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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library stands out due to several important features:
partner
Reaxense
upacc
P03923
UPID:
NU6M_HUMAN
Alternative names:
NADH dehydrogenase subunit 6
Alternative UPACC:
P03923; Q34774; Q8HG30
Background:
NADH-ubiquinone oxidoreductase chain 6, also known as NADH dehydrogenase subunit 6, plays a pivotal role in cellular energy production. As a core component of the mitochondrial membrane respiratory chain Complex I, it facilitates the transfer of electrons from NADH to ubiquinone, a critical step in the mitochondrial respiratory chain that drives ATP synthesis.
Therapeutic significance:
The protein's involvement in diseases such as Leber hereditary optic neuropathy, mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes syndrome, and Leigh syndrome underscores its clinical importance. These conditions, linked to mutations affecting the protein, highlight the potential of targeting NADH-ubiquinone oxidoreductase chain 6 in therapeutic strategies aimed at mitigating mitochondrial dysfunction.