Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q99259
UPID:
DCE1_HUMAN
Alternative names:
67 kDa glutamic acid decarboxylase; Glutamate decarboxylase 67 kDa isoform
Alternative UPACC:
Q99259; Q49AK1; Q53TQ7; Q9BU91; Q9UHH4
Background:
Glutamate decarboxylase 1 (GAD1), also known as the 67 kDa glutamic acid decarboxylase or Glutamate decarboxylase 67 kDa isoform, plays a pivotal role in the central nervous system. It catalyzes the synthesis of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter, utilizing pyridoxal 5'-phosphate as a cofactor. Despite its enzymatic inactivity as glutamate decarboxylase, GAD1's contribution to neurotransmission and neural regulation is significant.
Therapeutic significance:
GAD1's association with Developmental and epileptic encephalopathy 89 (DEE89), a severe form of epileptic encephalopathy, underscores its therapeutic significance. DEE89 is characterized by profound developmental delays, absent speech, inability to sit or walk, and early-onset seizures. Understanding the role of GAD1 could open doors to potential therapeutic strategies for managing DEE89 and related neurological disorders.