Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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 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.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q8NBJ7
UPID:
SUMF2_HUMAN
Alternative names:
Paralog of formylglycine-generating enzyme; Sulfatase-modifying factor 2
Alternative UPACC:
Q8NBJ7; B4DU41; B4DWQ0; Q14DW5; Q53ZE3; Q96BH2; Q9BRN3; Q9BWI1; Q9Y405
Background:
Inactive C-alpha-formylglycine-generating enzyme 2, also known as Sulfatase-modifying factor 2, plays a crucial role in the post-translational modification of sulfatases. It is characterized by its inability to activate newly synthesized sulfatases, a process essential for their enzymatic activity. This protein acts by inhibiting the activation of sulfatases by SUMF1, highlighting its unique function in cellular mechanisms.
Therapeutic significance:
Understanding the role of Inactive C-alpha-formylglycine-generating enzyme 2 could open doors to potential therapeutic strategies. Its involvement in the regulation of sulfatase activity suggests a pivotal role in metabolic pathways, which, if manipulated, could offer novel approaches to treating diseases linked to sulfatase dysfunction.