Pterin is a heterocyclic compound composed of a pyrazine ring and a pyrimidine ring (a pteridine ring system). The pyrimidine ring includes a carbonyl oxygen and an amino group. Pterins are derivatives of 2-amino-4-oxopteridine with additional functional groups attached to the pyrazine ring. Pterins are known in the art and are used in a various applications. One of the most notable examples of pterin is folic acid. Another example is molybdopterin which is a substituted pteridine that binds molybdenum to give redox enzymes involved in biological hydroxylation and oxidation reactions. Pterins, substituted pterins, and derivatives thereof are of significant interest because of their potential uses in the fields of medicine and pharmaceuticals. It is contemplated that pterins can be used as a means for therapy in treating various medical conditions, such as cancer and molybdenum cofactor deficiency (MCD). Further, it is believed that pterins may possess antibacterial properties.
Pyran is a heterocyclic ring composed of five carbon atoms and one oxygen atom. There are many pyran derivatives that are known in the art as important biological molecules.
Molybdenum is an essential trace element for virtually all life forms. It is central to a cofactor for a number of enzymes that catalyze important chemical transformations. A biological form of molybdenum present in molybdenum-containing enzymes is known as the molybdenum cofactor. The molybdenum cofactor is a complicated molecule with multiple redox-active components delicately balanced having the following structure:

In some enzymes, the phosphate group substituent of the cofactor is modified with a dinucleotide. The chemical synthesis of the molybdenum cofactor and its precursors is very challenging.
An absence of or deficiency in molybdenum cofactor (known as MCD) in the human body can lead to serious illness and death. MCD is a lethal autosomal recessive disease for which treatment and cure is a focus of significant research efforts.
The biosynthetic pathway of molybdenum cofactor is a multi-step and evolutionarily conserved process involving four genes. Three of these four genes are linked to MCD. Patients are characterized by progressive neurological damage, leading to early childhood death in most cases. Symptoms are mainly caused by the sulfite oxidase (SO) enzyme deficiency. The SO enzymes remove toxic sulfite in the human body to protect the organs, particularly the brain, from an accumulation of sulfite. A deficiency of SO enzymes causes excess sulfite to accumulate in plasma and serum, it crosses the blood-brain barrier, and rapidly triggers neuronal death. Excess sulfite reacts with cystine, forming S-sulfocysteine, a potential agonist of glutamate receptors, which has been implicated for observed seizures, convulsions, contractions and twitching associated with MCD, causing damage of cortical neurons and loss of white matter.
There is a desire in the art to develop and synthesize new substituted pyrans and pterins for use in various applications including medicine and pharmaceuticals, such as, but not limited to, the treatment of MCD.