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 promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
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 distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q16822
UPID:
PCKGM_HUMAN
Alternative names:
-
Alternative UPACC:
Q16822; B4DW73; O43253; Q86U01; Q9BV62
Background:
Phosphoenolpyruvate carboxykinase [GTP], mitochondrial (PEPCK-M), encoded by the gene with accession number Q16822, plays a pivotal role in gluconeogenesis. It catalyzes the conversion of oxaloacetate to phosphoenolpyruvate, a critical step in the metabolic pathway that generates glucose from lactate and other precursors. This enzyme's activity is essential for maintaining glucose homeostasis, especially during fasting states.
Therapeutic significance:
PEPCK-M deficiency, a metabolic disorder characterized by impaired gluconeogenesis, highlights the enzyme's crucial role in energy metabolism. The condition manifests with hypotonia, hepatomegaly, and hypoglycemia, underscoring the potential of targeting PEPCK-M for therapeutic interventions in metabolic diseases.