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.
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 for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q5JWF2
UPID:
GNAS1_HUMAN
Alternative names:
Adenylate cyclase-stimulating G alpha protein; Extra large alphas protein
Alternative UPACC:
Q5JWF2; A2A2S3; E1P5G3; O75684; O75685; Q5JW67; Q5JWF1; Q9NY42
Background:
The Guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas, including alternative names such as Adenylate cyclase-stimulating G alpha protein and Extra large alphas protein, play a pivotal role in cellular signaling. These proteins function as transducers in signaling pathways controlled by G protein-coupled receptors (GPCRs), activating adenylyl cyclases and increasing cAMP levels.
Therapeutic significance:
Diseases such as GNAS hyperfunction, ACTH-independent macronodular adrenal hyperplasia 1, and various forms of Pseudohypoparathyroidism are linked to mutations in the GNAS gene. Understanding the role of Guanine nucleotide-binding protein G(s) subunit alpha isoforms XLas could open doors to potential therapeutic strategies for these conditions.