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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q96CU9
UPID:
FXRD1_HUMAN
Alternative names:
-
Alternative UPACC:
Q96CU9; B3KN84; B4DHU2; Q71MG0; Q9BU39; Q9UKY9
Background:
FAD-dependent oxidoreductase domain-containing protein 1 plays a crucial role in mitochondrial function, specifically in the assembly of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I). This protein's involvement in mid-late stages of complex I assembly is pivotal for cellular energy production.
Therapeutic significance:
Given its critical role in mitochondrial complex I assembly, understanding the function of FAD-dependent oxidoreductase domain-containing protein 1 could unveil new therapeutic avenues for treating mitochondrial complex I deficiency, nuclear type 19, and related mitochondrial disorders.