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.
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.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best 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
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q96MT8
UPID:
CEP63_HUMAN
Alternative names:
-
Alternative UPACC:
Q96MT8; D3DND8; D3DND9; D3DNE0; Q96CR0; Q9H8F5; Q9H8N0
Background:
Centrosomal protein of 63 kDa (Cep63) is pivotal in spindle assembly, centriole duplication, and DNA damage response. It forms a complex with CEP152, CDK5RAP2, and WDR62, crucial for centrosome function and cell division. Cep63's role in recruiting CDK1 and CDK2 to centrosomes underscores its importance in mitotic progression.
Therapeutic significance:
Cep63's mutation is linked to Seckel syndrome 6, characterized by dwarfism, microcephaly, and intellectual disability. Understanding Cep63's role could unveil therapeutic strategies for this rare autosomal recessive disorder.