Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries for protein-protein interfaces.
Fig. 1. The sreening workflow of Receptor.AI
This process entails comprehensive molecular simulations of the target protein, individually and in complex with essential partner proteins, along with ensemble virtual screening that focuses on conformational mobility in both its free and complex states. Potential binding pockets are considered at the protein-protein interaction interface and in remote allosteric locations to address every conceivable mechanism of action.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
P23510
UPID:
TNFL4_HUMAN
Alternative names:
Glycoprotein Gp34; OX40 ligand; TAX transcriptionally-activated glycoprotein 1
Alternative UPACC:
P23510; Q5JZA5; Q8IV74; Q9HCN9
Background:
Tumor necrosis factor ligand superfamily member 4 (TNFSF4), also known as OX40 ligand, Glycoprotein Gp34, and TAX transcriptionally-activated glycoprotein 1, plays a pivotal role in immune regulation. It binds to TNFRSF4, co-stimulating T-cell proliferation and cytokine production, which are crucial for an effective immune response.
Therapeutic significance:
TNFSF4's involvement in Systemic lupus erythematosus (SLE), a complex autoimmune disorder, underscores its therapeutic potential. The protein's elevated expression in SLE suggests that modulating TNFSF4 activity could offer new avenues for treatment, aiming to restore immune system balance and prevent disease progression.