Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved activity, selectivity, and safety.
Our selection of compounds is from a large virtual library of over 60 billion molecules. The production and distribution of these compounds are managed by our partner Reaxense.
The library features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
Our high-tech, dedicated method is applied to construct targeted libraries for receptors.
Fig. 1. The sreening workflow of Receptor.AI
This process includes extensive molecular simulations of the receptor in its native membrane environment, along with ensemble virtual screening that accounts for its conformational mobility. In the case of dimeric or oligomeric receptors, the entire functional complex is modelled, identifying potential binding pockets on and between the subunits to encompass all possible mechanisms of action.
Our library stands out due to several important features:
partner
Reaxense
upacc
P02708
UPID:
ACHA_HUMAN
Alternative names:
-
Alternative UPACC:
P02708; B4DRV6; D3DPE8
Background:
The Acetylcholine receptor subunit alpha plays a pivotal role in neuromuscular signaling, facilitating communication between nerve and muscle cells. Upon acetylcholine binding, it undergoes a significant conformational change, leading to the opening of an ion-conducting channel. This process is crucial for muscle contraction and coordination.
Therapeutic significance:
Mutations in this protein are linked to severe conditions such as Multiple pterygium syndrome, lethal type, and congenital myasthenic syndromes (CMS1A and CMS1B), characterized by muscle weakness and neuromuscular transmission failure. Targeting these pathways offers a promising avenue for therapeutic intervention in these genetic disorders.