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 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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q96EV8
UPID:
DTBP1_HUMAN
Alternative names:
Biogenesis of lysosome-related organelles complex 1 subunit 8; Dysbindin-1; Dystrobrevin-binding protein 1; Hermansky-Pudlak syndrome 7 protein
Alternative UPACC:
Q96EV8; A8K3V3; Q5THY3; Q5THY4; Q96NV2; Q9H0U2; Q9H3J5
Background:
Dysbindin, also known as Biogenesis of lysosome-related organelles complex 1 subunit 8, plays a crucial role in the biogenesis of lysosome-related organelles, such as platelet dense granules and melanosomes. It is involved in synaptic vesicle trafficking, neurotransmitter release, and may modulate MAPK8 phosphorylation and actin cytoskeleton reorganization.
Therapeutic significance:
Dysbindin's association with Hermansky-Pudlak syndrome 7, a disorder characterized by oculocutaneous albinism, bleeding, and lysosomal storage defects, highlights its potential as a target for therapeutic intervention. Understanding the role of Dysbindin could open doors to potential therapeutic strategies.