Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q86UC2
UPID:
RSPH3_HUMAN
Alternative names:
A-kinase anchor protein RSPH3; Radial spoke head-like protein 2
Alternative UPACC:
Q86UC2; Q96LQ5; Q96LX2; Q9BX75
Background:
Radial spoke head protein 3 homolog (RSPH3) is pivotal in the motility of sperm and cilia, functioning within axonemal radial spoke complexes. It acts as a scaffold for the cAMP-dependent protein kinase holoenzyme, integrating MAPK and PKA signaling pathways in cilia.
Therapeutic significance:
RSPH3's mutation leads to primary ciliary dyskinesia, 32, marked by chronic respiratory infections and bronchiectasis due to motile cilia abnormalities. Targeting RSPH3 could revolutionize treatments for respiratory diseases.