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 pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
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 employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize 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.