Secosteroid biosynthesis denotes the formation of secosteroids—steroidal compounds in which one of the parent rings of the tetracyclic nucleus, most commonly the B-ring, has undergone scission—through photochemical or enzymatic mechanisms ^[1]. The prototypical pathway is the UV-B–driven photolysis of a 5,7-diene sterol precursor: in vertebrates, 7-dehydrocholesterol in the skin absorbs UV-B radiation (290–315 nm), causing cleavage of the B-ring between C9 and C10 to yield previtamin D3, which then undergoes a temperature-dependent rearrangement to cholecalciferol (vitamin D3); an analogous photoconversion of ergosterol yields vitamin D2 in fungi ^[2]. Secosteroid biosynthesis also encompasses enzyme-catalyzed routes, notably cytochrome P450 CYP11A1–mediated hydroxylation of 7-dehydrocholesterol or vitamin D3, which generates hydroxylated secosteroid metabolites with modified A-ring or side-chain structures that can be further transformed by UV-B ^[3]. The term additionally covers the formation of diverse 9,11-, 5,6-, and other secosteroid classes in marine invertebrates and microorganisms, where oxidative cleavage of sterol rings produces structurally distinct secosteroid scaffolds ^[1][4]. Secosteroid biosynthesis thus spans non-enzymatic photochemical ring opening and enzyme-dependent oxidative routes that together generate the secosteroid class from sterol precursors ^[1][2][3].