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 features a range of promising modulators, each detailed with 38 ADME-Tox and 32 physicochemical and drug-likeness parameters. Plus, each compound is presented with its ideal docking poses, affinity scores, and activity scores, ensuring a thorough insight.
We utilise our cutting-edge, exclusive workflow to develop focused libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
The procedure entails thorough molecular simulations of the catalytic and allosteric binding pockets, accompanied by ensemble virtual screening that factors in their conformational flexibility. When developing modulators, the structural modifications brought about by reaction intermediates are factored in to optimize activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
P05186
UPID:
PPBT_HUMAN
Alternative names:
Alkaline phosphatase liver/bone/kidney isozyme; Phosphoamidase; Phosphocreatine phosphatase
Alternative UPACC:
P05186; A1A4E7; B2RMP8; B7Z387; B7Z4Y6; O75090; Q2TAI7; Q59EJ7; Q5BKZ5; Q5VTG5; Q6NZI8; Q8WU32; Q9UBK0
Background:
Alkaline phosphatase, tissue-nonspecific isozyme (ALPL), plays a pivotal role in skeletal mineralization and adaptive thermogenesis. It hydrolyzes phosphate compounds, aiding in hydroxyapatite crystal formation, essential for bone and dental health. ALPL's broad substrate specificity includes natural substrates like diphosphate and pyridoxal 5'-phosphate, crucial for vitamin B6 metabolism.
Therapeutic significance:
ALPL is linked to Hypophosphatasia, a metabolic bone disease with varying severity, from lethal perinatal forms to milder adult manifestations. Understanding ALPL's function and its genetic variants opens avenues for targeted therapies, potentially transforming treatment paradigms for affected individuals.