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 carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create 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
Q00526
UPID:
CDK3_HUMAN
Alternative names:
Cell division protein kinase 3
Alternative UPACC:
Q00526
Background:
Cyclin-dependent kinase 3 (CDK3), also known as Cell division protein kinase 3, is a serine/threonine-protein kinase pivotal in cell cycle control, particularly during the G0-G1 and G1-S transitions. It interacts with CCNC/cyclin-C in interphase, phosphorylating key substrates such as histone H1, ATF1, RB1, and CABLES1. Phosphorylation of ATF1 by CDK3 promotes cell proliferation and transformation, while its action on RB1 is essential for the G0-G1 transition. Additionally, CDK3 is believed to facilitate G1-S transition by activating E2F1, E2F2, and E2F3 in a RB1-independent manner.
Therapeutic significance:
Understanding the role of Cyclin-dependent kinase 3 could open doors to potential therapeutic strategies.