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.
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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q7KZN9
UPID:
COX15_HUMAN
Alternative names:
-
Alternative UPACC:
Q7KZN9; A8K6I9; O60556; O75878; Q5TD00; Q5TD01; Q7Z3Q3; Q9NTN0
Background:
The Cytochrome c oxidase assembly protein COX15 homolog plays a crucial role in cellular energy production, specifically in the biosynthesis of heme A, an essential component of the mitochondrial respiratory chain. This protein is integral to the assembly and proper functioning of cytochrome c oxidase, the terminal enzyme complex in the mitochondrial electron transport chain.
Therapeutic significance:
Given its pivotal role in mitochondrial function, mutations in the COX15 gene leading to Mitochondrial complex IV deficiency, nuclear type 6, underscore the protein's therapeutic significance. This condition manifests with a spectrum of severe clinical features, including encephalopathy, cardiomyopathy, and persistent lactic acidosis. Targeting the COX15 protein pathway offers a promising avenue for developing treatments for mitochondrial disorders.