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.
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.
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.
Our high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library stands out due to several important features:
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.