Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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.
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 employ our advanced, specialised process to create 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 distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q6NVY1
UPID:
HIBCH_HUMAN
Alternative names:
3-hydroxyisobutyryl-coenzyme A hydrolase
Alternative UPACC:
Q6NVY1; D3DPI4; Q53GA8; Q53GF2; Q53RF7; Q53TC6; Q92931; Q9BS94
Background:
The 3-hydroxyisobutyryl-CoA hydrolase, mitochondrial, known alternatively as 3-hydroxyisobutyryl-coenzyme A hydrolase, plays a crucial role in valine metabolism. It efficiently hydrolyzes 3-hydroxyisobutyryl-CoA (HIBYL-CoA) and has a high activity toward isobutyryl-CoA, indicating its potential involvement in isobutyryl-CoA dehydrogenase function and valine catabolism. Additionally, it can hydrolyze 3-hydroxypropanoyl-CoA.
Therapeutic significance:
3-hydroxyisobutyryl-CoA hydrolase deficiency, a disease linked to mutations in the gene encoding this protein, manifests as severely delayed psychomotor development, neurodegeneration, increased lactic acid, and brain lesions in the basal ganglia. Understanding the role of 3-hydroxyisobutyryl-CoA hydrolase could open doors to potential therapeutic strategies for treating this metabolic disorder.