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.
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 use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9BSV6
UPID:
SEN34_HUMAN
Alternative names:
Leukocyte receptor cluster member 5; tRNA-intron endonuclease Sen34
Alternative UPACC:
Q9BSV6; A6NNB1; B0V3J1; Q9BVT1; Q9H6H5
Background:
The tRNA-splicing endonuclease subunit Sen34, also known as Leukocyte receptor cluster member 5, plays a pivotal role in RNA processing. It is integral to the tRNA-splicing endonuclease complex, crucial for cleaving pre-tRNA at specific splice sites, thereby facilitating the removal of introns and the formation of functional tRNA molecules. This process is essential for the accurate translation of genetic information into proteins.
Therapeutic significance:
Pontocerebellar hypoplasia 2C, a severe neurological disorder, is linked to mutations affecting Sen34. Understanding the role of tRNA-splicing endonuclease subunit Sen34 could open doors to potential therapeutic strategies for this debilitating condition.