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.
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.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q16836
UPID:
HCDH_HUMAN
Alternative names:
Medium and short-chain L-3-hydroxyacyl-coenzyme A dehydrogenase; Short-chain 3-hydroxyacyl-CoA dehydrogenase
Alternative UPACC:
Q16836; J3KQ17; O00324; O00397; O00753; Q4W5B4
Background:
Hydroxyacyl-coenzyme A dehydrogenase, mitochondrial, known for its roles in mitochondrial fatty acid beta-oxidation, catalyzes the third step of the beta-oxidation cycle. This enzyme is crucial for the metabolism of medium and short-chain 3-hydroxy fatty acyl-CoAs, impacting energy production. Its alternative names include Medium and short-chain L-3-hydroxyacyl-coenzyme A dehydrogenase and Short-chain 3-hydroxyacyl-CoA dehydrogenase.
Therapeutic significance:
This protein's malfunction is linked to 3-alpha-hydroxyacyl-CoA dehydrogenase deficiency and Hyperinsulinemic hypoglycemia, familial, 4, both metabolic disorders with severe clinical manifestations. Understanding its role could lead to novel therapeutic strategies for these conditions.