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.
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
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9H0P0
UPID:
5NT3A_HUMAN
Alternative names:
7-methylguanosine phosphate-specific 5'-nucleotidase; Cytosolic 5'-nucleotidase 3; Cytosolic 5'-nucleotidase III; Pyrimidine 5'-nucleotidase 1; Uridine 5'-monophosphate hydrolase 1; p36
Alternative UPACC:
Q9H0P0; A8K253; B2RAA5; B8ZZC4; Q6IPZ1; Q6NXS6; Q7L3G6; Q9P0P5; Q9UC42; Q9UC43; Q9UC44; Q9UC45
Background:
Cytosolic 5'-nucleotidase 3A, also known as Pyrimidine 5'-nucleotidase 1 or Uridine 5'-monophosphate hydrolase 1, plays a pivotal role in nucleotide metabolism. It specifically acts on cytidine monophosphate (CMP) and 7-methylguanosine monophosphate (m(7)GMP), with a preference for CMP. This enzyme's activity is crucial for the proper functioning of cellular processes.
Therapeutic significance:
P5N deficiency, a condition linked to mutations in the gene encoding Cytosolic 5'-nucleotidase 3A, results in hemolytic anemia and potential learning difficulties. Understanding the role of Cytosolic 5'-nucleotidase 3A could open doors to potential therapeutic strategies for treating P5N deficiency and mitigating the effects of lead poisoning.