Carbon monoxide (CO)

Carbon monoxide is a **gaseous signaling molecule** produced endogenously in the body primarily through the action of heme oxygenase enzymes on heme. It acts as a gasotransmitter with roles in **vasodilation**, anti-inflammatory responses, cytoprotection, and modulation of neurotransmission. Abnormalities in carbon monoxide metabolism are linked to diseases such as neurodegeneration, hypertension, heart failure, and inflammation. Therapeutically, controlled delivery of carbon monoxide—often via specialized compounds called **carbon monoxide-releasing molecules (CO-RMs)**—has been explored for its potential benefits in cardiovascular diseases and inflammatory conditions. However, "carbon monoxide delivery" is not itself a molecular target or receptor but rather refers to the process or technology for administering CO therapeutically. The actual biological targets are various heme-containing proteins that bind CO—including hemoglobin (which mediates its toxic effects), myoglobin, cytochrome c oxidase (Complex IV), soluble guanylate cyclase (sGC), nitric oxide synthases, cytochrome P450 enzymes—and these mediate both physiological signaling effects at low concentrations and toxicity at high concentrations[1][2][3][4]. “All known biological functions of CO occur through binding to metal ions, primarily hemoproteins in the ferrous form.” [6] “There is significant interest in the therapeutic potential of carbon monoxide becoming pharmaceutical agent... Many pharmaceutical drug delivery initiatives have developed methods to safely administer carbon monoxide...” [1] In summary: "Carbon monoxide delivery" is not itself a canonical molecular target but describes an approach for modulating endogenous pathways by delivering exogenous CO; thus this entry is incorrect as a drug target per se.

Binds to heme-containing proteins (e.g., hemoglobin, myoglobin, cytochrome c oxidase); Modulates guanylate cyclase activity leading to increased cGMP and vasorelaxation[3][4]