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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner 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.
Our high-tech, dedicated method is applied to construct targeted 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
Q96M11
UPID:
HYLS1_HUMAN
Alternative names:
Hydrolethalus syndrome protein 1
Alternative UPACC:
Q96M11; B3KXI8; Q96BX9
Background:
Centriolar and ciliogenesis-associated protein HYLS1, also known as Hydrolethalus syndrome protein 1, is pivotal in ciliogenesis. This protein's involvement in the formation and function of cilia underscores its significance in cellular and developmental processes.
Therapeutic significance:
HYLS1 is linked to Hydrolethalus syndrome 1, a lethal condition marked by polydactyly, central nervous system malformations, and hydrocephalus. Understanding the role of HYLS1 could open doors to potential therapeutic strategies for this devastating syndrome.