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.
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 use our state-of-the-art dedicated workflow for designing focused 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 is unique due to several crucial aspects:
partner
Reaxense
upacc
Q5XKP0
UPID:
MIC13_HUMAN
Alternative names:
Protein P117
Alternative UPACC:
Q5XKP0; A0A0B4J2A5; K7EKR0; Q86YE5
Background:
MICOS complex subunit MIC13, also known as Protein P117, is integral to the mitochondrial inner membrane. It plays a pivotal role in maintaining crista junctions and the inner membrane's architecture, crucial for cellular energy production. MIC13 is essential for incorporating MICOS10/MIC10 into the MICOS complex, thereby ensuring the proper formation and maintenance of cristae morphology.
Therapeutic significance:
The dysfunction of MIC13 is linked to Combined oxidative phosphorylation deficiency 37, a severe mitochondrial disorder characterized by neurodegeneration, liver dysfunction, and often early mortality. Understanding MIC13's role could pave the way for novel therapeutic strategies targeting mitochondrial diseases.