Explore the Potential with AI-Driven Innovation
Our detailed focused library is generated on demand with advanced virtual screening and parameter assessment technology powered by the Receptor.AI drug discovery platform. This method surpasses traditional approaches, delivering compounds of better quality with enhanced 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 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 utilise our cutting-edge, exclusive workflow to develop focused libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
O95954
UPID:
FTCD_HUMAN
Alternative names:
Formiminotransferase-cyclodeaminase; LCHC1
Alternative UPACC:
O95954; B9EGD0; Q86V03; Q9HCT4; Q9HCT5; Q9HCT6; Q9UHJ2
Background:
Formimidoyltransferase-cyclodeaminase, also known as Formiminotransferase-cyclodeaminase or LCHC1, is a folate-dependent enzyme pivotal in one-carbon metabolism. It channels one-carbon units from formiminoglutamate to the folate pool and binds to vimentin filaments, influencing their bundling from the Golgi.
Therapeutic significance:
Glutamate formiminotransferase deficiency, an autosomal recessive disorder linked to this protein, manifests in severe to mild phenotypes, ranging from megaloblastic anemia and intellectual disability to mild developmental delays. Understanding the role of Formimidoyltransferase-cyclodeaminase could open doors to potential therapeutic strategies.