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.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed 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.
Our high-tech, dedicated method is applied to construct targeted 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.