Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior activity, selectivity and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
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 use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q06210
UPID:
GFPT1_HUMAN
Alternative names:
D-fructose-6-phosphate amidotransferase 1; Glutamine:fructose-6-phosphate amidotransferase 1; Hexosephosphate aminotransferase 1
Alternative UPACC:
Q06210; Q53QE6; Q9BXF8
Background:
Glutamine--fructose-6-phosphate aminotransferase [isomerizing] 1, also known as D-fructose-6-phosphate amidotransferase 1, plays a pivotal role in glucose metabolism by controlling the flux into the hexosamine pathway. This enzyme is crucial for the synthesis of N- and O-linked glycoproteins, impacting cellular communication and signaling.
Therapeutic significance:
The enzyme's involvement in congenital myasthenic syndrome 12, characterized by muscle weakness and neuromuscular junction dysfunction, highlights its therapeutic potential. Understanding its role could lead to targeted treatments for this syndrome, leveraging its response to acetylcholinesterase inhibitors.