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
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P49918
UPID:
CDN1C_HUMAN
Alternative names:
Cyclin-dependent kinase inhibitor p57; p57Kip2
Alternative UPACC:
P49918
Background:
Cyclin-dependent kinase inhibitor 1C, known as p57Kip2, is a crucial regulator of cell cycle progression. It inhibits several G1 cyclin/CDK complexes, including cyclin E-CDK2, cyclin D2-CDK4, and cyclin A-CDK2, playing a pivotal role in controlling cell proliferation and maintaining cells in a non-proliferative state.
Therapeutic significance:
p57Kip2's involvement in Beckwith-Wiedemann syndrome and a condition characterized by growth retardation and adrenal hypoplasia highlights its potential as a target for therapeutic intervention. Understanding the role of Cyclin-dependent kinase inhibitor 1C could open doors to potential therapeutic strategies.