Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior activity, selectivity and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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 high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q13303
UPID:
KCAB2_HUMAN
Alternative names:
K(+) channel subunit beta-2; Kv-beta-2
Alternative UPACC:
Q13303; A0AVM9; A8K1A4; B0AZR7; O43659; Q2YD85; Q5TG82; Q5TG83; Q6ZNE4; Q99411
Background:
Voltage-gated potassium channel subunit beta-2 (Kv-beta-2) plays a pivotal role in modulating potassium channel activity, crucial for nerve signaling and preventing neuronal hyperexcitability. It enhances the expression and activity of various potassium channels, including KCNA4 and KCNB2, and possesses NADPH-dependent aldoketoreductase activity with broad substrate specificity.
Therapeutic significance:
Understanding the role of Voltage-gated potassium channel subunit beta-2 could open doors to potential therapeutic strategies, particularly in neurological disorders where dysregulation of potassium channels contributes to disease pathology.