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.
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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
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
Q92838
UPID:
EDA_HUMAN
Alternative names:
Ectodermal dysplasia protein
Alternative UPACC:
Q92838; A0AUZ2; A2A337; B7ZLU2; B7ZLU4; O75910; Q5JS00; Q5JUM7; Q9UP77; Q9Y6L0; Q9Y6L1; Q9Y6L2; Q9Y6L3; Q9Y6L4
Background:
Ectodysplasin-A, also known as Ectodermal dysplasia protein, plays a pivotal role in the development of ectodermal organs through epithelial-mesenchymal signaling. It activates the DEATH-domain containing receptors EDAR and EDA2R, essential for morphogenesis. Additionally, it may contribute to cell adhesion processes.
Therapeutic significance:
Ectodysplasin-A is crucial in understanding Ectodermal dysplasia 1, hypohidrotic, X-linked, and selective tooth agenesis, X-linked, 1. These conditions, caused by gene variants affecting Ectodysplasin-A, highlight its potential as a target for therapeutic intervention, promising advancements in treatment strategies.