Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our high-tech, dedicated method is applied to construct targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Our library stands out due to several important features:
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.