Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
P60880
UPID:
SNP25_HUMAN
Alternative names:
Super protein; Synaptosomal-associated 25 kDa protein
Alternative UPACC:
P60880; B2RAU4; D3DW16; D3DW17; P13795; P36974; P70557; P70558; Q53EM2; Q5U0B5; Q8IXK3; Q96FM2; Q9BR45
Background:
Synaptosomal-associated protein 25 (SNAP-25), also known as Super protein and Synaptosomal-associated 25 kDa protein, plays a pivotal role in the regulation of neurotransmitter release. It is involved in the molecular mechanisms of vesicle docking and membrane fusion, essential for synaptic function in neuronal systems. SNAP-25's interaction with CENPF influences plasma membrane recycling, and it modulates the gating characteristics of the KCNB1 potassium channel in pancreatic beta cells.
Therapeutic significance:
The association of SNAP-25 with congenital myasthenic syndrome 18, characterized by muscle weakness and developmental delays, underscores its clinical relevance. Understanding the role of SNAP-25 could open doors to potential therapeutic strategies for treating neuromuscular transmission disorders.