DNA Repair Drug Development Services for Brain Tumors

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Chromatin was the first identified target for cancer therapy. Epigenetic abnormalities are not only associated with the development of certain cancers but may also affect the efficacy and prognosis of anticancer drugs by modifying pharmacokinetic-related genes such as drug absorption, distribution, metabolism, and excretion, as well as pharmacodynamic-related genes such as signaling pathways and targets of action. As research progresses, there is increasing evidence that epigenetic mechanisms have an important impact on the clinical efficacy of many drugs, especially anti-brain tumor drugs.

We provide services for the development of targeted brain tumor drugs targeting epigenetic genes

Drugs that exert anti-brain tumor effects by modulating epigenetic genes are becoming a hot topic of research. Alfa Cytology provides epigenetically targeted drug development services for clients in the field of brain tumor research. Given a large number of potential targets, we have developed a systematic approach to discover and validate potential drug targets to focus on helping our clients in brain tumor drug development and improving drug efficacy.

Drug type	Drug development services
DNA methyltransferase inhibitors (DNMTsI)	Alfa Cytology can develop DNMTsI for aberrant DNA methylation, including nucleoside class inhibitors, non-nucleoside class inhibitors, and antisense oligonucleotide class inhibitors. We also offer chemical structure modifications to obtain novel derivatives with good stability, high selectivity for brain tumor cells, lower adverse drug reactions, and good water solubility.
Histone target inhibitors	The histone target inhibitors in Alfa Cytology' pipeline are mainly histone methyltransferase inhibitors and histone deacetylase inhibitors.

Other targets that could be developed

DNMT1, 3A, and 3B. Methylates cytosines on DNA, and mutation can lead to aberrant methylation
EZH2. Methylates histone H3K27
DOT1L. Methylates histone H3K79
KMT2A-D, SETD2, NSDI. Methylate histone lysines
EP300, CREBBP. Acetylate histone lysines
TET2. Is the first step in cytosine demethylation, and it is inhibited by 2-hydroxyglutarate (2-HG)
IDH1, IDH2. Mutated protein produces 2-HG from isocitrate that inhibits TET2 and lysine demethylases
HDAC1-3, 8 and HDAC6. Deacetylase removes acetyl groups from histone lysines
KDMIA, KDM6A (UTX). Demethylates histone lysines
BRD4. Bromodomain proteins read acetyl groups on histone lysines
CBX family, CHD1. Chromodomain proteins read methyl groups
ARIDIA, ARID1B, ARID2, SMARCA2, SMARCA4, SMARCBI, CHD1. Proteins in the chromatin remodeling complex use ATP to move nucleosomes away from DNA. The loss-of-function mutations common in cancer
HIST1H1B, HIST1HIC, HISTIH3B, H3F3A, H3F3B. Structural histone proteins acquire mutations that can be oncogenic
CTCF, STAG2, RAD21, CHD8. Normal binding to CTCF sites on DNA defines and protects gene neighborhoods from the inappropriate expression

Epigenetic assay development

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Disorders of chromatin epigenetic modifications are seen in the pathology of many major diseases such as brain tumors, and cardiovascular and cerebrovascular. Therefore, there is an urgent need for drugs that can intervene in epigenetic modification disorders in disease states. In response to this need, Alfa Cytology offers its clients epigenetically targeted drug development services for brain tumors. You can contact us at any time to receive updates on our services.

All of our services and products are intended for preclinical research use only and cannot be used to diagnose, treat or manage patients.