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.
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.
Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.
We employ our advanced, specialised process to create targeted 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.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q71U36
UPID:
TBA1A_HUMAN
Alternative names:
Alpha-tubulin 3; Tubulin B-alpha-1; Tubulin alpha-3 chain
Alternative UPACC:
Q71U36; A8K0B8; G3V1U9; P04687; P05209
Background:
Tubulin alpha-1A chain, also known as Alpha-tubulin 3, Tubulin B-alpha-1, and Tubulin alpha-3 chain, plays a pivotal role in cell structure and function. It is a major constituent of microtubules, essential for cell division, intracellular transport, and the maintenance of cell shape. The dynamic assembly of tubulin into microtubules, facilitated by the addition of GTP-tubulin dimers, is critical for cellular processes.
Therapeutic significance:
Lissencephaly 3, a neurological disorder characterized by brain malformations, intellectual disability, and seizures, is linked to mutations in the gene encoding Tubulin alpha-1A chain. Understanding the role of Tubulin alpha-1A chain could open doors to potential therapeutic strategies for treating or managing conditions like Lissencephaly 3.