Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced activity, selectivity, and safety.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed 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.
Our high-tech, dedicated method is applied to construct 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 stands out due to several important features:
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.