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.
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 for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
P13569
UPID:
CFTR_HUMAN
Alternative names:
ATP-binding cassette sub-family C member 7; Channel conductance-controlling ATPase; cAMP-dependent chloride channel
Alternative UPACC:
P13569; Q20BG8; Q20BH2; Q2I0A1; Q2I102
Background:
The Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) is pivotal in epithelial ion and water transport, crucial for maintaining fluid homeostasis. Known alternatively as ATP-binding cassette sub-family C member 7, this protein facilitates chloride ion transport across cell membranes, influencing airway fluid balance and pathogen defense.
Therapeutic significance:
CFTR's malfunction is central to Cystic Fibrosis, a prevalent genetic disorder affecting exocrine glands, leading to severe respiratory and digestive issues. Insights into CFTR's function and regulation offer avenues for correcting the defective chloride channel activity, presenting potential therapeutic strategies for Cystic Fibrosis and related conditions.