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.
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 employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q8NCW5
UPID:
NNRE_HUMAN
Alternative names:
Apolipoprotein A-I-binding protein; NAD(P)HX epimerase; YjeF N-terminal domain-containing protein 1
Alternative UPACC:
Q8NCW5; B4DGY3; Q496C6; Q5T3I2
Background:
NAD(P)H-hydrate epimerase, also known as Apolipoprotein A-I-binding protein and YjeF N-terminal domain-containing protein 1, plays a crucial role in cellular metabolism. It catalyzes the epimerization of NAD(P)HX, a damaged form of NAD(P)H, facilitating its repair. This protein also enhances cholesterol efflux from endothelial cells to HDL, influencing angiogenesis.
Therapeutic significance:
The protein is linked to a severe neurometabolic disorder, early-onset progressive encephalopathy with brain edema and/or leukoencephalopathy 1, caused by gene variants. Understanding the role of NAD(P)H-hydrate epimerase could open doors to potential therapeutic strategies for this devastating condition.