AI-ACCELERATED DRUG DISCOVERY

Focused On-demand Library for Translation initiation factor eIF-2B subunit alpha

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.

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 top-notch dedicated system is used to design specialised libraries.

 Fig. 1. The sreening workflow of Receptor.AI

Our strategy employs molecular simulations to explore an extensive range of proteins, capturing their dynamics both individually and within complexes with other proteins. Through ensemble virtual screening, we address proteins' conformational mobility, uncovering key binding sites at both functional regions and remote allosteric locations. This comprehensive investigation ensures a thorough assessment of all potential mechanisms of action, with the goal of discovering innovative therapeutic targets and lead molecules across across diverse biological functions.

Our library is unique due to several crucial aspects:

  • Receptor.AI compiles all relevant data on the target protein, such as past experimental results, literature findings, known ligands, and structural data, thereby enhancing the likelihood of focusing on the most significant compounds.
  • By utilizing advanced molecular simulations, the platform is adept at locating potential binding sites, rendering the compounds in the focused library well-suited for unearthing allosteric inhibitors and binders for hidden pockets.
  • The platform is supported by more than 50 highly specialized AI models, all of which have been rigorously tested and validated in diverse drug discovery and research programs. Its design emphasizes efficiency, reliability, and accuracy, crucial for producing focused libraries.
  • Receptor.AI extends beyond just creating focused libraries; it offers a complete spectrum of services and solutions during the preclinical drug discovery phase, with a success-dependent pricing strategy that reduces risk and fosters shared success in the project.

partner

Reaxense

upacc

Q14232

UPID:

EI2BA_HUMAN

Alternative names:

eIF-2B GDP-GTP exchange factor subunit alpha

Alternative UPACC:

Q14232; A6NLY9; B4DGX0; Q3SXP4

Background:

Translation initiation factor eIF-2B subunit alpha, also known as eIF-2B GDP-GTP exchange factor subunit alpha, plays a pivotal role in protein synthesis. It catalyzes the exchange of eukaryotic initiation factor 2-bound GDP for GTP, a critical step in the initiation of protein translation. This protein's function underscores its importance in cellular biology and its potential impact on understanding disease mechanisms.

Therapeutic significance:

Leukoencephalopathy with vanishing white matter 1, a devastating brain disease, is directly linked to mutations affecting this protein. The disease's progression and its impact on neurological functions highlight the critical role of eIF-2B subunit alpha in brain health. Understanding the role of Translation initiation factor eIF-2B subunit alpha could open doors to potential therapeutic strategies for this and related neurological 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.