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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q9UPT6
UPID:
JIP3_HUMAN
Alternative names:
JNK MAP kinase scaffold protein 3; Mitogen-activated protein kinase 8-interacting protein 3
Alternative UPACC:
Q9UPT6; A2A2B3; A7E2B3; Q96RY4; Q9H4I4; Q9H7P1; Q9NUG0
Background:
C-Jun-amino-terminal kinase-interacting protein 3, also known as JNK MAP kinase scaffold protein 3, plays a pivotal role in neuronal development and regeneration. It orchestrates JNK signaling, essential for axon elongation, by aggregating MAPK cascade components. This protein also facilitates vesicle transport and cortical neuronal migration by interacting with motor proteins and mediating NTRK2/TRKB transport.
Therapeutic significance:
The protein is linked to a neurodevelopmental disorder characterized by developmental delays, speech impairments, and brain anomalies. Understanding the role of C-Jun-amino-terminal kinase-interacting protein 3 could open doors to potential therapeutic strategies for treating such neurological conditions.