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 carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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.
Our high-tech, dedicated method is applied to construct targeted libraries for ion channels.
Fig. 1. The sreening workflow of Receptor.AI
It includes extensive molecular simulations of the channel in its native membrane environment in open, closed and inactivated forms and the ensemble virtual screening accounting for conformational mobility in each of these states. Tentative binding pockets are considered inside the pore, in the gating region and in the allosteric locations to cover the whole spectrum of possible mechanisms of action.
Our library distinguishes itself through several key aspects:
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.