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 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 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.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q96KG9
UPID:
SCYL1_HUMAN
Alternative names:
Coated vesicle-associated kinase of 90 kDa; SCY1-like protein 1; Telomerase regulation-associated protein; Telomerase transcriptional element-interacting factor; Teratoma-associated tyrosine kinase
Alternative UPACC:
Q96KG9; A6NJF1; Q96G50; Q96KG8; Q96KH1; Q9HAW5; Q9HBL3; Q9NR53
Background:
The N-terminal kinase-like protein, known by alternative names such as Coated vesicle-associated kinase of 90 kDa and SCY1-like protein 1, plays a pivotal role in cellular processes. It regulates COPI-mediated retrograde protein traffic between the Golgi apparatus and the endoplasmic reticulum, crucial for maintaining Golgi apparatus morphology. Despite lacking detectable kinase activity in vitro, its isoform 6 acts as a transcriptional activator, influencing the beta-polymerase and TERT promoter regions.
Therapeutic significance:
Spinocerebellar ataxia, autosomal recessive, 21 (SCAR21), characterized by cerebellar atrophy, ataxia, liver failure, and peripheral neuropathy, is linked to variants affecting this protein. Understanding the role of N-terminal kinase-like protein could open doors to potential therapeutic strategies for SCAR21 and related cerebellar disorders.