Explore the Potential with AI-Driven Innovation
This comprehensive focused library is produced on demand with state-of-the-art virtual screening and parameter assessment technology driven by Receptor.AI drug discovery platform. This approach outperforms traditional methods and provides higher-quality compounds with superior 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 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.
Our high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library is unique due to several crucial aspects:
partner
Reaxense
upacc
Q8IZF0
UPID:
NALCN_HUMAN
Alternative names:
CanIon; Sodium leak channel non-selective protein; Voltage gated channel-like protein 1
Alternative UPACC:
Q8IZF0; Q6P2S6; Q6ZMI7; Q8IZZ1; Q8TAH1
Background:
The Sodium leak channel NALCN, also known as CanIon, Sodium leak channel non-selective protein, and Voltage gated channel-like protein 1, plays a pivotal role in neuronal excitability. It is the voltage-sensing, pore-forming subunit of the NALCN channel complex, which is essential for the resting Na(+) permeability. This channel complex, including NALCN, NALF1, UNC79, and UNC80, is constitutively active, conducting monovalent cations but blocked by extracellular divalent cations. NALCN's functions extend to regulating respiratory rhythm, systemic osmoregulation, and intestinal pace-making activity.
Therapeutic significance:
NALCN's involvement in diseases such as Hypotonia, infantile, with psychomotor retardation and characteristic facies 1, and Congenital contractures of the limbs and face, hypotonia, and developmental delay, underscores its therapeutic potential. Understanding the role of Sodium leak channel NALCN could open doors to potential therapeutic strategies for these neurodegenerative and developmental disorders.