addition of methyl groups to DNA, leading to DNA demethylation. This can reactivate silenced genes, potentially offering therapeutic avenues for conditions like cancer.
  • HDAC inhibitors: HDACs remove acetyl groups from histone proteins, contributing to gene repression. Small molecule HDAC inhibitors, such as Vorinostat and Romidepsin, can reverse this process by increasing histone acetylation, allowing genes to be more accessible for transcription. These inhibitors are being explored for cancer therapy and other conditions.
  • Histone Methyltransferase Inhibitors: Small molecules like GSK126 inhibit specific histone methyltransferases, affecting histone methylation patterns. This can alter gene expression, making them promising candidates for cancer and other diseases with epigenetic dysregulation.
  • RNA Modulators: Small molecules can also target non-coding RNAs involved in epigenetic regulation. For instance, small molecules called small interfering RNAs (siRNAs) can be designed to target and degrade specific long non-coding RNAs, influencing gene expression.
  • Epigenetic Reader Domain Inhibitors: These small molecules target proteins that recognize and bind to specific epigenetic marks. Examples include inhibitors of bromodomain-containing proteins (BET inhibitors), which can disrupt gene regulation by interfering with protein-DNA interactions.

Small molecules in epigenetics research not only provide insights into the fundamental biology of gene regulation but also hold immense promise for developing novel therapeutics. Their ability to selectively modulate specific epigenetic marks and pathways has led to ongoing clinical trials and drug development efforts for various diseases, including cancer, neurological disorders, and inflammatory conditions. Understanding and harnessing the power of these small molecules is at the forefront of modern epigenetics research, offering new hope for precision medicine and targeted therapies.


3 key components involved in the regulation of epigenetic modifications

Epigenetics Writer

Epigenetics writers are enzymes responsible for adding chemical marks or modifications to DNA or histone proteins. These marks include DNA methylation (addition of methyl groups to DNA) and histone modifications (such as acetylation, methylation, phosphorylation, etc.).

Epigenetics Reader

Function: Epigenetics readers are proteins that can recognize and bind to specific epigenetic marks on DNA or histones. These reader proteins interpret the epigenetic code and facilitate downstream cellular processes, such as gene activation or repression.

Epigenetics Eraser

Function: Epigenetics erasers are enzymes responsible for removing or reversing epigenetic marks on DNA or histones. This process allows for the dynamic regulation of gene expression and the resetting of epigenetic states during various stages of development and in response to environmental changes.

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  1. pan-PIM/FLT3 inhibitor

    SEL24-B489 HCl is a potent, dual pan-PIM/FLT3 inhibitor.
  2. FLT3 inhibitor

    FLT3-IN-1 is a novel potent and selective Flt3 inhibitor with IC50 of 10 nM; against FLT3-ITD-expressing MV4-11 cells with IC50 of 6 nM.
  3. FLT3 inhibitor

    FLT3-IN-2 is potent FLT3 inhibitor.
  4. FLT3 inhibitor

    FLT3-IN-4 is a potent and orally effective Fms-like tyrosine receptor kinase 3 (FLT3; IC50=7 nM) inhibitor for treating acute myelogenous leukemia.
  5. FLT-3 ITD degrader

    PROTAC FLT-3 degrader 1 is an FLT-3 internal tandem duplication (ITD) degrader with an IC50 0.6 nM. Anti-proliferative activity; apoptosis induction.
  6. FLT3 inhibitor

    BSc5371 is a potent and irreversible FLT3 inhibitor, with Kds of 1.3, 0.83, 1.5, 5.8 and 2.3 nM for mutant FLT3(D835H), FLT3(ITD, D835V), FLT3(ITD, F691L), FLT3-ITD and wild type FLT3wt, respectively.
  7. FLT3 inhibitor

    FLT3-IN-3 is a potent FLT3 inhibitor with IC50s of 13 and 8 nM for FLT3 WT and FLT3 D835Y, respectively.
  8. FLT3 inhibitor

    HM-43239 is a Novel Potent Small Molecule FLT3 Inhibitor, in Acute Myeloid Leukemia (AML) with FMS-like Tyrosine Kinase 3 (FLT3) Mutations
  9. FLT3 inhibitor

    5'-Fluoroindirubinoxime (5'-FIO, compound 13), an Indirubin derivative, is a potent FLT3 inhibitor, with an IC50 of 15 nM.

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