Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q8IYD1
UPID:
ERF3B_HUMAN
Alternative names:
G1 to S phase transition protein 2 homolog
Alternative UPACC:
Q8IYD1; Q9H909; Q9NVY0; Q9NY44
Background:
Eukaryotic peptide chain release factor GTP-binding subunit ERF3B, also known as GSPT2/ERF3B, plays a crucial role in translation termination. It forms part of the eRF1-eRF3-GTP ternary complex, which is essential for mediating translation termination at stop codons UAA, UAG, and UGA. This protein is also a component of the SURF complex, involved in nonsense-mediated decay (NMD) of mRNAs with premature stop codons.
Therapeutic significance:
Understanding the role of Eukaryotic peptide chain release factor GTP-binding subunit ERF3B could open doors to potential therapeutic strategies.