Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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.
We use our state-of-the-art dedicated workflow for designing focused 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
Q9UI95
UPID:
MD2L2_HUMAN
Alternative names:
Mitotic arrest deficient 2-like protein 2; REV7 homolog
Alternative UPACC:
Q9UI95; B3KNE3; Q5TGW7; Q9UNA7; Q9Y6I6
Background:
Mitotic spindle assembly checkpoint protein MAD2B, also known as Mitotic arrest deficient 2-like protein 2 and REV7 homolog, plays a pivotal role in cellular processes. It acts as an adapter protein, interacting with various proteins to mediate different biological functions. These include translesion DNA synthesis, crucial for bypassing DNA lesions and ensuring replication continuity, and the formation of the shieldin complex, vital for DNA double-stranded break repair. MAD2B's involvement in cell cycle regulation and DNA damage response underscores its importance in maintaining genomic stability.
Therapeutic significance:
MAD2B's association with Fanconi anemia, complementation group V, a disorder marked by bone marrow failure and cancer predisposition, highlights its therapeutic significance. Understanding the role of MAD2B could open doors to potential therapeutic strategies for treating Fanconi anemia and possibly other related malignancies by targeting its pathway and interaction networks.