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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Our library stands out due to several important features:
partner
Reaxense
upacc
O60282
UPID:
KIF5C_HUMAN
Alternative names:
Kinesin heavy chain neuron-specific 2; Kinesin-1
Alternative UPACC:
O60282; O95079; Q2YDC5
Background:
Kinesin heavy chain isoform 5C, also known as Kinesin heavy chain neuron-specific 2 or Kinesin-1, is a microtubule-associated protein crucial for organelle transport. It exhibits ATPase activity and is pivotal in synaptic transmission and dendritic mRNA trafficking. This protein is essential for the anterograde axonal transportation of MAPK8IP3/JIP3, facilitating axon elongation.
Therapeutic significance:
Kinesin heavy chain isoform 5C is linked to Cortical dysplasia, complex, with other brain malformations 2, a disorder characterized by abnormal neuronal migration and axonal guidance. Understanding the role of this protein could unveil new therapeutic strategies for treating such complex cortical dysplasias.