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.
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.
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.
We employ our advanced, specialised process to create targeted 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q9Y6M5
UPID:
ZNT1_HUMAN
Alternative names:
Solute carrier family 30 member 1; Zinc transporter 1
Alternative UPACC:
Q9Y6M5; Q0VAK9; Q9BZF6
Background:
The Proton-coupled zinc antiporter SLC30A1, also known as Zinc transporter 1 and Solute carrier family 30 member 1, plays a crucial role in zinc homeostasis. It functions as a zinc ion:proton antiporter, facilitating zinc efflux from cells to prevent intracellular zinc accumulation and toxicity. Additionally, SLC30A1 modulates the expression of L-type calcium channels by preventing the transport of their regulatory subunit, CACNB2, to the plasma membrane, thereby controlling calcium and zinc influx, as well as heavy metal entry into cells.
Therapeutic significance:
Understanding the role of Proton-coupled zinc antiporter SLC30A1 could open doors to potential therapeutic strategies.