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.
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.
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 utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes comprehensive molecular simulations of the catalytic and allosteric binding pockets and the ensemble virtual screening accounting for their conformational mobility. In the case of designing modulators, the structural changes induced by reaction intermediates are taken into account to leverage activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q6VVB1
UPID:
NHLC1_HUMAN
Alternative names:
Malin; NHL repeat-containing protein 1; RING-type E3 ubiquitin transferase NHLRC1
Alternative UPACC:
Q6VVB1; Q3SYB1; Q5VUK7; Q6IMH1
Background:
E3 ubiquitin-protein ligase NHLRC1, also known as Malin, plays a crucial role in cellular homeostasis. It functions alongside EPM2A/laforin and HSP70 in the clearance of toxic polyglucosans and protein aggregates through the ubiquitin-proteasome system (UPS) and macroautophagy pathway. This protein is involved in ubiquitinating and targeting specific glycogen-targeting protein phosphatase subunits and AGL for proteasome-dependent degradation, thereby regulating glycogen accumulation.
Therapeutic significance:
NHLRC1's involvement in Epilepsy, progressive myoclonic 2 (EPM2), characterized by severe adolescent-onset progressive epilepsy and neurodegeneration, underscores its therapeutic significance. Understanding the role of NHLRC1 could open doors to potential therapeutic strategies for EPM2 by targeting the pathways involved in the accumulation of Lafora bodies, offering hope for treatments that could alleviate symptoms or slow the disease's progression.