Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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.
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
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 stands out due to several important features:
partner
Reaxense
upacc
Q9H0K6
UPID:
PUS7L_HUMAN
Alternative names:
Pseudouridylate synthase 7 homolog-like protein
Alternative UPACC:
Q9H0K6; B3KUJ1; Q05CU0; Q6AHZ3; Q6NUP2
Background:
Pseudouridylate synthase PUS7L, also known as Pseudouridylate synthase 7 homolog-like protein, plays a crucial role in the pseudouridylation of mRNAs. This enzymatic process is essential for the modification of RNA, influencing its stability, translation, and overall function within the cell.
Therapeutic significance:
Understanding the role of Pseudouridylate synthase PUS7L could open doors to potential therapeutic strategies. Its involvement in RNA modification processes positions it as a key player in cellular function and disease mechanisms.