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.
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.
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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q15399
UPID:
TLR1_HUMAN
Alternative names:
Toll/interleukin-1 receptor-like protein
Alternative UPACC:
Q15399; D1CS39; D1CS41; O15452; Q32MK3; Q32MK4; Q9UG90
Background:
Toll-like receptor 1 (TLR1), also known as Toll/interleukin-1 receptor-like protein, plays a crucial role in the innate immune response against microbial agents. It recognizes diacylated and triacylated lipopeptides, cooperating with TLR2 to mediate response to bacterial lipoproteins. The activation cluster TLR2:TLR1:CD14, formed in response to triacylated lipopeptides, initiates signaling from the cell surface and is targeted to the Golgi in a lipid-raft dependent pathway. This process involves MYD88 and TRAF6, leading to NF-kappa-B activation, cytokine secretion, and the inflammatory response.
Therapeutic significance:
Understanding the role of Toll-like receptor 1 could open doors to potential therapeutic strategies.