Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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 high-tech, dedicated method is applied to construct 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.
Our library is unique due to several crucial 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.