Explore the Potential with AI-Driven Innovation
The specialised, focused library is developed on demand with the most recent virtual screening and parameter assessment technology, guided by the Receptor.AI drug discovery platform. This approach exceeds the capabilities of traditional methods and offers compounds with higher 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:
partner
Reaxense
upacc
Q6ZN17
UPID:
LN28B_HUMAN
Alternative names:
-
Alternative UPACC:
Q6ZN17; A1L165; B2RPN6; Q5TCM4
Background:
Protein lin-28 homolog B plays a crucial role in the suppression of microRNA (miRNA) biogenesis, notably affecting let-7 and potentially miR107, miR-143, and miR-200c. It binds to primary let-7 transcripts, sequestering them in the nucleolus and preventing their maturation into miRNA. This suppression is vital for normal development and maintaining the pluripotency of embryonic stem cells by inhibiting let-7-mediated differentiation. Additionally, its overexpression can lead to the degradation of pre-let-7 transcripts, although this may not be significant in vivo.
Therapeutic significance:
Understanding the role of Protein lin-28 homolog B could open doors to potential therapeutic strategies.