Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q9NX02
UPID:
NALP2_HUMAN
Alternative names:
Nucleotide-binding site protein 1; PYRIN domain and NACHT domain-containing protein 1; PYRIN-containing APAF1-like protein 2
Alternative UPACC:
Q9NX02; B4DZL7; I3L0G4; Q53FL5; Q59G09; Q8IXT0; Q9BVN5; Q9H6G6; Q9HAV9; Q9NWK3
Background:
NACHT, LRR, and PYD domains-containing protein 2, also known as Nucleotide-binding site protein 1, plays a crucial role in immune response regulation. It suppresses TNF- and CD40-induced NFKB1 activity, inhibiting NFKBIA degradation. This protein, in association with PYCARD, activates CASP1, leading to IL1B cytokine secretion, and may be part of the inflammasome complex, crucial for pro-inflammatory caspases activation.
Therapeutic significance:
Understanding the role of NACHT, LRR, and PYD domains-containing protein 2 could open doors to potential therapeutic strategies.