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.
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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
Our high-tech, dedicated method is applied to construct targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9NS61
UPID:
KCIP2_HUMAN
Alternative names:
A-type potassium channel modulatory protein 2; Cardiac voltage-gated potassium channel modulatory subunit; Potassium channel-interacting protein 2
Alternative UPACC:
Q9NS61; A6NJE5; A8MQ75; Q3YAC6; Q3YAC8; Q3YAC9; Q7Z6F1; Q96K86; Q96T41; Q96T42; Q96T43; Q96T44; Q9H0N4; Q9HD10; Q9HD11; Q9NS60; Q9NY10; Q9NZI1
Background:
Kv channel-interacting protein 2, also known as A-type potassium channel modulatory protein 2, plays a crucial role in regulating Kv4/D (Shal)-type voltage-gated rapidly inactivating A-type potassium channels. It influences channel density, inactivation kinetics, and recovery rate from inactivation in a calcium-dependent and isoform-specific manner, primarily modulating KCND2/Kv4.2 and KCND3/Kv4.3 currents. This protein is pivotal for KCND2 and KCND3 trafficking to the cell surface and is essential for the expression of I(To) currents in the heart.
Therapeutic significance:
Understanding the role of Kv channel-interacting protein 2 could open doors to potential therapeutic strategies.