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.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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 employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q8N442
UPID:
GUF1_HUMAN
Alternative names:
Elongation factor 4 homolog; GTPase GUF1; Ribosomal back-translocase
Alternative UPACC:
Q8N442; Q5XKM8; Q9H710; Q9H8U4
Background:
Translation factor GUF1, mitochondrial, also known as Elongation factor 4 homolog, GTPase GUF1, and Ribosomal back-translocase, plays a pivotal role in mitochondrial protein synthesis. It ensures the accuracy of protein translation by facilitating a one-codon backward translocation of tRNAs on ribosomes that have translocated improperly, binding to mitochondrial ribosomes in a GTP-dependent manner.
Therapeutic significance:
Linked to Developmental and epileptic encephalopathy 40 (DEE40), a severe early-onset epilepsy with neurodevelopmental impairment, the study of Translation factor GUF1, mitochondrial, offers a promising avenue for therapeutic intervention. Understanding its function could lead to novel strategies for managing DEE40, improving prognosis and quality of life for affected individuals.