Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P08754
UPID:
GNAI3_HUMAN
Alternative names:
G(i) alpha-3
Alternative UPACC:
P08754; P17539; Q5TZX1
Background:
Guanine nucleotide-binding protein G(i) subunit alpha-3, also known as G(i) alpha-3, plays a pivotal role in cellular signaling as a transducer downstream of G protein-coupled receptors (GPCRs). It alternates between an active GTP-bound state and an inactive GDP-bound state, modulating various signaling cascades. This protein inhibits adenylate cyclase activity, reducing cAMP levels, and stimulates receptor-regulated K(+) channels. It is also involved in cell division by affecting the localization of RGS14.
Therapeutic significance:
G(i) alpha-3's involvement in Auriculocondylar syndrome 1, a craniofacial malformation syndrome, underscores its potential as a therapeutic target. Understanding the role of G(i) alpha-3 could open doors to potential therapeutic strategies for treating this syndrome and possibly other related disorders.