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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated 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 utilise our cutting-edge, exclusive workflow to develop focused libraries for ion channels.
Fig. 1. The sreening workflow of Receptor.AI
This includes extensive molecular simulations of the ion channel in its native membrane environment, in open, closed, and inactivated forms, paired with ensemble virtual screening that factors in conformational mobility in each state. Tentative binding pockets are considered in the pore, the gating region, and allosteric areas to capture the full range of mechanisms of action.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q15858
UPID:
SCN9A_HUMAN
Alternative names:
Neuroendocrine sodium channel; Peripheral sodium channel 1; Sodium channel protein type IX subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.7
Alternative UPACC:
Q15858; A1BUH5; Q6B4R9; Q6B4S0; Q6B4S1; Q70HX1; Q70HX2; Q8WTU1; Q8WWN4
Background:
The Sodium channel protein type 9 subunit alpha, also known as Nav1.7, plays a crucial role in the voltage-dependent sodium ion permeability of excitable membranes. It transitions between opened or closed conformations in response to voltage changes, forming a sodium-selective channel. This protein is pivotal in pain perception mechanisms, particularly in inflammatory pain.
Therapeutic significance:
Nav1.7 is linked to several autosomal disorders, including Primary erythermalgia, Indifference to pain, congenital, autosomal recessive, and Paroxysmal extreme pain disorder. These associations highlight its potential as a target for developing treatments for pain disorders and conditions involving sodium ion channel dysfunctions.