Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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.
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 use our state-of-the-art dedicated workflow for designing focused 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.
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.