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.
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.
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.
Our top-notch dedicated system is used to design specialised 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
Q6IA69
UPID:
NADE_HUMAN
Alternative names:
NAD(+) synthase [glutamine-hydrolyzing]; NAD(+) synthetase
Alternative UPACC:
Q6IA69; B3KUU4; Q86SN2; Q9HA25; Q9NVM8
Background:
Glutamine-dependent NAD(+) synthetase, also known as NAD(+) synthase [glutamine-hydrolyzing] or NAD(+) synthetase, plays a pivotal role in the biosynthesis of nicotinamide adenine dinucleotide (NAD). This enzyme catalyzes the final step of the NAD de novo synthesis pathway, utilizing ATP and L-glutamine to convert deamido-NAD to NAD(+), a crucial coenzyme in cellular redox reactions.
Therapeutic significance:
The enzyme's link to Vertebral, cardiac, renal, and limb defects syndrome 3, a severe disorder marked by cardiac and renal anomalies, underscores its potential as a target for therapeutic intervention. Understanding the role of Glutamine-dependent NAD(+) synthetase could open doors to potential therapeutic strategies for this lethal condition.