Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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.
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.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q13794
UPID:
APR_HUMAN
Alternative names:
Immediate-early-response protein APR; Protein Noxa
Alternative UPACC:
Q13794; B2R4T7; Q8N589
Background:
Phorbol-12-myristate-13-acetate-induced protein 1, also known as Immediate-early-response protein APR or Protein Noxa, plays a pivotal role in apoptosis. It promotes caspase activation, mitochondrial membrane changes, and the release of apoptogenic proteins. Furthermore, it contributes to p53/TP53-dependent apoptosis post-radiation and facilitates the proteasomal degradation of MCL1. Notably, it competes with BAK1 and BIM/BCL2L11 for MCL1 binding, displacing them from their binding sites.
Therapeutic significance:
Understanding the role of Phorbol-12-myristate-13-acetate-induced protein 1 could open doors to potential therapeutic strategies.