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.
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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
Our top-notch dedicated system is used to design specialised libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P05107
UPID:
ITB2_HUMAN
Alternative names:
Cell surface adhesion glycoproteins LFA-1/CR3/p150,95 subunit beta; Complement receptor C3 subunit beta
Alternative UPACC:
P05107; B3KTS8; D3DSM1; Q16418; Q53HS5; Q9UD72
Background:
Integrin beta-2, also known as Integrin ITGAL/ITGB2, plays a pivotal role in immune response, mediating leukocyte adhesion, transmigration, and natural killer cell cytotoxicity. It serves as a receptor for ICAMs, fibrinogen, and the complement component, facilitating crucial interactions in the immune system.
Therapeutic significance:
Given its involvement in Leukocyte adhesion deficiency 1 (LAD1), where patients suffer from recurrent bacterial infections due to leukocyte function deficiencies, targeting Integrin beta-2 could offer therapeutic avenues for enhancing immune response and treating LAD1.