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.
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 enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8N490
UPID:
PNKD_HUMAN
Alternative names:
Myofibrillogenesis regulator 1; Paroxysmal nonkinesiogenic dyskinesia protein; Trans-activated by hepatitis C virus core protein 2
Alternative UPACC:
Q8N490; A8K1F2; Q96A48; Q9BU26; Q9NSX4; Q9ULN6; Q9Y4T1
Background:
Probable hydrolase PNKD, also known as Myofibrillogenesis regulator 1, plays a pivotal role in muscle function and movement regulation. It is implicated in Dystonia 8, a disorder characterized by involuntary muscle contractions and abnormal postures triggered by stress or stimulants. This protein's alternative names include Paroxysmal nonkinesiogenic dyskinesia protein and Trans-activated by hepatitis C virus core protein 2, reflecting its diverse biological implications.
Therapeutic significance:
The association of PNKD with Dystonia 8, where it aggravates cardiac hypertrophy via the NF-kappa-B signaling pathway, highlights its potential as a therapeutic target. Understanding the role of PNKD could open doors to potential therapeutic strategies for managing and treating involuntary muscle contractions and related cardiovascular complications.