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.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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.
We utilise our cutting-edge, exclusive workflow to develop focused 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
Q9Y3D2
UPID:
MSRB2_HUMAN
Alternative names:
-
Alternative UPACC:
Q9Y3D2; Q17R44; Q4G1C7; Q9Y5W6
Background:
Methionine-R-sulfoxide reductase B2, located in the mitochondria, plays a crucial role in cellular defense against oxidative stress by reducing methionine (R)-sulfoxide back to methionine. This enzymatic activity not only helps in maintaining protein functionality but also in preserving mitochondrial integrity, which is vital for cell survival.
Therapeutic significance:
Understanding the role of Methionine-R-sulfoxide reductase B2 could open doors to potential therapeutic strategies. Its ability to mitigate oxidative stress suggests its potential in treating conditions where oxidative damage is a key factor.