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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
O15350
UPID:
P73_HUMAN
Alternative names:
p53-like transcription factor; p53-related protein
Alternative UPACC:
O15350; B7Z7J4; B7Z8Z1; B7Z9C1; C9J521; O15351; Q17RN8; Q5TBV5; Q5TBV6; Q8NHW9; Q8TDY5; Q8TDY6; Q9NTK8
Background:
Tumor protein p73, also known as a p53-like transcription factor, plays a crucial role in the apoptotic response to DNA damage. It exists in multiple isoforms, with some promoting apoptosis and others inhibiting it, thereby regulating the function of p53 and p73 isoforms. Additionally, it activates FOXJ1 expression and is vital for lung ciliated cell differentiation.
Therapeutic significance:
Given its involvement in primary ciliary dyskinesia, characterized by respiratory infections and neurologic features due to motile cilia abnormalities, understanding the role of Tumor protein p73 could open doors to potential therapeutic strategies.