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Precisely modulate gene expression by rewriting chemical marks on DNA and histones without altering the underlying sequence. Our CRISPR-dCas9 platform enables surgical accuracy in epigenetic regulation for groundbreaking research and therapeutic development.
Trusted by leading research and pharmaceutical institutions
Targeted CpG methylation/demethylation for gene silencing
H3K27ac and other histone marks for activation
Reversible gene regulation without permanent changes
Our epigenome editing platform enables targeted modulation of gene expression by rewriting chemical marks on DNA or histones, offering unprecedented precision for basic research and therapeutic development.
Our advanced CRISPR-dCas9 platform utilizes catalytically inactive Cas9 fused to various epigenetic effector domains. This approach allows precise targeting of specific genomic loci without introducing double-strand breaks, ensuring superior safety and precision.
Unlike traditional CRISPR editing that introduces DNA breaks, epigenome editing modifies gene expression without altering the underlying DNA sequence. This approach avoids mutations, translocations, and p53-mediated toxicity.
DNA methylation changes can be stably inherited through cell divisions for lasting phenotypic changes.
Target multiple promoters or enhancers simultaneously to regulate entire metabolic networks.
High-efficiency ribonucleoprotein delivery minimizes cytotoxicity in primary cells.
Get expert consultation for your epigenome editing project.
Our comprehensive platform offers multiple effector options to meet diverse research needs.
Targeted DNA methylation using dCas9 fused to DNMT3A catalytic domain for stable gene silencing.
Targeted demethylation using TET1 dioxygenase to reactivate silenced genes.
Epigenetic writers and erasers for precise histone mark manipulation.
Comprehensive specifications to meet your research requirements.
| Parameter | DNA Methylation | DNA Demethylation | Histone Editing |
|---|---|---|---|
| Effector Proteins | dCas9-DNMT3A, dCas9-DNMT3L | dCas9-TET1, dCas9-TETv4 | dCas9-p300, dCas9-KRAB, dCas9-LSD1 |
| Modification Type | CpG methylation | 5mC demethylation | H3K27ac, H3K9me3, H3K4me |
| Modification Range | 300-500 bp | 150-200 bp | Target-specific |
| Heritability | Stable, heritable | Variable | Often transient |
| Reversibility | Can be reversed by TET | Permanent once established | Generally reversible |
| Cell Types | Dividing and non-dividing | Dividing and non-dividing | All cell types |
Our proven workflow ensures quality and efficiency at every stage.
Bioinformatic analysis of chromatin accessibility (ATAC-seq/ChIP-seq)
Select optimal dCas9 effector fusion based on desired outcome
Custom gRNA library design for high-precision targeting
RNP/mRNA/viral delivery with real-time monitoring
Bisulfite-seq/ChIP-qPCR and transcriptional analysis
Our epigenome editing services support a broad spectrum of research areas.
Enhance immune cell function by modulating checkpoint genes through epigenome editing. Silence immune checkpoint genes like PD-1 via repressive histone marks to enhance anti-tumor performance without permanent DNA alteration.
Study neurological disorders by precisely manipulating epigenetic marks in neurons and iPSC-derived models. Target genes implicated in Alzheimer's, Parkinson's, and rare imprinting diseases.
Demethylate hypermethylated tumor suppressor gene promoters to restore their expression. Target BRCA1, p15/CDKN2B, and other critical genes silenced in cancer.
Apply epigenome editing tools to precisely regulate genes involved in stress resistance, yield traits, and nutritional content without introducing foreign DNA.
Trusted by scientists worldwide for epigenome editing research.
"The epigenome editing platform allowed us to precisely study the role of DNA methylation in gene regulation without introducing DNA breaks. The results were highly reproducible across multiple cell types."
Senior Scientist
Biotechnology Company
"Using dCas9-TET1 for targeted demethylation, we successfully reactivated silenced tumor suppressor genes in our cancer model. The precision and efficiency exceeded our expectations."
Research Director
Pharmaceutical Research Institution
"The service's flexibility in designing custom gRNA libraries for our imprinting disease research was invaluable. The technical support team provided excellent consultation throughout."
Principal Investigator
Academic Research Institution
Our epigenome editing platform is backed by peer-reviewed research.
Linn Amanda Syding, Petr Nickl, Petr Kasparek, Radislav Sedlacek | Cells (2020)
View DOISaunderson E.A, Encabo H.H, Devis J, et al. | PNAS (2023)
View DOIAgustin Sgro, Pilar Blancafort | Nucleic Acids Research (2020)
View DOIJun Ueda, Taiga Yamazaki, Hiroshi Funakoshi | IJMS (2023)
View DOIRuijie Cai, Runyu Lv, Xin'e Shi, Gongshe Yang, Jianjun Jin | IJMS (2023)
View DOIFind answers to common questions about epigenome editing services.
It depends on the modification type. Histone modifications are often transient, while DNA methylation via dCas9-DNMT can lead to stable, heritable gene silencing across cell divisions. DNA demethylation using dCas9-TET1 can permanently remove methylation marks once established.
Absolutely. One of the greatest strengths of epigenome editing is targeting distal enhancers and insulators to study the "dark matter" of the genome and its role in long-range gene regulation. This capability is essential for understanding complex regulatory networks.
We use specialized assays including Methylation-Specific PCR, Bisulfite Sequencing, and ChIP-qPCR to verify the addition or removal of chemical marks at the target site. RNA-seq can confirm downstream transcriptional changes.
Yes. Since epigenome editing does not rely on HDR, it is highly effective in post-mitotic cells such as primary neurons, cardiomyocytes, and resting immune cells. This makes it ideal for studying differentiated cells and hard-to-transfect primary tissues.
We offer multiple delivery options: RNP complexes for minimal toxicity, lentiviral vectors for stable integration, AAV for in vivo applications, and mRNA for transient expression. The optimal method depends on your cell type and experimental goals.
DNA methylation editors typically affect 300-500 bp regions, while demethylation editors (TET1) work within 150-200 bp downstream of the PAM site. Histone editors provide target-specific modifications without defined ranges. These can be tailored based on your experimental requirements.
Still have questions? Our technical team is here to help.
Get a customized quote for your Epigenome Editing Services project. Our experts will respond within 24 hours.
CD Biosynsis is a leading customer-focused biotechnology company dedicated to providing high-quality products, comprehensive service packages, and tailored solutions to support and facilitate the applications of synthetic biology in a wide range of areas.