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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We employ our advanced, specialised process to create targeted 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
O43707
UPID:
ACTN4_HUMAN
Alternative names:
Non-muscle alpha-actinin 4
Alternative UPACC:
O43707; A4K467; D6PXK4; O76048
Background:
Alpha-actinin-4, a non-muscle alpha-actinin, plays a pivotal role in actin filament cross-linking and anchoring. It is involved in various cellular processes, including vesicular trafficking and tight junction assembly, through its interaction with the CART complex and MICALL2, respectively. Additionally, it acts as a transcriptional coactivator for PPARG and RARA.
Therapeutic significance:
Alpha-actinin-4's mutation is linked to Focal segmental glomerulosclerosis 1, a renal disease leading to end-stage renal disease. Understanding its role could pave the way for novel therapeutic strategies targeting kidney disorders.