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.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P33316
UPID:
DUT_HUMAN
Alternative names:
dUTP pyrophosphatase
Alternative UPACC:
P33316; A8K650; B4DPR5; O14785; Q16708; Q16860; Q6FHN1; Q6NSA3; Q96Q81
Background:
Deoxyuridine 5'-triphosphate nucleotidohydrolase, mitochondrial, also known as dUTP pyrophosphatase, plays a crucial role in DNA synthesis and repair. It catalyzes the conversion of dUTP to dUMP, preventing uracil misincorporation into DNA and supplying dUMP for thymidylate biosynthesis. This enzyme's action is vital for maintaining the integrity of the genetic material and is essential for embryonic development.
Therapeutic significance:
The enzyme's link to Bone marrow failure and diabetes mellitus syndrome highlights its clinical importance. Variants affecting this gene cause a spectrum of bone marrow failures and non-autoimmune insulin-dependent diabetes mellitus. Understanding the role of Deoxyuridine 5'-triphosphate nucleotidohydrolase could open doors to potential therapeutic strategies for these conditions.