Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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.
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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P61978
UPID:
HNRPK_HUMAN
Alternative names:
Transformation up-regulated nuclear protein
Alternative UPACC:
P61978; Q07244; Q15671; Q59F98; Q5T6W4; Q60577; Q6IBN1; Q922Y7; Q96J62
Background:
Heterogeneous nuclear ribonucleoprotein K (HNRNPK) is a key player in the nuclear metabolism of hnRNAs, especially those containing cytidine-rich sequences. It binds strongly to poly(C) sequences and has a pivotal role in the p53/TP53 response to DNA damage, influencing both transcription activation and repression. Its interaction with lincRNA-p21 is crucial for apoptosis induction.
Therapeutic significance:
Given its involvement in Au-Kline syndrome, a disorder marked by intellectual disability and skeletal abnormalities, understanding HNRNPK's role could open doors to potential therapeutic strategies.