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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P45954
UPID:
ACDSB_HUMAN
Alternative names:
2-methyl branched chain acyl-CoA dehydrogenase; 2-methylbutyryl-coenzyme A dehydrogenase
Alternative UPACC:
P45954; B4DQ51; Q5SQN6; Q96CX7
Background:
Short/branched chain specific acyl-CoA dehydrogenase, mitochondrial, known alternatively as 2-methyl branched chain acyl-CoA dehydrogenase or 2-methylbutyryl-coenzyme A dehydrogenase, plays a pivotal role in fatty acid metabolism. It specifically catalyzes the dehydrogenation of short and branched chain acyl-CoA derivatives, crucial for the catabolism of L-isoleucine, a key amino acid.
Therapeutic significance:
The enzyme's deficiency leads to Short/branched-chain acyl-CoA dehydrogenase deficiency, a disorder marked by seizures and psychomotor delay due to impaired L-isoleucine catabolism. Understanding the role of this protein could open doors to potential therapeutic strategies.