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.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q8N8U9
UPID:
BMPER_HUMAN
Alternative names:
Bone morphogenetic protein-binding endothelial cell precursor-derived regulator; Protein crossveinless-2
Alternative UPACC:
Q8N8U9; A8K1P8; Q8TF36
Background:
The BMP-binding endothelial regulator protein, also known as Protein crossveinless-2, plays a crucial role in skeletal development by inhibiting bone morphogenetic protein (BMP) function. This regulation is essential for the proper responsiveness of osteoblasts and chondrocytes, the cells responsible for bone formation and cartilage development, respectively.
Therapeutic significance:
Given its pivotal role in skeletal development, understanding the BMP-binding endothelial regulator protein's function could open doors to potential therapeutic strategies for Diaphanospondylodysostosis, a rare skeletal disorder linked to gene variants affecting this protein.