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.
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 includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
Our top-notch dedicated system is used to design specialised 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 distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q16134
UPID:
ETFD_HUMAN
Alternative names:
Electron-transferring-flavoprotein dehydrogenase
Alternative UPACC:
Q16134; B4E3R9; J3KND9; Q7Z347
Background:
Electron transfer flavoprotein-ubiquinone oxidoreductase, mitochondrial, also known as Electron-transferring-flavoprotein dehydrogenase, plays a pivotal role in the mitochondrial respiratory chain. It accepts electrons from the electron transfer flavoprotein and reduces ubiquinone, facilitating the transfer of electrons from various substrates to the mitochondrial electron transport chain.
Therapeutic significance:
The protein is directly linked to Glutaric aciduria 2C, a metabolic disorder affecting fatty acid, amino acid, and choline metabolism. This association highlights its critical role in metabolic pathways and underscores the potential for targeted therapeutic strategies to address the underlying genetic variants causing this disorder.