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.
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 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.
Our high-tech, dedicated method is applied to construct targeted 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
Q14696
UPID:
MESD_HUMAN
Alternative names:
LDLR chaperone MESD; Mesoderm development LRP chaperone MESD; Mesoderm development candidate 2; Mesoderm development protein; Renal carcinoma antigen NY-REN-61
Alternative UPACC:
Q14696; B4DW84; D3DW96; Q969U1
Background:
The LRP chaperone MESD plays a pivotal role in the folding of beta-propeller/EGF modules within low-density lipoprotein receptors, crucial for Wnt pathway modulation, embryonic polarity, mesoderm induction, and neuromuscular junction formation. Known alternatively as LDLR chaperone MESD, it is essential for LRP5 and LRP6 coreceptor trafficking to the plasma membrane.
Therapeutic significance:
Osteogenesis imperfecta 20, a progressive disorder marked by bone fragility and skeletal deformity, is linked to mutations in the gene encoding LRP chaperone MESD. Understanding its role could lead to novel treatments for this and potentially other related conditions.