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
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q695T7
UPID:
S6A19_HUMAN
Alternative names:
Solute carrier family 6 member 19; System B(0) neutral amino acid transporter AT1
Alternative UPACC:
Q695T7; A8K446
Background:
The Sodium-dependent neutral amino acid transporter B(0)AT1, also known as Solute carrier family 6 member 19, plays a crucial role in the resorption of neutral amino acids across the apical membrane of renal and intestinal epithelial cells. This process is sodium-dependent and chloride-independent, requiring CLTRN in the kidney or ACE2 in the intestine for cell surface expression and amino acid transporter activity.
Therapeutic significance:
Mutations in B(0)AT1 are linked to Hartnup disorder, characterized by abnormal amino acid transport leading to a variety of symptoms, including a pellagra-like rash and neurological issues. Understanding the role of B(0)AT1 could open doors to potential therapeutic strategies for Hartnup disorder, Hyperglycinuria, and Iminoglycinuria, diseases associated with amino acid transport defects.