Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher activity, selectivity, and safety.
We pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate Reaxense.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We employ our advanced, specialised process to create 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 stands out due to several important features:
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Reaxense
upacc
Q12934
UPID:
BFSP1_HUMAN
Alternative names:
Beaded filament structural protein 1; Lens fiber cell beaded-filament structural protein CP 115; Lens intermediate filament-like heavy
Alternative UPACC:
Q12934; F5H0G1; O43595; O76034; O95676; Q8IVZ6; Q9HBX4
Background:
Filensin, also known as Beaded filament structural protein 1, plays a crucial role in the formation of lens intermediate filaments, essential for eye lens transparency. It forms a complex with BFSP1, BFSP2, and CRYAA, vital for lens structure integrity (PubMed:28935373). Additionally, Filensin is involved in modulating the calcium regulation of MIP water permeability, highlighting its significance in lens physiology (PubMed:30790544).
Therapeutic significance:
Filensin's mutation is directly linked to Cataract 33, multiple types, characterized by juvenile-onset opacities in the lens cortex. Understanding the role of Filensin could open doors to potential therapeutic strategies for cataract treatment, emphasizing the importance of targeted genetic research in ophthalmology.