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.
Our top-notch dedicated system is used to design specialised libraries for ion channels.
Fig. 1. The sreening workflow of Receptor.AI
This process includes comprehensive molecular simulations of the ion channel in its native membrane environment, depicting its open, closed, and inactivated states, and ensemble virtual screening that accounts for conformational mobility in each state. Tentative binding pockets are investigated inside the pore, at the gating region, and in allosteric sites to cover the full spectrum of possible mechanisms of action.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q08289
UPID:
CACB2_HUMAN
Alternative names:
Calcium channel voltage-dependent subunit beta 2; Lambert-Eaton myasthenic syndrome antigen B
Alternative UPACC:
Q08289; A6PVM5; A6PVM7; A6PVM8; O00304; Q5QJ99; Q5QJA0; Q5VVG9; Q5VVH0; Q5VWV6; Q6TME1; Q6TME2; Q6TME3; Q8WX81; Q96NZ3; Q96NZ4; Q96NZ5; Q9BWU2; Q9HD32; Q9Y340; Q9Y341
Background:
The Voltage-dependent L-type calcium channel subunit beta-2, also known as Calcium channel voltage-dependent subunit beta 2 and Lambert-Eaton myasthenic syndrome antigen B, plays a crucial role in cardiac function. It enhances peak calcium current, modulates voltage dependencies, and contributes to beta-adrenergic augmentation of Ca(2+) influx in cardiomyocytes. This protein is pivotal in regulating heart rate and contractile force.
Therapeutic significance:
Given its involvement in Brugada syndrome 4, a heart disease leading to potentially fatal arrhythmias, understanding the role of Voltage-dependent L-type calcium channel subunit beta-2 could open doors to potential therapeutic strategies. Its function in calcium channel modulation and cardiomyocyte activity makes it a target for developing treatments aimed at heart rhythm disorders.