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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
The library includes a list of the most effective modulators, each annotated with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Furthermore, each compound is shown with its optimal docking poses, affinity scores, and activity scores, offering a detailed summary.
We use our state-of-the-art dedicated workflow for designing focused 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.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q96FE5
UPID:
LIGO1_HUMAN
Alternative names:
Leucine-rich repeat and immunoglobulin domain-containing protein 1; Leucine-rich repeat neuronal protein 1; Leucine-rich repeat neuronal protein 6A
Alternative UPACC:
Q96FE5; D3DW80; Q6NUK3; Q6UXM3; Q6VVG0; Q6VVG1; Q6VVG2; Q8N3K5; Q96K52
Background:
Leucine-rich repeat and immunoglobulin-like domain-containing nogo receptor-interacting protein 1 (LRRN1) plays a pivotal role in the Nogo receptor signaling complex, crucial for RhoA activation and myelin-associated factors' inhibition of axonal regeneration. It also negatively regulates oligodendrocyte differentiation and axonal myelination, and is involved in neuronal precursor cell motility during cortical development.
Therapeutic significance:
LRRN1's involvement in Intellectual developmental disorder, autosomal recessive 64, characterized by severe intellectual disability and delayed motor development, highlights its potential as a therapeutic target. Understanding LRRN1's role could open doors to novel therapeutic strategies for neurological disorders.