AI-ACCELERATED DRUG DISCOVERY

Focused On-demand Library for Transport and Golgi organization protein 1 homolog

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.

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 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 use our state-of-the-art dedicated workflow for designing focused libraries.

 Fig. 1. The sreening workflow of Receptor.AI

By deploying molecular simulations, our approach comprehensively covers a broad array of proteins, tracking their flexibility and dynamics individually and within complexes. Ensemble virtual screening is utilised to take into account conformational dynamics, identifying pivotal binding sites located within functional regions and at allosteric locations. This thorough exploration ensures that every conceivable mechanism of action is considered, aiming to identify new therapeutic targets and advance lead compounds throughout a vast spectrum of biological functions.

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.

partner

Reaxense

upacc

Q5JRA6

UPID:

TGO1_HUMAN

Alternative names:

C219-reactive peptide; D320; Melanoma inhibitory activity protein 3

Alternative UPACC:

Q5JRA6; A8K2S0; A8MT05; A8MT13; B7Z430; Q14083; Q3S4X3; Q5JRA5; Q5JRB0; Q5JRB1; Q5JRB2; Q6UVY8; Q86Y60; Q8N8M5; Q92580

Background:

Transport and Golgi organization protein 1 homolog, also known as C219-reactive peptide, D320, and Melanoma inhibitory activity protein 3, is pivotal in the transport of large cargos from the endoplasmic reticulum. It specifically facilitates the secretion of collagen VII and lipoproteins by incorporating them into membrane-bound carriers. This protein also plays a crucial role in the assembly of COPII coat components at endoplasmic reticulum exit sites, essential for protein secretion.

Therapeutic significance:

Linked to Odontochondrodysplasia 2 with hearing loss and diabetes, understanding the role of Transport and Golgi organization protein 1 homolog could open doors to potential therapeutic strategies. Its specific function in collagen VII secretion and lipoprotein export from the endoplasmic reticulum highlights its potential as a target in treating related disorders.

Looking for more information on this library or underlying technology? Fill out the form below and we'll be in touch with all the details you need.
Thank you! Your submission has been received!
Oops! Something went wrong while submitting the form.
No Spam. Cancel Anytime.