AI-ACCELERATED DRUG DISCOVERY

Focused On-demand Library for Large ribosomal subunit protein bL28m

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.

Contained in the library are leading modulators, each labelled with 38 ADME-Tox and 32 physicochemical and drug-likeness qualities. In addition, each compound is illustrated with its optimal docking poses, affinity scores, and activity scores, giving a complete picture.

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

 Fig. 1. The sreening workflow of Receptor.AI

Our methodology leverages molecular simulations to examine a vast array of proteins, capturing their dynamics in both isolated forms and in complexes with other proteins. Through ensemble virtual screening, we thoroughly account for the protein's conformational mobility, identifying critical binding sites within functional regions and distant allosteric locations. This detailed exploration ensures that we comprehensively assess every possible mechanism of action, with the objective of identifying novel therapeutic targets and lead compounds that span a wide spectrum of 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

Q13084

UPID:

RM28_HUMAN

Alternative names:

39S ribosomal protein L28, mitochondrial; Melanoma antigen p15; Melanoma-associated antigen recognized by T-lymphocytes

Alternative UPACC:

Q13084; B2RCM4; D3DU46; Q4TT39; Q96S26; Q9BQD8; Q9BR04

Background:

The Large ribosomal subunit protein bL28m, also known as 39S ribosomal protein L28, mitochondrial, Melanoma antigen p15, and Melanoma-associated antigen recognized by T-lymphocytes, plays a crucial role in the mitochondrial ribosome. Its primary function is to contribute to the synthesis of proteins within the mitochondria, a process essential for cellular energy production and metabolic functions.

Therapeutic significance:

Understanding the role of Large ribosomal subunit protein bL28m could open doors to potential therapeutic strategies. Its involvement in mitochondrial protein synthesis positions it as a key player in cellular metabolism and energy production, making it a potential target for addressing metabolic disorders and diseases related to mitochondrial dysfunction.

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.