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.
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.
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 high-tech, dedicated method is applied to construct targeted 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.
Key features that set our library apart include:
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.