Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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.
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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
P62633
UPID:
CNBP_HUMAN
Alternative names:
Cellular nucleic acid-binding protein; Zinc finger protein 9
Alternative UPACC:
P62633; A8K7V4; B2RAV9; B4DP17; D3DNB9; D3DNC0; D3DNC1; E9PDR7; P20694; Q4JGY0; Q4JGY1; Q5QJR0; Q5U0E9; Q6PJI7; Q96NV3
Background:
The CCHC-type zinc finger nucleic acid binding protein, also known as Cellular nucleic acid-binding protein or Zinc finger protein 9, plays a crucial role in cellular processes. It preferentially binds to single-stranded DNA and RNA, mediating transcriptional repression and supporting translation by resolving stable structures on mRNAs. Its ability to bind G-rich elements in mRNA coding sequences is vital for preventing G-quadruplex structure formation.
Therapeutic significance:
Linked to Dystrophia myotonica 2, a multisystem disease, the protein's mutation involves a CCTG expansion in the CNBP gene. Understanding its role could lead to novel therapeutic strategies for managing symptoms like muscle weakness, myotonia, and cardiac manifestations.