Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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.
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 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
Q9Y3Z3
UPID:
SAMH1_HUMAN
Alternative names:
Dendritic cell-derived IFNG-induced protein; Monocyte protein 5; SAM domain and HD domain-containing protein 1
Alternative UPACC:
Q9Y3Z3; B4E2A5; E1P5V2; Q5JXG8; Q8N491; Q9H004; Q9H005; Q9H3U9
Background:
Deoxynucleoside triphosphate triphosphohydrolase SAMHD1, also known as Dendritic cell-derived IFNG-induced protein, plays a crucial role in cellular defense against viral infections and in DNA repair mechanisms. It exhibits dNTPase activity, crucial for limiting viral replication by reducing cellular dNTP levels, and aids in the regulation of DNA precursor pools.
Therapeutic significance:
SAMHD1's involvement in Aicardi-Goutieres syndrome 5 and Chilblain lupus 2, through gene variants, highlights its potential as a target for therapeutic intervention. Understanding SAMHD1's functions could pave the way for novel treatments for these conditions.