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.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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 for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library stands out due to several important features:
partner
Reaxense
upacc
Q9NYL2
UPID:
M3K20_HUMAN
Alternative names:
Human cervical cancer suppressor gene 4 protein; Leucine zipper- and sterile alpha motif-containing kinase; MLK-like mitogen-activated protein triple kinase; Mitogen-activated protein kinase kinase kinase MLT; Mixed lineage kinase 7; Mixed lineage kinase-related kinase; Sterile alpha motif- and leucine zipper-containing kinase AZK
Alternative UPACC:
Q9NYL2; B3KPG2; Q53SX1; Q580W8; Q59GY5; Q86YW8; Q9HCC4; Q9HCC5; Q9HDD2; Q9NYE9
Background:
Mitogen-activated protein kinase kinase kinase 20 (MAP3K20) is a pivotal stress-activated component in protein kinase signal transduction cascades, crucial for programmed cell death in response to various stresses including ribosomal stress and ionizing radiation. It activates JNK and MAP kinase p38 pathways through phosphorylation, playing a key role in cellular responses to adrenergic stimulation and cardiac stress.
Therapeutic significance:
MAP3K20's involvement in split-foot malformation with mesoaxial polydactyly and centronuclear myopathy highlights its potential as a therapeutic target. Understanding the role of MAP3K20 could open doors to potential therapeutic strategies for these genetic disorders.