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.
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.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library is unique due to several crucial aspects:
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.