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.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
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.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q969Y2
UPID:
GTPB3_HUMAN
Alternative names:
GTP-binding protein 3; Mitochondrial GTP-binding protein 1
Alternative UPACC:
Q969Y2; A6NFH1; A6NIG5; A6NKR4; A8K7B4; B7Z4V8; Q8TCY6; Q8WUW9; Q969G4; Q9BX61
Background:
The tRNA modification GTPase GTPBP3, mitochondrial, also known as GTP-binding protein 3 or Mitochondrial GTP-binding protein 1, plays a crucial role in mitochondrial tRNA modification. Specifically, it is involved in the 5-carboxymethylaminomethyl modification of the wobble uridine base in mitochondrial tRNAs, a process essential for proper mitochondrial function and protein synthesis.
Therapeutic significance:
GTPBP3 is linked to Combined oxidative phosphorylation deficiency 23, a mitochondrial disorder with symptoms ranging from hypertrophic cardiomyopathy to neurologic issues. Understanding the role of GTPBP3 could open doors to potential therapeutic strategies for this condition, highlighting its importance in mitochondrial diseases.