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.
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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q15628
UPID:
TRADD_HUMAN
Alternative names:
TNFRSF1A-associated via death domain
Alternative UPACC:
Q15628; B2RDS3; B3KQZ9; Q52NZ1
Background:
The Tumor necrosis factor receptor type 1-associated DEATH domain protein (TRADD) serves as a crucial adapter molecule for TNFRSF1A/TNFR1, facilitating its interaction with FADD. This interaction is pivotal for the activation of apoptosis and NF-kappa-B pathways following TNF induction. Additionally, TRADD's nuclear form acts as a tumor suppressor by stabilizing isoform p19ARF/ARF of CDKN2A, preventing its degradation.
Therapeutic significance:
Understanding the role of Tumor necrosis factor receptor type 1-associated DEATH domain protein could open doors to potential therapeutic strategies.