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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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 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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P51795
UPID:
CLCN5_HUMAN
Alternative names:
Chloride channel protein 5; Chloride transporter ClC-5
Alternative UPACC:
P51795; A1L475; B3KPN6; Q5JQD5; Q7RTN8
Background:
H(+)/Cl(-) exchange transporter 5, also known as Chloride channel protein 5 or Chloride transporter ClC-5, plays a crucial role in the body's renal tubular function. It operates as a proton-coupled chloride transporter, facilitating the exchange of chloride ions against protons, essential for the acidification of the endosome lumen.
Therapeutic significance:
Mutations in H(+)/Cl(-) exchange transporter 5 are linked to a spectrum of renal diseases within the 'Dent disease complex', including Hypophosphatemic rickets, Dent disease 1, Nephrolithiasis with renal failure, and Low molecular weight proteinuria with hypercalciuria and nephrocalcinosis. Understanding the role of this protein could open doors to potential therapeutic strategies for these conditions.