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.
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 includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our top-notch dedicated system is used to design specialised 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
Q9BYW2
UPID:
SETD2_HUMAN
Alternative names:
HIF-1; Huntingtin yeast partner B; Huntingtin-interacting protein 1; Huntingtin-interacting protein B; Lysine N-methyltransferase 3A; Protein-lysine N-methyltransferase SETD2; SET domain-containing protein 2; p231HBP
Alternative UPACC:
Q9BYW2; O75397; O75405; Q17RW8; Q5BKS9; Q5QGN2; Q69YI5; Q6IN64; Q6ZN53; Q6ZS25; Q8N3R0; Q8TCN0; Q9C0D1; Q9H696; Q9NZW9
Background:
Histone-lysine N-methyltransferase SETD2, known for its role in trimethylating 'Lys-36' of histone H3, is pivotal in epigenetic transcriptional activation, DNA repair, and tumor suppression. Its activity influences chromatin structure, facilitating transcriptional elongation and DNA mismatch repair. SETD2's involvement in angiogenesis and endoderm development underscores its broad biological significance.
Therapeutic significance:
SETD2's mutation is linked to renal cell carcinoma, Luscan-Lumish syndrome, and various forms of leukemia, highlighting its role in disease. Understanding SETD2's function could lead to breakthroughs in cancer therapy, offering hope for targeted treatments.