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.
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 includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our high-tech, dedicated method is applied to construct targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q96S37
UPID:
S22AC_HUMAN
Alternative names:
Organic anion transporter 4-like protein; Renal-specific transporter; Urate anion exchanger 1; Urate:anion antiporter SLC22A12
Alternative UPACC:
Q96S37; B7WPG1; G3XAN7; Q19PF7; Q19PF8; Q19PF9; Q19PG0; Q6UXW3; Q96DT2
Background:
Solute carrier family 22 member 12 (SLC22A12), also known as Urate anion exchanger 1, plays a pivotal role in urate homeostasis. It functions as an electroneutral antiporter, facilitating the exchange of urate with organic or inorganic anions across the renal proximal tubule cells. This process is crucial for the renal reabsorption of urate, thereby maintaining optimal blood levels of uric acid.
Therapeutic significance:
Mutations in SLC22A12 are linked to Hypouricemia renal 1, a condition characterized by impaired uric acid reabsorption, leading to high urinary urate excretion. This can result in acute renal failure, chronic renal dysfunction, and nephrolithiasis. Understanding the role of SLC22A12 could open doors to potential therapeutic strategies for managing urate-related disorders.