Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We employ our advanced, specialised process to create targeted 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
P01008
UPID:
ANT3_HUMAN
Alternative names:
Serpin C1
Alternative UPACC:
P01008; B2R6P0; P78439; P78447; Q13815; Q5TC78; Q7KZ43; Q7KZ97; Q9UC78
Background:
Antithrombin-III, also known as Serpin C1, plays a pivotal role in the regulation of blood coagulation, acting as the primary serine protease inhibitor in plasma. It targets key factors in the coagulation cascade, including thrombin, matriptase-3/TMPRSS7, and factors IXa, Xa, and XIa, with its activity significantly amplified in the presence of heparin.
Therapeutic significance:
Antithrombin III deficiency, a risk factor for hereditary thrombophilia, underscores the critical function of Antithrombin-III in preventing thrombosis. This condition manifests in various forms, from decreased antigenic and functional levels to mutations affecting thrombin and heparin-binding domains, highlighting the therapeutic potential of targeting Antithrombin-III in coagulation disorders.