Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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.
Our high-tech, dedicated method is applied to construct targeted 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
P16219
UPID:
ACADS_HUMAN
Alternative names:
Butyryl-CoA dehydrogenase
Alternative UPACC:
P16219; P78331
Background:
Short-chain specific acyl-CoA dehydrogenase, mitochondrial, also known as Butyryl-CoA dehydrogenase, plays a pivotal role in mitochondrial fatty acid beta-oxidation. This process is crucial for breaking down fatty acids into acetyl-CoA, facilitating energy production from fats. The enzyme specifically targets acyl-CoAs with 4 to 6 carbon long primary chains, catalyzing the first step of fatty acid beta-oxidation by removing hydrogen from C-2 and C-3, leading to trans-2-enoyl-CoA formation.
Therapeutic significance:
Acyl-CoA dehydrogenase short-chain deficiency, a disease linked to mutations in the gene encoding this enzyme, manifests as acute acidosis and muscle weakness in infants, and lipid-storage myopathy in adults. Understanding the role of Short-chain specific acyl-CoA dehydrogenase could open doors to potential therapeutic strategies for treating this metabolic disorder.