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 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.
We utilise our cutting-edge, exclusive workflow to develop 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
P53004
UPID:
BIEA_HUMAN
Alternative names:
Biliverdin-IX alpha-reductase
Alternative UPACC:
P53004; A8K747; O95019; Q86UX0; Q96QL4; Q9BRW8
Background:
Biliverdin reductase A, also known as Biliverdin-IX alpha-reductase, plays a pivotal role in the heme degradation pathway. It catalyzes the conversion of biliverdin IX alpha to bilirubin, utilizing NADH or NADPH as cofactors. This enzyme's activity is crucial for maintaining the balance between biliverdin and bilirubin levels in the body, with preferences for NADH in acidic conditions and NADPH in alkaline.
Therapeutic significance:
Hyperbiliverdinemia, characterized by green discoloration of the skin and bodily fluids, is linked to mutations affecting Biliverdin reductase A. Understanding the role of Biliverdin reductase A could open doors to potential therapeutic strategies for treating this condition and related disorders of bilirubin metabolism.