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 includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P04629
UPID:
NTRK1_HUMAN
Alternative names:
Neurotrophic tyrosine kinase receptor type 1; TRK1-transforming tyrosine kinase protein; Tropomyosin-related kinase A; Tyrosine kinase receptor; Tyrosine kinase receptor A; gp140trk; p140-TrkA
Alternative UPACC:
P04629; B2R6T5; B7ZM34; P08119; Q15655; Q15656; Q5D056; Q5VZS2; Q7Z5C3; Q9UIU7
Background:
The High affinity nerve growth factor receptor, also known as Neurotrophic tyrosine kinase receptor type 1 or TrkA, plays a pivotal role in the development and maturation of the central and peripheral nervous systems. It regulates proliferation, differentiation, and survival of neurons through high affinity binding to NGF. TrkA's activation involves dimerization, autophosphorylation, and recruitment of downstream effectors, driving cell survival and differentiation.
Therapeutic significance:
TrkA's involvement in congenital insensitivity to pain with anhidrosis highlights its therapeutic potential. Understanding TrkA's mechanisms could lead to treatments for this rare disorder by targeting the pathways that contribute to sensory neuropathy and anhidrosis, offering hope for affected individuals.