Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
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.
Our high-tech, dedicated method is applied to construct targeted 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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8N2H3
UPID:
PYRD2_HUMAN
Alternative names:
-
Alternative UPACC:
Q8N2H3; D3DR61; Q5TAA9; Q9BRQ1
Background:
Pyridine nucleotide-disulfide oxidoreductase domain-containing protein 2, encoded by the gene with accession number Q8N2H3, is identified as a probable oxidoreductase. This protein is believed to play a pivotal role in regulating mitochondrial function, which is crucial for energy production and cellular metabolism.
Therapeutic significance:
Understanding the role of Pyridine nucleotide-disulfide oxidoreductase domain-containing protein 2 could open doors to potential therapeutic strategies. Its involvement in mitochondrial regulation suggests its potential impact on diseases related to mitochondrial dysfunction.