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 carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q9NPI9
UPID:
KCJ16_HUMAN
Alternative names:
Inward rectifier K(+) channel Kir5.1; Potassium channel, inwardly rectifying subfamily J member 16
Alternative UPACC:
Q9NPI9
Background:
Inward rectifier potassium channel 16 (KCNJ16), also known as Kir5.1, plays a pivotal role in maintaining potassium ion balance across cell membranes. This channel's unique property of allowing potassium ions to flow more readily into the cell than out underlies its critical function in regulating cell excitability and potassium homeostasis. KCNJ16, alongside KCNJ10, is instrumental in the basolateral recycling of potassium in kidney distal tubules, a process essential for sodium reabsorption and fluid and pH balance.
Therapeutic significance:
KCNJ16's involvement in Hypokalemic tubulopathy and deafness, a disease characterized by renal tubulopathy, hypokalemia, salt wasting, and sensorineural deafness, underscores its therapeutic potential. Targeting KCNJ16 could lead to innovative treatments for this autosomal recessive disorder, offering hope for patients suffering from its debilitating effects.