Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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 includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our top-notch dedicated system is used to design specialised 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
Q9NPI0
UPID:
TM138_HUMAN
Alternative names:
-
Alternative UPACC:
Q9NPI0; A6NGA7; B4E044; Q5JPE1
Background:
Transmembrane protein 138 plays a crucial role in ciliogenesis, the process by which cilia are formed. Cilia are small, hair-like structures on the surface of cells that play vital roles in movement, signaling, and sensory perception. The protein's involvement in this fundamental cellular process underscores its importance in maintaining cellular function and integrity.
Therapeutic significance:
Joubert syndrome 16, a disorder marked by oculomotor apraxia, coloboma, and kidney involvement, is directly linked to mutations in the gene encoding Transmembrane protein 138. Understanding the role of Transmembrane protein 138 could open doors to potential therapeutic strategies for this syndrome, highlighting the protein's significance in disease mechanisms and treatment.