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.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q16620
UPID:
NTRK2_HUMAN
Alternative names:
GP145-TrkB; Neurotrophic tyrosine kinase receptor type 2; TrkB tyrosine kinase; Tropomyosin-related kinase B
Alternative UPACC:
Q16620; B1ANZ4; B4DFV9; Q16675; Q59GJ1; Q8WXJ5; Q8WXJ6; Q8WXJ7
Background:
The BDNF/NT-3 growth factors receptor, also known as Neurotrophic tyrosine kinase receptor type 2 or TrkB, plays a pivotal role in the development and maturation of the central and peripheral nervous systems. It regulates neuron survival, proliferation, migration, differentiation, and synapse formation and plasticity, primarily through its interaction with BDNF, NTF4, and to a lesser extent, NTF3. Upon ligand binding, TrkB undergoes homodimerization, autophosphorylation, and activation, engaging several downstream effectors that influence neuronal differentiation, growth, survival, and synaptic plasticity.
Therapeutic significance:
TrkB is implicated in Developmental and epileptic encephalopathy 58, characterized by severe early-onset epilepsies, and a disorder involving early-onset obesity, hyperphagia, and developmental delay. Understanding the role of TrkB could open doors to potential therapeutic strategies for these conditions.