EpiCypher was founded in 2012 by Drs. Mark Bedford, Or Gozani, Brian Strahl, and James Bone in response to the growing demand for high-quality reagents and tools to study chromatin regulation and enable epigenetics-focused drug development.

EpiCypher is the global leader in recombinant nucleosome manufacturing and development. Using proprietary methods, we are continuously adding to the world’s largest collection of highly pure modified recombinant “designer” nucleosomes (dNucs). EpiCypher’s broad dNuc diversity is providing a powerful tool to decipher the histone code and accelerate drug development. Shah et al., Wang et al., and Weinburg et al. (see below) are just a few examples of the many benefits of using nucleosome substrates for epigenetics studies.

EpiCypher leverages dNuc technology for a wide range of applications, including: SNAP-ChIP® Spike-in Controls (for antibody profiling and quantitative ChIP), EpiDyne® substrates (for characterizing chromatin remodeling enzyme complexes and inhibitors), and dCypher™ assays (for interrogation of epigenetic protein-histone PTM binding interactions). We also offer a suite of high-quality recombinant histone binding proteins, enzymes, peptides, antibodies, and custom assay development services to complement these platforms.

EpiCypher continuously pushes technology boundaries to deliver innovative products, solutions, and services to epigenetics and chromatin biology researchers. Most recently, EpiCypher has been at the leading edge of chromatin mapping technology improvements with the recent launch of the highly sensitive epigenomic mapping CUTANA assays for ChIC, CUT&RUN, and CUT&Tag.

From our strong scientific expertise and rigor to our focus on customer success, EpiCypher is proud to be a company For Scientists, By Scientists.

Shah RN, Grzybowski AT, Cornett EM, Johnstone AL, Dickson BM, Boone BA, Cheek MA, Cowles MW, Maryanski D, Meiners MJ, Tiedemann RL, Vaughan RM, Arora N, Sun ZW, Rothbart SB, Keogh MC & Ruthenberg AJ. Examining the roles of H3K4 methylation states with systematically characterized antibodies. Mol Cell. 72, 162-177 (2018). (PMID: 30244833)

This study established SNAP-ChIP Recombinant Nucleosome Spike-ins as a robust and essential technology for defining histone PTM antibody binding in ChIP experiments. Direct comparison of SNAP-ChIP (also known as ICeChIP) Spike-ins and histone peptide arrays revealed that modified histone peptides had no predictive ability for antibody performance in ChIP, and many “ChIP-grade” antibodies to H3K4me1, me2, and me3 exhibited off-target binding and poor pull-down efficiency. Instead, SNAP-ChIP Spike-in Controls were able to accurately characterize antibody performance within the context of a ChIP assay.

Wang Z, Hausmann S, Lyu R, Li T, Lofgren SM, Flores NM, Fuentes ME, Caporicci M, Yang Z, Meiners MJ, Cheek MA, Howard SA, Zhang L, Elias JE, Kim MP, Maitra A, Wang H, Bassik MC, Keogh MC, Sage J, Gozani O &Mazur PK. SETD5-coordinated chromatin reprogramming regulates adaptive resistance to targeted pancreatic cancer therapy. Cancer Cell. 37, 834-849.e13 (2020). (PMID: 32442403)

This study utilized EpiCypher’s library of dNucs to identify epigenetic pathways underlying the development of drug-resistant pancreatic cancer. Several of our lysine-acetylated recombinant nucleosomes were used to characterize the novel SETD5-HDAC3-G9a corepressor complex, revealing SETD5 as a master regulator that coordinates selective inactivation of key genes required for drug sensitivity.

Weinberg DN, Papillon-Cavanaugh S, Chen H, Yue Y, Chen X, Rajagopalan KN, Horth C, McGuire JT, Xu X, Nikbakht H, Lemeisz AE, Marchione DM, Marunde MR, Meiners M, Cheek M, Keogh MC, Bareke E, Djedid A, Harutyunyan AS, Jabado N, Garcia BA, Li H, Allis CD, Majewski J & Lu C. H3K36me2 recruits DNMT3A and shapes the intergenic DNA methylation landscape. Nature 573, 281-286 (2019). (PMID: 31485078)

Here, dCypher nucleosome panels illuminated the binding preference of chromatin reader DNMT3A towards NSD1-catalyzed H3K36me2, highlighting the importance of the nucleosome context when defining histone PTM interactions. Notably, alterations in each of these chromatin regulators results in childhood overgrowth syndromes (mutation of DNMT3A is associated with Tatton-Brown-Rahman syndrome, while changes in NSD1 cause Sotos syndrome). This work established a new regulatory link between the two growth disorders, as loss of NSD1 leads to misregulated localization of DNMT3A and altered DNA methylation in intergenic regions.