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.
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 top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library stands out due to several important features:
partner
Reaxense
upacc
P35609
UPID:
ACTN2_HUMAN
Alternative names:
Alpha-actinin skeletal muscle isoform 2; F-actin cross-linking protein
Alternative UPACC:
P35609; B1ANE4; B2RCS5; Q86TF4; Q86TI8
Background:
Alpha-actinin-2, also known as the skeletal muscle isoform 2 or F-actin cross-linking protein, plays a crucial role in the structural integrity of muscle cells by anchoring actin to various intracellular structures. This protein is pivotal in maintaining the cytoskeletal architecture, facilitating cellular movement, and muscle contraction.
Therapeutic significance:
Mutations in Alpha-actinin-2 are linked to severe diseases such as familial hypertrophic cardiomyopathy, dilated cardiomyopathy, congenital myopathy, and adult-onset distal myopathy. These conditions underscore the protein's critical role in cardiac and skeletal muscle function, presenting it as a potential target for therapeutic intervention in muscle-related diseases.