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.
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.
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.
We utilise our cutting-edge, exclusive workflow to develop focused 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
P06730
UPID:
IF4E_HUMAN
Alternative names:
eIF-4F 25 kDa subunit; mRNA cap-binding protein
Alternative UPACC:
P06730; B7Z6V1; D6RCQ6; Q96E95
Background:
Eukaryotic translation initiation factor 4E (EIF4E), also known as the mRNA cap-binding protein, plays a pivotal role in the initiation of protein synthesis. It is a key component of the eIF4F complex, facilitating ribosome binding by unwinding mRNA secondary structures and recognizing the 7-methylguanosine cap. EIF4E's involvement extends to regulating translation and stability in the cytoplasm, and it is part of complexes that mediate translational repression and mRNA storage.
Therapeutic significance:
EIF4E's deregulation is linked to Autism 19, where a heterozygous single-nucleotide insertion increases promoter activity, affecting gene expression. Understanding the role of EIF4E could open doors to potential therapeutic strategies for autism and other translation-related disorders.