Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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
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.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9UKI8
UPID:
TLK1_HUMAN
Alternative names:
PKU-beta; Tousled-like kinase 1
Alternative UPACC:
Q9UKI8; B3KR15; B4DX87; Q14150; Q8N591; Q9NYH2; Q9Y4F6
Background:
Serine/threonine-protein kinase tousled-like 1, known as PKU-beta and Tousled-like kinase 1, plays a crucial role in DNA repair and cell cycle regulation. It is rapidly and transiently inhibited by phosphorylation following DNA double-stranded breaks during S-phase, indicating its involvement in the ATM-pathway dependent cell cycle checkpoint. This kinase also phosphorylates histone H3 at 'Ser-10', contributing to chromatin assembly processes.
Therapeutic significance:
Understanding the role of Serine/threonine-protein kinase tousled-like 1 could open doors to potential therapeutic strategies.