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.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P02647
UPID:
APOA1_HUMAN
Alternative names:
Apolipoprotein A1
Alternative UPACC:
P02647; A8K866; Q6LDN9; Q6Q785; Q9UCS8; Q9UCT8
Background:
Apolipoprotein A-I, known for its pivotal role in lipid metabolism, facilitates the reverse transport of cholesterol from tissues back to the liver, aiding in its excretion. It acts as a crucial cofactor for the lecithin cholesterol acyltransferase (LCAT) and is instrumental in activating spermatozoa motility as part of the SPAP complex.
Therapeutic significance:
Apolipoprotein A-I is directly linked to several lipid metabolism disorders, including Hypoalphalipoproteinemia and Familial apolipoprotein gene cluster deletion syndrome, which are characterized by severe HDL-C deficiency and increased cardiovascular risk. Understanding its function and the genetic variants affecting it could lead to novel therapeutic strategies targeting these lipid-related diseases.