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.
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.
We employ our advanced, specialised process to create targeted libraries for receptors.
Fig. 1. The sreening workflow of Receptor.AI
It includes extensive molecular simulations of the receptor in its native membrane environment and the ensemble virtual screening accounting for its conformational mobility. In the case of dimeric or oligomeric receptors, the whole functional complex is modelled, and the tentative binding pockets are determined on and between the subunits to cover the whole spectrum of possible mechanisms of action.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q15116
UPID:
PDCD1_HUMAN
Alternative names:
-
Alternative UPACC:
Q15116; O00517; Q8IX89
Background:
Programmed cell death protein 1 (PD-1) is a critical regulator of T-cell activation and immune response. By binding to its ligands, PD-L1 and PD-L2, PD-1 delivers inhibitory signals that maintain immune tolerance and prevent autoimmunity. Its role in suppressing T-cell activation through the recruitment of SHP-2 phosphatase highlights its importance in immune regulation.
Therapeutic significance:
The exploitation of PD-1's inhibitory pathway by tumors underscores its therapeutic significance in cancer. Blocking PD-1 interactions can rejuvenate exhausted T-cells, enhancing anti-tumor immunity. This mechanism forms the basis of PD-1 targeted cancer immunotherapies, offering hope for effective treatment strategies.