Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
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 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
O95500
UPID:
CLD14_HUMAN
Alternative names:
-
Alternative UPACC:
O95500
Background:
Claudin-14, encoded by the gene with accession number O95500, is pivotal in maintaining the integrity of tight junctions in cellular structures. Its primary function involves the obliteration of the intercellular space, facilitating calcium-independent cell-adhesion activity. This protein plays a crucial role in the architecture of epithelial and endothelial barriers, ensuring selective permeability and cellular cohesion.
Therapeutic significance:
Claudin-14's mutation has been directly linked to Deafness, autosomal recessive, 29, a form of non-syndromic sensorineural hearing loss. This condition underscores the protein's vital role in auditory function, suggesting that targeting Claudin-14 pathways could offer new avenues for treating sensorineural deafness. Understanding the role of Claudin-14 could open doors to potential therapeutic strategies.