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 effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P23763
UPID:
VAMP1_HUMAN
Alternative names:
Synaptobrevin-1
Alternative UPACC:
P23763; A8MVP3; D3DUR3; O75468; Q15857; Q6FG94; Q8IVC9
Background:
Vesicle-associated membrane protein 1 (VAMP1), also known as Synaptobrevin-1, plays a crucial role in the targeting and/or fusion of transport vesicles to their target membrane. This protein is pivotal in the process of neurotransmitter release, a fundamental mechanism in neuronal communication.
Therapeutic significance:
VAMP1 is linked to Spastic ataxia 1, autosomal dominant (SPAX1), where mutations lead to neurotransmitter exocytosis impairment, and to congenital myasthenic syndrome 25, characterized by muscle weakness from birth. Understanding the role of VAMP1 could open doors to potential therapeutic strategies for these neurological disorders.