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.
We employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P28482
UPID:
MK01_HUMAN
Alternative names:
ERT1; Extracellular signal-regulated kinase 2; MAP kinase isoform p42; Mitogen-activated protein kinase 2
Alternative UPACC:
P28482; A8CZ64
Background:
Mitogen-activated protein kinase 1 (MAPK1), also known as Extracellular signal-regulated kinase 2 (ERK2), plays a pivotal role in the MAP kinase signal transduction pathway. It is involved in various cellular processes including growth, adhesion, survival, and differentiation. MAPK1 mediates its effects through phosphorylation of numerous substrates across different cellular compartments, influencing transcription, translation, and cytoskeletal rearrangements.
Therapeutic significance:
MAPK1's involvement in Noonan syndrome 13, characterized by congenital heart defects, facial dysmorphia, and a risk of juvenile myelomonocytic leukemia, underscores its therapeutic potential. Targeting MAPK1 could lead to innovative treatments for this syndrome and its associated complications.