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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated 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.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9UNE0
UPID:
EDAR_HUMAN
Alternative names:
Anhidrotic ectodysplasin receptor 1; Downless homolog; EDA-A1 receptor; Ectodermal dysplasia receptor; Ectodysplasin-A receptor
Alternative UPACC:
Q9UNE0; B2R9H2; B4DLC5; D3DX74; E9PC98; Q52LL5; Q9UND9
Background:
Tumor necrosis factor receptor superfamily member EDAR, also known as Anhidrotic ectodysplasin receptor 1, plays a crucial role in ectodermal development. It specifically binds to EDA isoform A1, activating NF-kappa-B and JNK pathways, and may promote caspase-independent cell death. This receptor's involvement in ectodermal dysplasias highlights its importance in hair, teeth, and sweat gland development.
Therapeutic significance:
EDAR's mutation leads to ectodermal dysplasia 10A and 10B, affecting hair, teeth, and sweat glands. Understanding EDAR's role could open doors to potential therapeutic strategies for these conditions, offering hope for targeted treatments.