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.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner 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 utilise our cutting-edge, exclusive workflow to develop 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.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9NRP7
UPID:
STK36_HUMAN
Alternative names:
Fused homolog
Alternative UPACC:
Q9NRP7; B7WPM3; Q8TC32; Q9H9N9; Q9UF35; Q9ULE2
Background:
Serine/threonine-protein kinase 36, also known as Fused homolog, plays a pivotal role in the sonic hedgehog (Shh) pathway, regulating GLI transcription factors' activity. It is essential for the construction of the central pair apparatus of motile cilia and is crucial for postnatal development by possibly regulating cerebral spinal fluid homeostasis or ciliary function.
Therapeutic significance:
The protein's involvement in primary ciliary dyskinesia, specifically Ciliary dyskinesia, primary, 46, underscores its therapeutic significance. Understanding the role of Serine/threonine-protein kinase 36 could open doors to potential therapeutic strategies for treating this autosomal recessive disorder.