Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated 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 high-tech, dedicated method is applied to construct targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q12756
UPID:
KIF1A_HUMAN
Alternative names:
Axonal transporter of synaptic vesicles; Microtubule-based motor KIF1A; Unc-104- and KIF1A-related protein
Alternative UPACC:
Q12756; B0I1S5; F5H045; O95068; Q13355; Q14752; Q2NKJ6; Q4LE42; Q53T78; Q59GH1; Q63Z40; Q6P1R9; Q7KZ57
Background:
Kinesin-like protein KIF1A, also known as Axonal transporter of synaptic vesicles and Microtubule-based motor KIF1A, plays a crucial role in anterograde axonal transport of synaptic vesicle precursors. Its interaction with CALM1 enhances vesicle motility, facilitating the transport of neuronal dense core vesicles to dendritic spines and axons.
Therapeutic significance:
KIF1A is implicated in several neurodegenerative disorders, including Spastic paraplegia 30, Neuropathy, hereditary sensory, 2C, and NESCAV syndrome. These associations highlight its potential as a target for therapeutic intervention in conditions characterized by progressive weakness, spasticity, and cognitive dysfunction.