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 effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q5VWQ0
UPID:
RSBN1_HUMAN
Alternative names:
Round spermatid basic protein 1
Alternative UPACC:
Q5VWQ0; A8K937; Q6AI21; Q8TC33; Q9HA80; Q9NUP6
Background:
Lysine-specific demethylase 9 (LSD9), also known as Round spermatid basic protein 1, plays a crucial role in epigenetic regulation by specifically demethylating dimethylated 'Lys-20' of histone H4 (H4K20me2). This action is pivotal in modulating chromosome architecture, impacting gene expression and cellular differentiation.
Therapeutic significance:
Understanding the role of Lysine-specific demethylase 9 could open doors to potential therapeutic strategies. Its unique function in epigenetic regulation presents opportunities for targeted interventions in diseases where chromatin architecture and gene expression are disrupted.