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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q56NI9
UPID:
ESCO2_HUMAN
Alternative names:
Establishment factor-like protein 2; Establishment of cohesion 1 homolog 2
Alternative UPACC:
Q56NI9; B3KW59; Q49AP4
Background:
N-acetyltransferase ESCO2, also known as Establishment factor-like protein 2, plays a crucial role in sister chromatid cohesion. This protein ensures that only sister chromatids are paired together by acetylating the cohesin component SMC3, a process vital for DNA replication and cell division.
Therapeutic significance:
Mutations in ESCO2 are linked to Roberts-SC phocomelia syndrome and Juberg-Hayward syndrome, disorders characterized by limb and facial abnormalities. Understanding the role of N-acetyltransferase ESCO2 could open doors to potential therapeutic strategies for these genetic conditions.