Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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 promising modulators annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Also, each compound is presented with its optimal docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries.
Fig. 1. The sreening workflow of Receptor.AI
Utilising molecular simulations, our approach thoroughly examines a wide array of proteins, tracking their conformational changes individually and within complexes. Ensemble virtual screening enables us to address conformational flexibility, revealing essential binding sites at functional regions and allosteric locations. Our rigorous analysis guarantees that no potential mechanism of action is overlooked, aiming to uncover new therapeutic targets and lead compounds across diverse biological functions.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9NPL8
UPID:
TIDC1_HUMAN
Alternative names:
Protein M5-14; Translocase of inner mitochondrial membrane domain-containing protein 1
Alternative UPACC:
Q9NPL8; D3DN81; Q6IAJ7; Q6UWU6; Q9NPR3; Q9NPS5; Q9P0Y6
Background:
Complex I assembly factor TIMMDC1, mitochondrial, also known as Protein M5-14 and Translocase of inner mitochondrial membrane domain-containing protein 1, plays a crucial role in the assembly of the mitochondrial NADH:ubiquinone oxidoreductase complex (complex I). This protein is instrumental in constructing the membrane arm of complex I, essential for cellular energy production.
Therapeutic significance:
The protein is linked to Mitochondrial complex I deficiency, nuclear type 31, a condition with autosomal recessive inheritance. This disease manifests in a spectrum from lethal neonatal disease to adult-onset neurodegenerative disorders. Understanding the role of Complex I assembly factor TIMMDC1 could open doors to potential therapeutic strategies.