Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We use our state-of-the-art dedicated workflow for designing focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q15526
UPID:
SURF1_HUMAN
Alternative names:
-
Alternative UPACC:
Q15526; Q5T8T3; Q5T8T4
Background:
Surfeit locus protein 1 plays a crucial role as part of the MITRAC complex, essential for regulating the assembly of cytochrome c oxidase, a key component of the mitochondrial respiratory chain. This protein's involvement in mitochondrial function highlights its importance in cellular energy production.
Therapeutic significance:
Given its pivotal role in mitochondrial function, Surfeit locus protein 1 is linked to diseases such as Mitochondrial complex IV deficiency, nuclear type 1, and Charcot-Marie-Tooth disease 4K. These associations underscore the potential of targeting this protein in therapeutic strategies aimed at mitigating mitochondrial and neurological disorders.