Non-reducing polyketide synthase; part of the cluster A that mediates the biosynthesis of azasperpyranones, members of the azaphilone family that exhibit anti-cancer activities (PubMed:31908094). Azasperpyranones are synthesized by 2 clusters, A and B (PubMed:31908094). Cluster A is responsible for the production of the polyhydric phenol moiety while the azaphilonoid scaffold is produced by the cluster B (PubMed:31908094). The non-reducing polyketide synthase ATEG_03629 produces 5-methyl orsellinic acid, which is then reduced to 5-methyl orsellinic aldehyde by the NRPS-like protein ATEG_03630 (PubMed:24412543). 5-methyl orsellinic aldehyde is then first hydroxylated by the FAD-dependent monooxygenase ATEG_03635 and subsequently hydroxylated by the cytochrome P450 monooxygenase ATEG_03631 to produce the unstable polyhydric phenol precursor of azasperpyranones (PubMed:31908094). On the other hand, the polyketide synthase ATEG_07659 is responsible for producing the 3,5-dimethyloctadienone moiety from acetyl-CoA, three malonyl-CoA, and two S-adenosyl methionines (SAM) (Probable). The 3,5-dimethyloctadienone moiety is then loaded onto the SAT domain of ATEG_07661 and extended with four malonyl-CoA and one SAM, which leads to the formation of 2,4-dihydroxy-6-(5,7-dimethyl-2-oxo-trans-3-trans-5-nonadienyl)-3-methylbenzaldehyde (compound 8) after reductive release and aldol condensation (Probable). The FAD-dependent monooxygenase ATEG_07662 is the next enzyme in the biosynthesis sequence and hydroxylates the side chain at the benzylic position of compound 8 (Probable). In Aspergillus nidulans, afoF, the ortholog of the FAD-dependent oxygenase ATEG_07660, is the key enzyme for the biosynthesis of asperfuranone by catalyzing the hydroxylation at C-8 of to prevent the formation of a six-membered ring hemiacetal intermediate and thus facilitatings the formation of a five-membered ring to produce asperfuranone (Probable). In Aspergillus terreus, ATEG_07660 is probably not functional, which leads to the formation of the six-membered ring hemiacetal intermediate presperpyranone instead of asperfuranone (Probable). Finally, ATEG_03636 is involved in the condensation of the polyhydric phenol moiety produced by cluster A and the perasperpyranone precursor produced by cluster B, to yield azasperpyranone A (Probable). Further modifications of azasperpyranone A result in the production of derivatives, including azasperpyranone B to F (PubMed:31908094). acetyl-CoA + H(+) + 3 malonyl-CoA + S-adenosyl-L-methionine = 5-methylorsellinate + 3 CO2 + 4 CoA + S-adenosyl-L-homocysteine Secondary metabolite biosynthesis. Expression is induced by the azasperpyranone cluster A-specific transcription factor ATEG_03638 which is itself regulated by the azasperpyranone transcriptional regulator ATEG_07667. Multidomain protein; including a starter unit:ACP transacylase (SAT) that selects the starter unit; a ketosynthase (KS) that catalyzes repeated decarboxylative condensation to elongate the polyketide backbone; a malonyl-CoA:ACP transacylase (MAT) that selects and transfers the extender unit malonyl-CoA; a product template (PT) domain that controls the immediate cyclization regioselectivity of the reactive polyketide backbone; and 2 acyl-carrier proteins (ACPs) that serve as the tether of the growing and completed polyketide via its phosphopantetheinyl arm. Abolishes the production of 5-methyl orsellinic acid and azasperpyranone A (AZA-A). Azasperpyranones display potential anti-cancer activities (PubMed:31908094). Azasperpyranones A, C, D, and F exhibit potent growth-inhibitory activity against the A549, HepG2, HCT-116, and HL-60 cell lines, with IC(50) values of 2.39-14.42 mm, respectively (PubMed:31908094). Moreover, azasperpyranone D significantly inhibits HCT-116 xenograft tumor growth in BALB/c-nu mice (PubMed:31908094). In addition, azasperpyranones A and C can bind with four kinds of therapeutic targets for cancer, eEF2K, FGFR, survivin, and TNF-a (PubMed:31908094).