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 carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
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 utilise our cutting-edge, exclusive workflow to develop 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
Q92629
UPID:
SGCD_HUMAN
Alternative names:
35 kDa dystrophin-associated glycoprotein
Alternative UPACC:
Q92629; A8K9S9; Q53XA5; Q99644
Background:
Delta-sarcoglycan, a 35 kDa dystrophin-associated glycoprotein, plays a crucial role in the sarcoglycan complex, linking the F-actin cytoskeleton to the extracellular matrix. This protein's function is pivotal in maintaining muscle integrity and function.
Therapeutic significance:
Delta-sarcoglycan mutations are implicated in limb-girdle muscular dystrophy type 6 and dilated cardiomyopathy 1L, both leading to severe muscular and cardiac dysfunctions. Targeting delta-sarcoglycan pathways offers a promising avenue for therapeutic interventions in these conditions.