Focused On-demand Library for Voltage-dependent T-type calcium channel subunit alpha-1G

Available from Reaxense
Predicted by Alphafold

Focused On-demand Libraries - Reaxense Collaboration

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.

From a virtual chemical space containing more than 60 billion molecules, we precisely choose certain compounds. Our collaborator, Reaxense, aids in their synthesis and provision.

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.

We utilise our cutting-edge, exclusive workflow to develop focused libraries for ion channels.

 Fig. 1. The sreening workflow of Receptor.AI

This process includes comprehensive molecular simulations of the ion channel in its native membrane environment, depicting its open, closed, and inactivated states, and ensemble virtual screening that accounts for conformational mobility in each state. Tentative binding pockets are investigated inside the pore, at the gating region, and in allosteric sites to cover the full spectrum of possible mechanisms of action.

Several key aspects differentiate our library:

  • Receptor.AI compiles an all-encompassing dataset on the target protein, including historical experiments, literature data, known ligands, and structural insights, maximising the chances of prioritising the most pertinent compounds.
  • The platform employs state-of-the-art molecular simulations to identify potential binding sites, ensuring the focused library is primed for discovering allosteric inhibitors and binders of concealed pockets.
  • Over 50 customisable AI models, thoroughly evaluated in various drug discovery endeavours and research projects, make Receptor.AI both efficient and accurate. This technology is integral to the development of our focused libraries.
  • In addition to generating focused libraries, Receptor.AI offers a full range of services and solutions for every step of preclinical drug discovery, with a pricing model based on success, thereby reducing risk and promoting joint project success.







Alternative names:

Cav3.1c; NBR13; Voltage-gated calcium channel subunit alpha Cav3.1

Alternative UPACC:

O43497; D6RA64; E7EPR0; O43498; O94770; Q19QY8; Q19QY9; Q19QZ0; Q19QZ1; Q19QZ2; Q19QZ3; Q19QZ4; Q19QZ5; Q19QZ6; Q19QZ7; Q19QZ8; Q19QZ9; Q19R00; Q19R01; Q19R02; Q19R03; Q19R04; Q19R05; Q19R06; Q19R07; Q19R08; Q19R09; Q19R10; Q19R11; Q19R12; Q19R13; Q19R15; Q19R16; Q19R17; Q19R18; Q2TAC4; Q9NYU4; Q9NYU5; Q9NYU6; Q9NYU7; Q9NYU8; Q9NYU9; Q9NYV0; Q9NYV1; Q9UHN9; Q9UHP0; Q9ULU6; Q9UNG7; Q9Y5T2; Q9Y5T3


The Voltage-dependent T-type calcium channel subunit alpha-1G, known alternatively as Cav3.1c, NBR13, and Voltage-gated calcium channel subunit alpha Cav3.1, plays a pivotal role in mediating calcium ion entry into excitable cells. This protein is integral to various calcium-dependent processes such as muscle contraction, neurotransmitter release, and cell division. Its unique feature is the ability to open at negative potentials, contributing to pacemaking functions in neurons and cardiac cells.

Therapeutic significance:

Spinocerebellar ataxia 42 and its severe early-onset form with neurodevelopmental deficits are directly linked to mutations affecting the Voltage-dependent T-type calcium channel subunit alpha-1G. Understanding the role of this protein could lead to novel therapeutic strategies targeting these debilitating neurological disorders.

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