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.
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 includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Our library distinguishes itself through several key aspects:
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.