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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
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 use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
P36382
UPID:
CXA5_HUMAN
Alternative names:
Connexin-40
Alternative UPACC:
P36382; Q5T3B6; Q5U0N6
Background:
Gap junction alpha-5 protein, also known as Connexin-40, plays a pivotal role in cell communication by forming channels that allow the diffusion of small molecules between adjacent cells. This protein is essential for the coordinated function of tissues, particularly in the heart where it facilitates electrical conduction.
Therapeutic significance:
Mutations in Gap junction alpha-5 protein are linked to Atrial standstill 1 and Familial Atrial fibrillation, 11. These conditions underscore the protein's critical role in maintaining heart rhythm. Understanding the role of Gap junction alpha-5 protein could open doors to potential therapeutic strategies for these arrhythmias.