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 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.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q53EL6
UPID:
PDCD4_HUMAN
Alternative names:
Neoplastic transformation inhibitor protein; Nuclear antigen H731-like; Protein 197/15a
Alternative UPACC:
Q53EL6; B2RCV4; B5ME91; O15501; Q5VZS6; Q6PJI5; Q8TAR5; Q99834
Background:
Programmed cell death protein 4, also known as Neoplastic transformation inhibitor protein, plays a crucial role in inhibiting translation initiation and cap-dependent translation. It functions by obstructing the interaction between EIF4A1 and EIF4G, and inhibiting EIF4A's helicase activity. Additionally, it modulates JUN kinase activation, down-regulates MAP4K1 expression, and may play a role in apoptosis. As a tumor suppressor, it inhibits tumor promoter-induced neoplastic transformation and binds RNA.
Therapeutic significance:
Understanding the role of Programmed cell death protein 4 could open doors to potential therapeutic strategies.