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.
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.
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 top-notch dedicated system is used to design specialised libraries.
Fig. 1. The sreening workflow of Receptor.AI
Our methodology employs molecular simulations to explore a wide array of proteins, capturing their dynamic states both individually and within complexes. Through ensemble virtual screening, we address conformational mobility, uncovering binding sites within functional regions and remote allosteric locations. This thorough exploration ensures no potential mechanism of action is overlooked, aiming to discover novel therapeutic targets and lead compounds across an extensive spectrum of biological functions.
Several key aspects differentiate our library:
partner
Reaxense
upacc
O14949
UPID:
QCR8_HUMAN
Alternative names:
Complex III subunit 8; Complex III subunit VIII; Ubiquinol-cytochrome c reductase complex 9.5 kDa protein; Ubiquinol-cytochrome c reductase complex ubiquinone-binding protein QP-C
Alternative UPACC:
O14949; Q5FVE2; Q9BV88; Q9T2V7
Background:
Cytochrome b-c1 complex subunit 8, also known as Complex III subunit 8, plays a crucial role in the mitochondrial electron transport chain, driving oxidative phosphorylation. This protein is a component of the ubiquinol-cytochrome c oxidoreductase, facilitating electron transfer and proton translocation across the mitochondrial inner membrane, essential for ATP synthesis.
Therapeutic significance:
Mutations in Cytochrome b-c1 complex subunit 8 are linked to Mitochondrial complex III deficiency, nuclear type 4, characterized by encephalopathy, liver dysfunction, and muscle weakness. Understanding its role could lead to targeted therapies for mitochondrial disorders.