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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9H845
UPID:
ACAD9_HUMAN
Alternative names:
Acyl-CoA dehydrogenase family member 9
Alternative UPACC:
Q9H845; D3DNB8; Q8WXX3
Background:
Complex I assembly factor ACAD9, mitochondrial, also known as Acyl-CoA dehydrogenase family member 9, is pivotal in the assembly of mitochondrial complex I, crucial for oxidative phosphorylation. It exhibits dehydrogenase activity, preferentially targeting long-chain unsaturated acyl-CoAs, although this function seems secondary in vivo.
Therapeutic significance:
Linked to Mitochondrial complex I deficiency, nuclear type 20, a severe metabolic disorder, understanding ACAD9's role could unveil novel therapeutic avenues.