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.
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.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P28347
UPID:
TEAD1_HUMAN
Alternative names:
NTEF-1; Protein GT-IIC; TEA domain family member 1; Transcription factor 13
Alternative UPACC:
P28347; A4FUP2; E7EV65
Background:
Transcriptional enhancer factor TEF-1, also known as NTEF-1, Protein GT-IIC, and TEA domain family member 1, is a pivotal transcription factor in the Hippo signaling pathway. This pathway is crucial for organ size control and tumor suppression, functioning through a kinase cascade that ultimately inhibits YAP1 oncoprotein and WWTR1/TAZ, thereby regulating cell proliferation, migration, and epithelial-mesenchymal transition (EMT). TEF-1 binds specifically to enhansons, activating transcription in a cell-specific manner and playing a significant role in cardiac development.
Therapeutic significance:
TEF-1's involvement in Sveinsson chorioretinal atrophy, characterized by symmetrical lesions radiating from the optic disk, underscores its potential as a target for therapeutic intervention. Understanding the role of TEF-1 could open doors to potential therapeutic strategies.