Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our high-tech, dedicated method is applied to construct targeted 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
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.