Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.
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.
Key features that set our library apart include:
partner
Reaxense
upacc
Q5U5X0
UPID:
LYRM7_HUMAN
Alternative names:
LYR motif-containing protein 7
Alternative UPACC:
Q5U5X0; A8MPQ9; Q86Y68
Background:
Complex III assembly factor LYRM7, also known as LYR motif-containing protein 7, plays a crucial role in mitochondrial function. It acts as an assembly factor necessary for the incorporation of the Rieske Fe-S protein UQCRFS1 into the cytochrome b-c1 complex within the mitochondrial matrix. This process is vital for mitochondrial respiratory chain efficiency.
Therapeutic significance:
Given its pivotal role in mitochondrial complex III deficiency, nuclear type 8, understanding the function of LYRM7 could pave the way for innovative treatments. This disease manifests through a spectrum of symptoms, including mitochondrial encephalopathy and liver dysfunction, highlighting the therapeutic potential of targeting LYRM7.