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 pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P30084
UPID:
ECHM_HUMAN
Alternative names:
Enoyl-CoA hydratase 1; Short-chain enoyl-CoA hydratase
Alternative UPACC:
P30084; O00739; Q5VWY1; Q96H54
Background:
Enoyl-CoA hydratase, mitochondrial, also known as Enoyl-CoA hydratase 1 or Short-chain enoyl-CoA hydratase, plays a pivotal role in fatty acid oxidation. It specifically converts unsaturated trans-2-enoyl-CoA species to (3S)-3hydroxyacyl-CoA, facilitating the beta-oxidation spiral of short- and medium-chain fatty acids. This enzyme exhibits high substrate specificity for crotonyl-CoA and moderate specificity for several other enoyl-CoA thioesters.
Therapeutic significance:
The enzyme's deficiency is linked to Mitochondrial short-chain enoyl-CoA hydratase 1 deficiency, a severe metabolic disorder affecting valine metabolism, leading to neurodegeneration and increased lactic acid. Understanding the role of Enoyl-CoA hydratase could open doors to potential therapeutic strategies for this and related metabolic disorders.