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.
We carefully select specific compounds from a vast collection of over 60 billion molecules in virtual chemical space. Our partner Reaxense helps in synthesizing and delivering these compounds.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
Our high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance 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.