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 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.
Our top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9NZB8
UPID:
MOCS1_HUMAN
Alternative names:
Cell migration-inducing gene 11 protein; Molybdenum cofactor synthesis-step 1 protein A-B
Alternative UPACC:
Q9NZB8; B3KPT7; B4DTP1; O14940; O14941; O75710; Q5J7W0; Q5TCE1; Q5TCE2; Q5TCE6; Q5TCE9; Q5TCF0; Q5TCF1; Q8N418; Q9NZB7; Q9UEM1
Background:
Molybdenum cofactor biosynthesis protein 1, known as MOCS1, plays a pivotal role in the conversion of 5'-GTP to cyclic pyranopterin monophosphate (cPMP), a crucial step in molybdenum cofactor synthesis. This process involves two isoforms, MOCS1A and MOCS1B, working in tandem to catalyze this conversion, which is essential for the activity of molybdoenzymes.
Therapeutic significance:
MOCS1 is linked to Molybdenum cofactor deficiency, complementation group A, a metabolic disorder characterized by the loss of molybdoenzyme activities, leading to severe neurological symptoms and early childhood mortality. Understanding the role of MOCS1 could open doors to potential therapeutic strategies for this devastating condition.