Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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 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.
Our high-tech, dedicated method is applied to construct targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q15049
UPID:
MLC1_HUMAN
Alternative names:
-
Alternative UPACC:
Q15049; B3KW61; B7Z659; Q5JZ83; Q8TAG4; Q96RP5; Q9UGY8
Background:
Membrane protein MLC1 plays a pivotal role in regulating astrocyte response to hypo-osmosis, facilitating calcium influx. This protein's involvement in cellular osmoregulation underscores its importance in maintaining brain homeostasis.
Therapeutic significance:
MLC1's mutation leads to Leukoencephalopathy, megalencephalic, with subcortical cysts, 1, characterized by cerebral abnormalities and intellectual disability. Targeting MLC1 pathways offers a promising avenue for therapeutic intervention in this syndrome.