Explore the Potential with AI-Driven Innovation
This extensive focused library is tailor-made using the latest virtual screening and parameter assessment technology, operated by the Receptor.AI drug discovery platform. This technique is more effective than traditional methods, offering compounds with improved 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.
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 use our state-of-the-art dedicated workflow for designing focused 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.
Several key aspects differentiate our library:
partner
Reaxense
upacc
Q99707
UPID:
METH_HUMAN
Alternative names:
5-methyltetrahydrofolate--homocysteine methyltransferase; Cobalamin-dependent methionine synthase; Vitamin-B12 dependent methionine synthase
Alternative UPACC:
Q99707; A1L4N8; A9Z1W4; B7ZLW7; B9EGF7; Q99713; Q99723
Background:
Methionine synthase, also known as 5-methyltetrahydrofolate--homocysteine methyltransferase, plays a pivotal role in methionine biosynthesis by transferring a methyl group from methylcob(III)alamin to homocysteine, yielding methionine. This process is vital for DNA synthesis and repair, implicating the protein in crucial cellular functions.
Therapeutic significance:
The protein's malfunction is linked to Homocystinuria-megaloblastic anemia, cblG complementation type, and Neural tube defects, folate-sensitive, highlighting its therapeutic potential. Understanding the role of Methionine synthase could open doors to potential therapeutic strategies for these conditions.