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.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We use our state-of-the-art dedicated workflow for designing focused 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 distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q15306
UPID:
IRF4_HUMAN
Alternative names:
Lymphocyte-specific interferon regulatory factor; Multiple myeloma oncogene 1; NF-EM5
Alternative UPACC:
Q15306; Q5VUI7; Q99660
Background:
Interferon regulatory factor 4 (IRF4), also known as Multiple myeloma oncogene 1 and NF-EM5, plays a pivotal role in immune response regulation. It acts as a transcriptional activator, binding to specific elements of the MHC class I promoter and the immunoglobulin lambda light chain enhancer. Its involvement in CD8(+) dendritic cell differentiation highlights its significance in lymphoid cell-specific signal transduction pathways.
Therapeutic significance:
IRF4's aberration, particularly the translocation t(6;14)(p25;q32) with the IgH locus, is implicated in multiple myeloma, a malignant plasma cell tumor. This association underscores the potential of targeting IRF4 in therapeutic strategies aimed at treating multiple myeloma and possibly other related hematological malignancies.