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.
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 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 use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q8N6F1
UPID:
CLD19_HUMAN
Alternative names:
-
Alternative UPACC:
Q8N6F1; B7Z5I2; F5H5P9; Q5QT57; Q8N8X0
Background:
Claudin-19, encoded by the gene with accession number Q8N6F1, is pivotal in maintaining tight junction integrity in epithelial cells. It achieves this through calcium-independent cell-adhesion activity, crucial for cellular barrier functions.
Therapeutic significance:
Claudin-19 is directly implicated in Hypomagnesemia 5, a renal disorder marked by magnesium wasting, hypercalciuria, and nephrocalcinosis, often accompanied by severe ocular abnormalities. Targeting Claudin-19 could offer novel therapeutic avenues for managing this condition.