Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
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.
We use our state-of-the-art dedicated workflow for designing focused 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 distinguishes itself through several key aspects:
partner
Reaxense
upacc
P51800
UPID:
CLCKA_HUMAN
Alternative names:
ClC-K1
Alternative UPACC:
P51800; B4DPD3; E7EPH6; Q5T5P8; Q5T5Q4; Q7Z6D1; Q86VT1
Background:
The Chloride channel protein ClC-Ka, also known as ClC-K1, plays a pivotal role in the regulation of cell volume, membrane potential stabilization, signal transduction, and transepithelial transport. Its significance is underscored in urinary concentrating mechanisms, highlighting its essential function in maintaining electrolyte balance.
Therapeutic significance:
ClC-Ka's involvement in Bartter syndrome 4B, a condition characterized by impaired salt reabsorption, hypokalemic metabolic alkalosis, and sensorineural deafness, underscores its therapeutic potential. Targeting ClC-Ka could lead to innovative treatments for this syndrome, emphasizing the importance of understanding its biological mechanisms.