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 pick out particular compounds from an extensive virtual database of more than 60 billion molecules. The preparation and shipment of these compounds are facilitated by our associate 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 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.
Key features that set our library apart include:
partner
Reaxense
upacc
O43181
UPID:
NDUS4_HUMAN
Alternative names:
Complex I-18 kDa; Complex I-AQDQ; NADH-ubiquinone oxidoreductase 18 kDa subunit
Alternative UPACC:
O43181; Q9BS69
Background:
NADH dehydrogenase [ubiquinone] iron-sulfur protein 4, mitochondrial, also known as Complex I-18 kDa, Complex I-AQDQ, or NADH-ubiquinone oxidoreductase 18 kDa subunit, plays a crucial role in cellular energy production. It serves as an accessory subunit of the mitochondrial membrane respiratory chain NADH dehydrogenase (Complex I), facilitating the transfer of electrons from NADH to the respiratory chain, with ubiquinone being the immediate electron acceptor.
Therapeutic significance:
Given its pivotal role in mitochondrial function, mutations affecting this protein are linked to mitochondrial complex I deficiency, nuclear type 1. This condition manifests in a spectrum from lethal neonatal disease to adult-onset neurodegenerative disorders, including Leigh syndrome and some forms of Parkinson disease. Understanding the role of this protein could open doors to potential therapeutic strategies for these conditions.