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.
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.
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
Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
A1L188
UPID:
NDUF8_HUMAN
Alternative names:
-
Alternative UPACC:
A1L188
Background:
NADH dehydrogenase [ubiquinone] 1 alpha subcomplex assembly factor 8 plays a crucial role in the assembly of mitochondrial NADH:ubiquinone oxidoreductase complex (complex I, MT-ND1), essential for cellular energy production. It stabilizes NDUFAF5, highlighting its importance in mitochondrial function.
Therapeutic significance:
Linked to Mitochondrial complex I deficiency, nuclear type 34, a condition with a broad spectrum of severity, this protein's dysfunction can lead to various diseases, including neurodegenerative disorders and cardiomyopathy. Understanding its role could lead to novel therapeutic strategies for these conditions.