Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced activity, selectivity, and safety.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9NU63
UPID:
ZFP57_HUMAN
Alternative names:
Zinc finger protein 698
Alternative UPACC:
Q9NU63; B0S894; B0V254; B2RXJ7; Q5SSB1
Background:
Zinc finger protein 57 homolog (ZFP57) plays a pivotal role in maintaining gene imprinting and DNA methylation during early development. It partners with ZNF445 in humans for imprinting maintenance, differing from its predominant role in mice. ZFP57 is essential for maternal methylation imprints at the SNRPN locus and acts as a transcriptional repressor in Schwann cells, binding to specific DNA sequences.
Therapeutic significance:
ZFP57's mutation is linked to Diabetes mellitus, transient neonatal, 1, characterized by early-life hyperglycemia. Understanding ZFP57's function could lead to novel therapeutic strategies for managing this form of diabetes and enhancing our approach to gene imprinting disorders.