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.
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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We employ our advanced, specialised process to create 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
P04066
UPID:
FUCO_HUMAN
Alternative names:
Alpha-L-fucosidase I; Alpha-L-fucoside fucohydrolase 1
Alternative UPACC:
P04066; B2RBG3; Q14334; Q14335; Q3LID0; Q8NAC2
Background:
Tissue alpha-L-fucosidase, also known as Alpha-L-fucosidase I and Alpha-L-fucoside fucohydrolase 1, encoded by the gene with accession number P04066, plays a crucial role in cellular processes. It is responsible for hydrolyzing the alpha-1,6-linked fucose joined to the reducing-end N-acetylglucosamine of the carbohydrate moieties of glycoproteins. This enzymatic activity is vital for the proper degradation and recycling of glycoproteins within cells.
Therapeutic significance:
The dysfunction of Tissue alpha-L-fucosidase is directly linked to Fucosidosis, an autosomal recessive lysosomal storage disease. This condition is marked by the accumulation of fucose-containing glycolipids and glycoproteins, leading to severe symptoms including facial dysmorphism, dysostosis multiplex, moderate hepatomegaly, severe intellectual deficit, and deafness. Understanding the role of Tissue alpha-L-fucosidase could pave the way for innovative therapeutic strategies targeting the molecular basis of Fucosidosis.