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.
The compounds are cherry-picked from the vast virtual chemical space of over 60B molecules. The synthesis and delivery of compounds is facilitated by our partner Reaxense.
In the library, a selection of top modulators is provided, each marked with 38 ADME-Tox and 32 parameters related to physicochemical properties and drug-likeness. Also, every compound comes with its best docking poses, affinity scores, and activity scores, providing a comprehensive overview.
We employ our advanced, specialised process to create targeted libraries for enzymes.
Fig. 1. The sreening workflow of Receptor.AI
It includes in-depth molecular simulations of both the catalytic and allosteric binding pockets, with ensemble virtual screening focusing on their conformational flexibility. For modulators, the process includes considering the structural shifts due to reaction intermediates to boost activity and selectivity.
Our library distinguishes itself through several key aspects:
partner
Reaxense
upacc
O15270
UPID:
SPTC2_HUMAN
Alternative names:
Long chain base biosynthesis protein 2; Long chain base biosynthesis protein 2a; Serine-palmitoyl-CoA transferase 2
Alternative UPACC:
O15270; Q16685
Background:
Serine palmitoyltransferase 2 (SPTLC2) plays a pivotal role in de novo sphingolipid biosynthesis, essential for adipogenesis. This enzyme, forming a heterodimer with SPTLC1, exhibits substrate preference influenced by its complex composition; the SPTLC1-SPTLC2-SPTSSA complex favors C16-CoA, while the SPTLC1-SPTLC2-SPTSSB complex prefers C18-CoA.
Therapeutic significance:
SPTLC2 mutations lead to hereditary sensory and autonomic neuropathy 1C (HSAN1C), characterized by sensory abnormalities and severe infections. These mutations alter SPT's substrate specificity, causing the production of 1-deoxysphingolipids, which are toxic due to improper metabolism. Understanding SPTLC2's role could unveil new therapeutic strategies for HSAN1C.