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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We utilise our cutting-edge, exclusive workflow to develop 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P25963
UPID:
IKBA_HUMAN
Alternative names:
I-kappa-B-alpha; Major histocompatibility complex enhancer-binding protein MAD3
Alternative UPACC:
P25963; B2R8L6
Background:
NF-kappa-B inhibitor alpha, also known as I-kappa-B-alpha and Major histocompatibility complex enhancer-binding protein MAD3, plays a crucial role in inhibiting the activity of NF-kappa-B/REL complexes. This protein traps REL dimers in the cytoplasm, preventing their nuclear translocation. Upon cellular stimulation, it becomes phosphorylated, leading to its degradation and allowing RELA dimers to activate transcription in the nucleus.
Therapeutic significance:
Ectodermal dysplasia and immunodeficiency 2 (EDAID2), a disease marked by abnormal ectodermal development and increased infection susceptibility, is associated with mutations in NF-kappa-B inhibitor alpha. Understanding the role of NF-kappa-B inhibitor alpha could open doors to potential therapeutic strategies for EDAID2 and related immunodeficiencies.