Explore the Potential with AI-Driven Innovation
The focused library is created on demand with the latest virtual screening and parameter assessment technology, supported by the Receptor.AI drug discovery platform. This method is more effective than traditional methods and results in higher-quality compounds with better 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.
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 use our state-of-the-art dedicated workflow for designing focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
Q9UIV1
UPID:
CNOT7_HUMAN
Alternative names:
BTG1-binding factor 1; CCR4-associated factor 1; Caf1a
Alternative UPACC:
Q9UIV1; A8MZM5; B3KMP1; B3KN35; D3DSP6; G3V108; Q7Z530
Background:
CCR4-NOT transcription complex subunit 7, known as CCR4-associated factor 1 or Caf1a, exhibits 3'-5' poly(A) exoribonuclease activity, crucial for mRNA degradation and miRNA-mediated repression. It operates within the CCR4-NOT complex, a key cellular mRNA deadenylase linked to transcription regulation and translational repression. Its interaction with BTG family members like TOB1 and BTG2 underscores its role in anti-proliferative activity.
Therapeutic significance:
Understanding the role of CCR4-NOT transcription complex subunit 7 could open doors to potential therapeutic strategies.