Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
Our top-notch dedicated system is used to design specialised 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
Q8IY18
UPID:
SMC5_HUMAN
Alternative names:
-
Alternative UPACC:
Q8IY18; A6NM81; O60335; Q05D92; Q5VZ60; Q96SB9
Background:
Structural maintenance of chromosomes protein 5 (SMC5) is a core component of the SMC5-SMC6 complex, crucial for DNA double-strand break repair via homologous recombination. It facilitates sister chromatid cohesion, telomere maintenance in ALT cell lines, and sumoylation of shelterin complex components, essential for genomic stability and cell cycle progression.
Therapeutic significance:
Given its pivotal role in DNA repair and genomic stability, SMC5's dysfunction is linked to Atelis syndrome 2, characterized by neurodevelopmental disorders, congenital anomalies, and increased mortality. Targeting SMC5 pathways could offer novel therapeutic avenues for treating Atelis syndrome 2 and enhancing genomic integrity.