Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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 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.
We employ our advanced, specialised process to create targeted libraries for ion channels.
Fig. 1. The sreening workflow of Receptor.AI
The method involves in-depth molecular simulations of the ion channel in its native membrane environment, including its open, closed, and inactivated states, along with ensemble virtual screening that focuses on conformational mobility for each state. Tentative binding pockets are identified inside the pore, in the gating area, and at allosteric sites to address every conceivable mechanism of action.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q99250
UPID:
SCN2A_HUMAN
Alternative names:
HBSC II; Sodium channel protein brain II subunit alpha; Sodium channel protein type II subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.2
Alternative UPACC:
Q99250; A6NC14; A6NIQ5; Q14472; Q53T77; Q9BZC9; Q9BZD0
Background:
The Sodium channel protein type 2 subunit alpha, known as Nav1.2, plays a crucial role in the voltage-dependent sodium ion permeability of excitable membranes. It transitions between opened or closed conformations based on the voltage difference across the membrane, forming a sodium-selective channel. This protein is pivotal in regulating hippocampal replay within sharp wave ripples, essential for memory consolidation.
Therapeutic significance:
Nav1.2 is implicated in several neurological disorders, including benign familial infantile seizures, developmental and epileptic encephalopathy, and episodic ataxia. Understanding its function and the genetic variants affecting it opens avenues for targeted therapeutic strategies, potentially revolutionizing treatment for these conditions.