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.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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.
We employ our advanced, specialised process to create targeted 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
P30305
UPID:
MPIP2_HUMAN
Alternative names:
Dual specificity phosphatase Cdc25B
Alternative UPACC:
P30305; D3DVY1; D3DVY2; D3DVY3; D3DVY4; O43551; Q13971; Q5JX77; Q6RSS1; Q9BRA6
Background:
M-phase inducer phosphatase 2, also known as Dual specificity phosphatase Cdc25B, plays a pivotal role in cell cycle regulation. It acts as a tyrosine protein phosphatase, crucial for the progression through G2/M phases and successful cytokinesis, by dephosphorylating CDK1 to stimulate its kinase activity. The activity levels vary among its three isoforms, indicating a nuanced regulatory mechanism.
Therapeutic significance:
Understanding the role of M-phase inducer phosphatase 2 could open doors to potential therapeutic strategies. Its critical function in mitotic progression positions it as a key target for cancer research, where cell cycle dysregulation is a hallmark.