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.
The library features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q8N1B3
UPID:
CCNQ_HUMAN
Alternative names:
CDK10-activating cyclin; Cyclin-M; Cyclin-related protein FAM58A
Alternative UPACC:
Q8N1B3; Q2I380; Q330J9; Q96IU5; Q9BUU1
Background:
Cyclin-Q, also known as CDK10-activating cyclin, Cyclin-M, and Cyclin-related protein FAM58A, plays a pivotal role in cell cycle regulation by activating the cyclin-associated kinase CDK10. This activation is crucial for the proper progression of the cell cycle, impacting cell division and growth.
Therapeutic significance:
Cyclin-Q is implicated in the syndrome characterized by toe syndactyly, telecanthus, and anogenital and renal malformations. Understanding the role of Cyclin-Q could open doors to potential therapeutic strategies for this complex syndrome, highlighting its significance in genetic and developmental research.