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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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 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
P05062
UPID:
ALDOB_HUMAN
Alternative names:
Liver-type aldolase
Alternative UPACC:
P05062; Q13741; Q13742; Q5T7D6
Background:
Fructose-bisphosphate aldolase B, also known as Liver-type aldolase, plays a pivotal role in glycolysis and gluconeogenesis. It catalyzes the conversion of fructose 1,6-biphosphate into dihydroxyacetone phosphate and D-glyceraldehyde 3-phosphate, and vice versa. Beyond its enzymatic activity, it acts as a tumor suppressor by regulating oxidative pentose phosphate metabolism.
Therapeutic significance:
Hereditary fructose intolerance (HFI) is directly linked to mutations affecting Fructose-bisphosphate aldolase B. Understanding its function and the genetic variants that impair its activity is crucial for developing targeted therapies for HFI, offering hope for effective management and dramatic recovery from this autosomal recessive disease.