Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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.
We employ our advanced, specialised process to create targeted 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q92752
UPID:
TENR_HUMAN
Alternative names:
Janusin; Restrictin
Alternative UPACC:
Q92752; C9J563; Q15568; Q5R3G0
Background:
Tenascin-R, known alternatively as Janusin and Restrictin, is a neural extracellular matrix protein pivotal in cell-matrix interactions. It influences cellular behavior through adhesion, differentiation, repulsion, and inhibition of neurite growth. Its interactions with cell surface gangliosides and sulfatides play critical roles in cellular adhesion, detachment, and oligodendrocyte differentiation. Moreover, Tenascin-R's interaction with CNTN1 and SCN2B is essential for neuron repulsion and sodium channel regulation at nodes of Ranvier.
Therapeutic significance:
The involvement of Tenascin-R in neurodevelopmental disorder, non-progressive, with spasticity and transient opisthotonus, underscores its therapeutic potential. Understanding Tenascin-R's role could pave the way for innovative treatments targeting neural matrix interactions and cellular behavior modulation in neurodevelopmental disorders.