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 pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
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.
Our library stands out due to several important features:
partner
Reaxense
upacc
P00491
UPID:
PNPH_HUMAN
Alternative names:
Inosine phosphorylase; Inosine-guanosine phosphorylase
Alternative UPACC:
P00491; B2R8S5; D3DS00; Q15160; Q5PZ03
Background:
Purine nucleoside phosphorylase (PNP), also known as Inosine phosphorylase and Inosine-guanosine phosphorylase, plays a crucial role in the purine salvage pathway. It catalyzes the phosphorolytic breakdown of N-glycosidic bonds in beta-(deoxy)ribonucleoside molecules, leading to the formation of free purine bases and pentose-1-phosphate. This enzyme preferentially acts on 6-oxopurine nucleosides, including inosine and guanosine.
Therapeutic significance:
PNP deficiency disrupts the catabolism of inosine into hypoxanthine and guanosine into guanine, causing accumulation of guanosine and inosine. This leads to recurrent infections due to severe T-cell immunodeficiency and potential neurologic impairment. Understanding the role of PNP could open doors to potential therapeutic strategies for treating PNP deficiency.