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 pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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 use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
P98155
UPID:
VLDLR_HUMAN
Alternative names:
-
Alternative UPACC:
P98155; B2RMZ7; D3DRH6; Q5VVF6
Background:
The Very low-density lipoprotein receptor (VLDLR) plays a pivotal role in energy metabolism by mediating the endocytosis of VLDL. It binds a variety of molecules, including Reelin and apolipoprotein E-containing ligands, facilitating crucial cellular processes. VLDLR's interaction with DAB1 upon ligand binding is essential for neuron positioning and migration stop signals.
Therapeutic significance:
VLDLR's mutation is linked to Cerebellar ataxia, impaired intellectual development, and dysequilibrium syndrome 1, highlighting its critical role in neurological development. Understanding VLDLR's functions could pave the way for innovative treatments for this and potentially other neurodevelopmental disorders.