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 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 high-tech, dedicated method is applied to construct targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
This approach involves comprehensive molecular simulations of the catalytic and allosteric binding pockets and ensemble virtual screening that accounts for their conformational flexibility. In the case of designing modulators, the structural adjustments caused by reaction intermediates are considered to improve activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
Q9GZV9
UPID:
FGF23_HUMAN
Alternative names:
Phosphatonin; Tumor-derived hypophosphatemia-inducing factor
Alternative UPACC:
Q9GZV9; Q4V758
Background:
Fibroblast growth factor 23 (FGF23), also known as Phosphatonin and Tumor-derived hypophosphatemia-inducing factor, plays a pivotal role in phosphate homeostasis. It inhibits renal tubular phosphate transport, up-regulates EGR1 expression, and acts on the parathyroid to decrease PTH secretion. FGF23 is a key regulator of vitamin-D metabolism and negatively regulates osteoblast differentiation.
Therapeutic significance:
FGF23 is implicated in Hypophosphatemic rickets, autosomal dominant, characterized by renal phosphate wasting, and Tumoral calcinosis, hyperphosphatemic, familial, 2, marked by hyperphosphatemia and calcium deposits. Understanding the role of FGF23 could open doors to potential therapeutic strategies for these conditions.