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.
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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
Our top-notch dedicated system is used to design specialised 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
Q8NI60
UPID:
COQ8A_HUMAN
Alternative names:
Chaperone activity of bc1 complex-like; Coenzyme Q protein 8A; aarF domain-containing protein kinase 3
Alternative UPACC:
Q8NI60; Q5T7A5; Q63HK0; Q8NCJ6; Q9HBQ1; Q9NQ67
Background:
Atypical kinase COQ8A, mitochondrial, also known as Coenzyme Q protein 8A, plays a crucial role in the biosynthesis of coenzyme Q (ubiquinone). This lipid-soluble electron transporter is vital for aerobic cellular respiration. Despite its unclear substrate specificity, COQ8A does not exhibit traditional protein kinase activity but is suggested to act as a lipid kinase, phosphorylating a prenyl lipid in the ubiquinone biosynthesis pathway.
Therapeutic significance:
COQ8A is linked to Coenzyme Q10 deficiency, primary, 4, an autosomal recessive disorder characterized by cerebellar ataxia, exercise intolerance, and potential psychomotor retardation. Understanding the role of COQ8A could open doors to potential therapeutic strategies for this condition.