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.
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.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
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.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9BZI7
UPID:
REN3B_HUMAN
Alternative names:
Nonsense mRNA reducing factor 3B; Up-frameshift suppressor 3 homolog B; Up-frameshift suppressor 3 homolog on chromosome X
Alternative UPACC:
Q9BZI7; D3DWI3; D3DWI4; Q0VAK8; Q9H1J0
Background:
Regulator of nonsense transcripts 3B (RNT3B), also known as Nonsense mRNA reducing factor 3B, plays a crucial role in the nonsense-mediated decay (NMD) pathway. It is pivotal in degrading mRNAs with premature stop codons, thus preventing the synthesis of truncated, potentially harmful proteins. RNT3B functions by associating with the nuclear exon junction complex and recruiting UPF2 to activate NMD, showcasing its essential role in maintaining mRNA quality control.
Therapeutic significance:
RNT3B's involvement in Intellectual developmental disorder, X-linked, syndromic 14, highlights its therapeutic potential. Understanding RNT3B's mechanisms could pave the way for innovative treatments targeting genetic disorders caused by nonsense mutations, offering hope for patients with this and potentially other related conditions.