5-Azacytidine

Epigenetic modifier; Inhibits DNA methyltransferase (DNMT)

5-Azacytidine

Epigenetic modifier; Inhibits DNA methyltransferase (DNMT)

From: 70 USD
Catalog #
72012_C
Epigenetic modifier; Inhibits DNA methyltransferase (DNMT)

Overview

5-Azacytidine is an analog of the nucleoside cytidine which can be incorporated into DNA and RNA. 5-Azacytidine acts as an epigenetic modifier by incorporating into DNA where it irreversibly binds to DNA methyltransferases, thus inhibiting their activity.

REPROGRAMMING
· Increases reprogramming efficiency of mouse fibroblasts to induced pluripotent stem (iPS) cells by inducing full reprogramming of partially reprogrammed cells (Mikkelsen et al.).
· Resets epigenetic memory in mouse iPS cells, in combination with Trichostatin A (Kim et al.).

DIFFERENTIATION
· Enhances differentiation to cardiomyocytes from human embryonic stem cells (Yoon et al.).

CANCER RESEARCH
· Wide range of anti-metabolic activities when tested against cultured cancer cells and an effective chemotherapeutic agent for acute myelogenous leukemia
Alternative Names
5-AzaC; Antibiotic U 18496; Ladakamycin; Mylosar; NSC 103-627; NSC 102816; U 18496; WR 183027; Zcyd
Cell Type
Cancer Cells and Cell Lines, Cardiomyocytes, PSC-Derived, Leukemia/Lymphoma Cells, Pluripotent Stem Cells
Species
Human, Mouse, Rat, Non-Human Primate, Other
Application
Differentiation, Reprogramming
Area of Interest
Cancer, Stem Cell Biology
CAS Number
320-67-2
Chemical Formula
C₈H₁₂N₄O₅
Molecular Weight
244.2 g/mol
Purity
≥ 95%
Pathway
Epigenetic
Target
DNMT

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Product Name
5-Azacytidine
Catalog #
72012, 72014
Lot #
All
Language
English
Document Type
Safety Data Sheet
Product Name
5-Azacytidine
Catalog #
72012, 72014
Lot #
All
Language
English

Applications

This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.

Resources and Publications

Publications (6)

Rewriting the epigenetic code for tumor resensitization: a review. Oronsky B et al. Translational oncology 2014 OCT

Abstract

In cancer chemotherapy, one axiom, which has practically solidified into dogma, is that acquired resistance to antitumor agents or regimens, nearly inevitable in all patients with metastatic disease, remains unalterable and irreversible, rendering therapeutic rechallenge futile. However, the introduction of epigenetic therapies, including histone deacetylase inhibitors (HDACis) and DNA methyltransferase inhibitors (DNMTIs), provides oncologists, like computer programmers, with new techniques to overwrite" the modifiable software pattern of gene expression in tumors and challenge the "one and done" treatment prescription. Taking the epigenetic code-as-software analogy a step further�
Epigenetic memory in induced pluripotent stem cells. Kim K et al. Nature 2010 SEP

Abstract

Somatic cell nuclear transfer and transcription-factor-based reprogramming revert adult cells to an embryonic state, and yield pluripotent stem cells that can generate all tissues. Through different mechanisms and kinetics, these two reprogramming methods reset genomic methylation, an epigenetic modification of DNA that influences gene expression, leading us to hypothesize that the resulting pluripotent stem cells might have different properties. Here we observe that low-passage induced pluripotent stem cells (iPSCs) derived by factor-based reprogramming of adult murine tissues harbour residual DNA methylation signatures characteristic of their somatic tissue of origin, which favours their differentiation along lineages related to the donor cell, while restricting alternative cell fates. Such an 'epigenetic memory' of the donor tissue could be reset by differentiation and serial reprogramming, or by treatment of iPSCs with chromatin-modifying drugs. In contrast, the differentiation and methylation of nuclear-transfer-derived pluripotent stem cells were more similar to classical embryonic stem cells than were iPSCs. Our data indicate that nuclear transfer is more effective at establishing the ground state of pluripotency than factor-based reprogramming, which can leave an epigenetic memory of the tissue of origin that may influence efforts at directed differentiation for applications in disease modelling or treatment.
Dissecting direct reprogramming through integrative genomic analysis Mikkelsen TS et al. Nature 2008

Abstract

Somatic cells can be reprogrammed to a pluripotent state through the ectopic expression of defined transcription factors. Understanding the mechanism and kinetics of this transformation may shed light on the nature of developmental potency and suggest strategies with improved efficiency or safety. Here we report an integrative genomic analysis of reprogramming of mouse fibroblasts and B lymphocytes. Lineage-committed cells show a complex response to the ectopic expression involving induction of genes downstream of individual reprogramming factors. Fully reprogrammed cells show gene expression and epigenetic states that are highly similar to embryonic stem cells. In contrast, stable partially reprogrammed cell lines show reactivation of a distinctive subset of stem-cell-related genes, incomplete repression of lineage-specifying transcription factors, and DNA hypermethylation at pluripotency-related loci. These observations suggest that some cells may become trapped in partially reprogrammed states owing to incomplete repression of transcription factors, and that DNA de-methylation is an inefficient step in the transition to pluripotency. We demonstrate that RNA inhibition of transcription factors can facilitate reprogramming, and that treatment with DNA methyltransferase inhibitors can improve the overall efficiency of the reprogramming process.

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