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.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
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 utilise our cutting-edge, exclusive workflow to develop focused 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.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9BSB4
UPID:
ATGA1_HUMAN
Alternative names:
-
Alternative UPACC:
Q9BSB4; Q9HAE2; Q9HBN1
Background:
Autophagy-related protein 101 plays a pivotal role in cellular homeostasis by facilitating autophagosome formation. It achieves this by stabilizing ATG13, thereby preventing its degradation by the proteasome. This protein's function is crucial for the autophagy process, a cellular mechanism essential for the removal of damaged cellular components and pathogens.
Therapeutic significance:
Understanding the role of Autophagy-related protein 101 could open doors to potential therapeutic strategies. Its fundamental role in autophagy suggests that modulation of its activity could be beneficial in diseases where autophagy is dysregulated.