Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
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.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9UI33
UPID:
SCNBA_HUMAN
Alternative names:
Peripheral nerve sodium channel 5; Sensory neuron sodium channel 2; Sodium channel protein type XI subunit alpha; Voltage-gated sodium channel subunit alpha Nav1.9; hNaN
Alternative UPACC:
Q9UI33; A6NN05; C9JD48; C9JR31; Q68K15; Q8NDX3; Q9UHE0; Q9UHM0
Background:
The Sodium channel protein type 11 subunit alpha, known as Nav1.9, plays a crucial role in the voltage-dependent sodium ion permeability of excitable membranes. It switches between opened or closed conformations based on the voltage difference across the membrane, forming a sodium-selective channel. This tetrodotoxin-resistant sodium channel isoform, with NTRK2's contribution, facilitates rapid BDNF-evoked neuronal depolarization.
Therapeutic significance:
Nav1.9's involvement in hereditary sensory and autonomic neuropathy 7 (HSAN7) and familial episodic pain syndrome 3 highlights its therapeutic potential. Understanding Nav1.9's function could lead to novel treatments for these debilitating conditions, offering hope for patients suffering from congenital pain insensitivity and paroxysmal extremity pain.