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.
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.
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.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Our library stands out due to several important features:
partner
Reaxense
upacc
P06865
UPID:
HEXA_HUMAN
Alternative names:
Beta-N-acetylhexosaminidase subunit alpha; N-acetyl-beta-glucosaminidase subunit alpha
Alternative UPACC:
P06865; B4DKE7; E7ENH7; Q53HS8; Q6AI32
Background:
Beta-hexosaminidase subunit alpha, also known as N-acetyl-beta-glucosaminidase subunit alpha, plays a crucial role in the degradation of GM2 gangliosides. It hydrolyzes the non-reducing end N-acetyl-D-hexosamine of glycoconjugates, crucial for the breakdown of oligosaccharides from proteins and lipids.
Therapeutic significance:
The protein's deficiency is directly linked to GM2-gangliosidosis 1, a severe lysosomal storage disease causing neurodegeneration and early childhood death. Targeting this protein's pathway offers a promising avenue for therapeutic intervention in treating this genetic disorder.