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.
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 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q9UGI6
UPID:
KCNN3_HUMAN
Alternative names:
KCa2.3
Alternative UPACC:
Q9UGI6; B1ANX0; O43517; Q86VF9; Q8WXG7
Background:
Small conductance calcium-activated potassium channel protein 3 (KCa2.3) is a critical component in the regulation of neuronal excitability, forming a voltage-independent potassium channel activated by intracellular calcium. This protein plays a pivotal role in the slow component of synaptic afterhyperpolarization, contributing to the fine-tuning of synaptic transmission and neuronal signaling.
Therapeutic significance:
KCa2.3's involvement in Zimmermann-Laband syndrome 3, characterized by developmental disorders and potential intellectual disability, underscores its therapeutic significance. Targeting KCa2.3 could offer novel interventions for managing symptoms or altering the disease course, highlighting the importance of understanding its biological mechanisms.