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.
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
The method includes detailed molecular simulations of the catalytic and allosteric binding pockets, along with ensemble virtual screening that considers their conformational flexibility. In the design of modulators, structural changes induced by reaction intermediates are taken into account to enhance activity and selectivity.
Key features that set our library apart include:
partner
Reaxense
upacc
P23786
UPID:
CPT2_HUMAN
Alternative names:
Carnitine palmitoyltransferase II
Alternative UPACC:
P23786; B2R6S0; Q5SW68; Q9BQ26
Background:
Carnitine O-palmitoyltransferase 2, mitochondrial, also known as Carnitine palmitoyltransferase II, plays a crucial role in the intramitochondrial synthesis of acylcarnitines from accumulated acyl-CoA metabolites. It is pivotal for the mitochondrial uptake of long-chain fatty acids and their subsequent beta-oxidation, with activity on medium and long-chain acyl-CoA esters.
Therapeutic significance:
Carnitine palmitoyltransferase II deficiency manifests in various forms, including myopathic, infantile, and lethal neonatal types, alongside susceptibility to infection-induced encephalopathy. Understanding its function could lead to breakthroughs in treating these metabolic disorders.