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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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.
Our high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q7Z3V4
UPID:
UBE3B_HUMAN
Alternative names:
HECT-type ubiquitin transferase E3B
Alternative UPACC:
Q7Z3V4; A5D8Z3; Q05BX9; Q659F7; Q7Z7Q1; Q9BXZ4
Background:
Ubiquitin-protein ligase E3B, also known as HECT-type ubiquitin transferase E3B, plays a pivotal role in protein ubiquitination, a critical process in cellular regulation and homeostasis. By transferring ubiquitin from an E2 ubiquitin-conjugating enzyme to targeted substrates, it influences protein degradation, signal transduction, and DNA repair.
Therapeutic significance:
The protein is implicated in Kaufman oculocerebrofacial syndrome, a condition marked by developmental delays, intellectual disability, and various physical anomalies. Understanding the role of Ubiquitin-protein ligase E3B could open doors to potential therapeutic strategies for this syndrome.