AI-ACCELERATED DRUG DISCOVERY

Focused On-demand Library for Tubby-related protein 3

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.

In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.

We utilise our cutting-edge, exclusive workflow to develop 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.

Our library stands out due to several important features:

  • The Receptor.AI platform compiles comprehensive data on the target protein, encompassing previous experiments, literature, known ligands, structural details, and more, leading to a higher chance of selecting the most relevant compounds.
  • Advanced molecular simulations on the platform help pinpoint potential binding sites, making the compounds in our focused library ideal for finding allosteric inhibitors and targeting cryptic pockets.
  • Receptor.AI boasts over 50 tailor-made AI models, rigorously tested and proven in various drug discovery projects and research initiatives. They are crafted for efficacy, dependability, and precision, all of which are key in creating our focused libraries.
  • Beyond creating focused libraries, Receptor.AI offers comprehensive services and complete solutions throughout the preclinical drug discovery phase. Our success-based pricing model minimises risk and maximises the mutual benefits of the project's success.

partner

Reaxense

upacc

O75386

UPID:

TULP3_HUMAN

Alternative names:

Tubby-like protein 3

Alternative UPACC:

O75386; B3KNB7; B7Z6A2; D3DUQ4; F8WBZ9; Q8N5B0

Background:

Tubby-related protein 3, alternatively known as Tubby-like protein 3, plays a pivotal role in cellular processes by acting as a negative regulator of the Shh signaling transduction pathway. It is essential for the recruitment of G protein-coupled receptor GPR161 to cilia, influencing PKA-dependent basal repression machinery in Shh signaling. Its interaction with phosphorylated inositide lipids and the IFT complex A underscores its significance in regulating ciliary G protein-coupled receptor trafficking, particularly during adipogenesis.

Therapeutic significance:

Tubby-related protein 3's involvement in Hepatorenocardiac degenerative fibrosis, a disorder marked by liver fibrosis, kidney disease, and cardiomyopathy, highlights its potential as a therapeutic target. Understanding the role of Tubby-related protein 3 could open doors to potential therapeutic strategies for this autosomal recessive disorder.

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.