Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior activity, selectivity and safety.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
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.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q86UX7
UPID:
URP2_HUMAN
Alternative names:
Kindlin-3; MIG2-like protein; Unc-112-related protein 2
Alternative UPACC:
Q86UX7; Q8IUA1; Q8N207; Q9BT48
Background:
Fermitin family homolog 3, also known as Kindlin-3, plays a pivotal role in cell adhesion, particularly in hematopoietic cells. It activates integrin beta-1-3, essential for platelet and leukocyte adhesion to endothelial cells. Additionally, it is crucial for integrin beta-2 activation in polymorphonuclear granulocytes.
Therapeutic significance:
Leukocyte adhesion deficiency 3, a disorder marked by recurrent bacterial infections and bleeding disorders, is linked to mutations in the gene encoding Kindlin-3. Understanding the role of Kindlin-3 could open doors to potential therapeutic strategies for this condition.