Monooxygenase; part of the gene cluster that mediates the biosynthesis of agnestins, dihydroxy-xanthone metabolites (PubMed:30746079). The pathway begins with the assembly and cyclization of atrochrysone thioester by the non-reducing polyketide synthase Agnpks1 (PubMed:30746079). The atrochrysone carboxyl ACP thioesterase AgnL7 then breaks the thioester bond and releases the atrochrysone carboxylic acid as the first enzyme-free intermediate (PubMed:30746079). The decarboxylase AgnL1 then catalyzes the concerted decarboxylation-elimination required to convert atochrysone carboxylic acid into emodin anthrone, which is further oxidized to emodin by the anthrone oxygenase AgnL2 (PubMed:30746079). Emodin then undergoes reduction catalyzed by the oxidoreductase AgnL4 to yield the dihydroquinone tautomer which is the substrate for reduction by the short chain dehydrogenase AgnL6 reduction to produce hydroxyketone, followed by AgnL8 dehydration and likely spontaneous autoxidation to chrysophanol (PubMed:30746079). Baeyer-Villiger oxidation by the oxidase AgnL3 leads to monodictyphenone via cleavage of the C-10/C-10a bond of chrysophanol (PubMed:30746079). Alternative cleavage at the C-4a/C-10 bond of chrysophanol leads also to the formation some cephalone F (PubMed:30746079). Further conversion to agnestins A and B, requires reduction to dihydro-monodictyphenone, oxidation to agnestin C probably via an epoxide, and rearrangement to either agnestin A or agnestin B directly, although agnestin A or agnestin B can also interconvert (PubMed:30746079). Within the cluster, AgnR1 is the only unassigned oxidoreductase present which could be involved in this conversion. However, AgnR1 seems not to be involved in this step, and thus genes involved in the proposed oxidation/reduction may be located elsewhere on the genome (PubMed:30746079). Further agnestin A derivatives are probably formed by spontaneous decarboxylations, dehydrations and methanolysis reactions (PubMed:30746079). Does not affect the production of agnestins.