Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior activity, selectivity and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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 for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q8N568
UPID:
DCLK2_HUMAN
Alternative names:
CaMK-like CREB regulatory kinase 2; Doublecortin domain-containing protein 3B; Doublecortin-like and CAM kinase-like 2; Doublecortin-like kinase 2
Alternative UPACC:
Q8N568; C9J5Q9; Q59GC8; Q8N399
Background:
Serine/threonine-protein kinase DCLK2, also known as CaMK-like CREB regulatory kinase 2, plays a crucial role in cellular signaling pathways. It is characterized by a significantly reduced Ca2+/CAM affinity, distinguishing it from other CaMK family members. DCLK2 is involved in the phosphorylation of the CREB coactivator CRTC2/TORC2, which is essential for the regulation of CRE-dependent gene activation.
Therapeutic significance:
Understanding the role of Serine/threonine-protein kinase DCLK2 could open doors to potential therapeutic strategies. Its unique function in the down-regulation of CRE-dependent gene activation highlights its potential as a target in diseases where these pathways are dysregulated.