Mitochondrial oxidative phosphorylation

Scientific explanation

Despite Warburg metabolism, many tumours retain or upregulate OXPHOS, including residual disease, CSC-like fractions and some -driven subsets.

Cancers where relevant

Compounds that intersect this pathway

Metformin

Modest complex I inhibition raises AMP:ATP, activating and restraining hepatic and -linked anabolism. Direct antineoplastic efficacy is not established from that pharmacology alone.

Niclosamide

uncoupler in cestodes; mammalian models report , Wnt/β-catenin and modulation. Those host-signalling findings are investigational/preclinical.

Doxycycline

Tetracycline antibiotic that can inhibit matrix metalloproteinases and, at experimental exposures, protein synthesis. Oncology uses remain investigational.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

Azithromycin

Macrolide with immunomodulatory properties and experimental / observations. Not an anticancer indication.

Nitazoxanide

Antiparasitic interfering with PFOR in anaerobes. Broader in-vitro reports include metabolic and -related readouts; these are not clinical oncology indications.

Berberine

Isoquinoline alkaloid that can inhibit complex I and activate in metabolic models, with additional -independent reports. Not an approved antineoplastic.

Evidence in mapped cancers: In Vitro · In Vivo · Mechanistically Plausible

Convergence partners

Other pathways that co-occur with Mitochondrial oxidative phosphorylation on mapped adjunct records: AMPK, mTOR, Invasion, Cancer stemness.

This oncology atlas is educational. Pathway maps, adjunctive strategies, and compound listings describe mechanistic relevance. They do not establish clinical efficacy, do not recommend treatment, and are not a substitute for oncology care. Evidence tiers are not equivalent.