Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better activity, selectivity, and safety.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries for receptors.
Fig. 1. The sreening workflow of Receptor.AI
This process includes extensive molecular simulations of the receptor in its native membrane environment, along with ensemble virtual screening that accounts for its conformational mobility. In the case of dimeric or oligomeric receptors, the entire functional complex is modelled, identifying potential binding pockets on and between the subunits to encompass all possible mechanisms of action.
Our library stands out due to several important features:
partner
Reaxense
upacc
P43489
UPID:
TNR4_HUMAN
Alternative names:
ACT35 antigen; OX40L receptor; TAX transcriptionally-activated glycoprotein 1 receptor
Alternative UPACC:
P43489; Q13663; Q2M312; Q5T7M0
Background:
Tumor necrosis factor receptor superfamily member 4 (TNFRSF4), also known as OX40L receptor, ACT35 antigen, and TAX transcriptionally-activated glycoprotein 1 receptor, plays a pivotal role in immune system regulation. It serves as a receptor for TNFSF4/OX40L/GP34, enhancing long-term T-cell immunity and acting as a receptor for human herpesvirus 6B/HHV-6B.
Therapeutic significance:
TNFRSF4's involvement in Immunodeficiency 16, a condition marked by poor T-cell recall immune responses and susceptibility to classic Kaposi sarcoma, underscores its therapeutic potential. Targeting TNFRSF4 could lead to innovative treatments for this immunodeficiency and other T-cell related disorders.