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.
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 use our state-of-the-art dedicated workflow for designing focused 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
P78560
UPID:
CRADD_HUMAN
Alternative names:
Caspase and RIP adapter with death domain; RIP-associated protein with a death domain
Alternative UPACC:
P78560; B7Z2Q5
Background:
Death domain-containing protein CRADD, also known as Caspase and RIP adapter with death domain, plays a pivotal role in apoptosis by forming the PIDDosome complex with PIDD1 and caspase CASP2. This complex is crucial for CASP2 activation and apoptosis initiation. CRADD also facilitates the recruitment of CASP2 to the TNFR-1 signaling complex, indicating its involvement in tumor necrosis factor-mediated signaling.
Therapeutic significance:
CRADD's association with Intellectual developmental disorder, autosomal recessive 34, with variant lissencephaly highlights its potential as a therapeutic target. Understanding CRADD's role could pave the way for innovative treatments for this and possibly other neurodevelopmental disorders.