Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best 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 procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P35575
UPID:
G6PC1_HUMAN
Alternative names:
Glucose-6-phosphatase; Glucose-6-phosphatase alpha
Alternative UPACC:
P35575; A1L4C0; B4E1C3; K7EL82
Background:
Glucose-6-phosphatase catalytic subunit 1, also known as Glucose-6-phosphatase or Glucose-6-phosphatase alpha, plays a pivotal role in glucose homeostasis. It hydrolyzes glucose-6-phosphate to glucose in the endoplasmic reticulum, partnering with the glucose-6-phosphate transporter to facilitate glucose production in glycogenolysis and gluconeogenesis.
Therapeutic significance:
The enzyme's dysfunction is linked to Glycogen storage disease 1A, a metabolic disorder marked by hypoglycemia, hepatomegaly, kidney enlargement, and growth retardation. Understanding its mechanism opens avenues for targeted therapies in metabolic diseases.