Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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.
The library includes a list of the most promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
Our top-notch dedicated system is used to design specialised 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
O75880
UPID:
SCO1_HUMAN
Alternative names:
-
Alternative UPACC:
O75880; B2RDM0
Background:
Protein SCO1 homolog, mitochondrial, plays a pivotal role in cellular energy production. It acts as a copper metallochaperone, crucial for the maturation of cytochrome c oxidase subunit II, a key component of the mitochondrial respiratory complex IV. This protein ensures the proper transportation and stabilization of copper, facilitating efficient electron transport and ATP synthesis.
Therapeutic significance:
Mitochondrial complex IV deficiency, nuclear type 4, a severe disorder characterized by metabolic acidosis, hypotonia, and early infant mortality, is linked to mutations in the SCO1 gene. Understanding the role of Protein SCO1 homolog, mitochondrial, could open doors to potential therapeutic strategies, offering hope for targeted treatments.