Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
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.
We use our state-of-the-art dedicated workflow for designing focused libraries for ion channels.
Fig. 1. The sreening workflow of Receptor.AI
It features detailed molecular simulations of the ion channel in its native membrane environment across its open, closed, and inactivated forms, coupled with ensemble virtual screening considering conformational mobility in these states. Potential binding sites are explored within the pore, in the gating region, and at allosteric locations to encompass all potential mechanisms of action.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q14654
UPID:
KCJ11_HUMAN
Alternative names:
IKATP; Inward rectifier K(+) channel Kir6.2; Potassium channel, inwardly rectifying subfamily J member 11
Alternative UPACC:
Q14654; B4DWI4; E9PNK0; Q2M1H7; Q58EX3; Q8IW96
Background:
ATP-sensitive inward rectifier potassium channel 11 (KCNJ11), also known as Kir6.2, plays a pivotal role in cellular physiology by regulating potassium flow. This receptor, controlled by G proteins, allows potassium to flow into cells, a process essential for maintaining the cell's electrical stability. KCNJ11 partners with ABCC9 to form ATP-sensitive potassium channels (KATP), crucial in cardiac and smooth muscle functions.
Therapeutic significance:
KCNJ11's malfunction is linked to several metabolic disorders, including Hyperinsulinemic hypoglycemia, familial, 2 (HHF2), and various forms of diabetes mellitus. These conditions underscore the protein's critical role in glucose homeostasis and insulin regulation. Understanding KCNJ11's function and its genetic variants offers a pathway to targeted treatments for these metabolic diseases.