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.
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.
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 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
P51788
UPID:
CLCN2_HUMAN
Alternative names:
-
Alternative UPACC:
P51788; B4DQT9; B4DZ58; E9PBD9; E9PCD2; O14864; Q6IPA9; Q8WU13
Background:
Chloride Channel Protein 2 (CLCN2) is a voltage-gated chloride channel, crucial for various physiological processes including cell volume regulation, membrane potential stabilization, and transepithelial transport. It plays a pivotal role in aldosterone production by depolarizing cell membranes in the adrenal gland, leading to increased aldosterone synthase expression.
Therapeutic significance:
CLCN2 is implicated in several neurological disorders and hypertension, such as idiopathic generalized epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy, leukoencephalopathy with ataxia, and familial hyperaldosteronism. Targeting CLCN2 could offer novel therapeutic avenues for these conditions.