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.
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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We utilise our cutting-edge, exclusive workflow to develop 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q7L5Y1
UPID:
ENOF1_HUMAN
Alternative names:
Antisense RNA to thymidylate synthase; L-fuconate dehydratase
Alternative UPACC:
Q7L5Y1; A6NMP3; A8K9R5; B3KSL6; B3KXE4; D3DUH0; Q15407; Q15594; Q15595; Q6ZS08; Q9HAS5; Q9HAS6
Background:
Mitochondrial enolase superfamily member 1, also known as Antisense RNA to thymidylate synthase and L-fuconate dehydratase, plays a crucial role in the catabolism of L-fucose. This process involves the dehydration of L-fuconate to 2-keto-3-deoxy-L-fuconate, a reaction essential for the metabolism of carbohydrates attached to cellular glycoproteins.
Therapeutic significance:
The protein's involvement in Dyskeratosis congenita, digenic, highlights its potential as a target for therapeutic intervention. Understanding the role of Mitochondrial enolase superfamily member 1 could open doors to potential therapeutic strategies, especially considering its impact on telomere maintenance and the pathogenic mechanism involving ENOSF1-TYMS RNA-RNA interactions.