Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library stands out due to several important features:
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.