Named Bioactive Compounds · Compound
Pomiferin
Moderate Evidencecompound
Hermetica Superfood Encyclopedia
Pomiferin is a prenylated isoflavone derived primarily from Maclura pomifera (Osage orange) that exerts anticancer and anti-inflammatory effects by modulating apoptotic pathways and suppressing neuroinflammatory signaling. Its prenyl side chain enhances membrane permeability and potentiates interaction with targets including Bcl-2 family proteins and NF-κB, distinguishing it from non-prenylated flavonoids.
Pomiferin is a prenylated isoflavone extracted from the fruits of Maclura pomifera (Osage Orange), a tree native to North America. It is typically isolated through solvent extraction methods from the fruit material, where it occurs alongside osajin as one of the major bioactive constituents.
No human clinical trials exist for pomiferin; all evidence comes from preclinical studies. Key research includes neuroinflammation effects in BV2 microglial cells (PMID: 35418806), synergy with chemotherapy drugs in neuroblastoma (PMID: 40332068), and reversal of multidrug resistance in mouse cancer models (PMID: 37061145).
No clinically established dosage ranges exist for pomiferin in humans. Preclinical studies have used varying concentrations in cell culture (typically micromolar ranges), but these cannot be translated to human therapeutic doses. Consult a healthcare provider before starting any new supplement.
Pomiferin is not a nutritional food source but rather a prenylated isoflavone (chemical formula C₂₅H₂₄O₆, molecular weight ~420.46 g/mol) primarily isolated from the fruit and wood of Maclura pomifera (Osage orange) and related Maclura species. It belongs to the broader class of isoflavonoids and is structurally characterized as 3',4'-dimethoxy-5-hydroxy-6,7-(2'',2''-dimethylchromeno)isoflavone. Key bioactive compound details: • Pomiferin typically co-occurs with osajin (another prenylated isoflavone) in Osage orange fruit at concentrations ranging from approximately 1–10 mg/g of dried fruit material, depending on extraction method and plant part. • It functions as a potent antioxidant with reported ORAC values significantly higher than many conventional dietary flavonoids; its radical-scavenging activity is attributed to the hydroxyl group at the C-5 position and the prenyl/chromenyl moiety. • Bioavailability is considered low due to poor aqueous solubility (typical of prenylated isoflavonoids), significant first-pass metabolism, and rapid glucuronidation/sulfation in hepatic and intestinal tissues. Lipid-based delivery systems or nanoformulations have been explored to improve absorption. • No established dietary reference intakes, recommended daily allowances, or standard nutritional values (calories, protein, fat, carbohydrates, fiber, vitamins, minerals) exist, as pomiferin is studied as a bioactive phytochemical/pharmacological agent rather than consumed as a food or supplement. • Additional co-occurring bioactive compounds in Maclura pomifera extracts include osajin, auriculasin, and various other prenylated flavonoids, which may contribute synergistic biological effects. • The compound demonstrates lipophilic character (estimated LogP ~4.5–5.0), favoring partitioning into lipid-rich environments and potentially accumulating in cell membranes, which is relevant to its mechanisms of action in modulating membrane-associated signaling pathways.
Pomiferin promotes cancer cell death by activating both intrinsic apoptotic pathways (via cytochrome c release and caspase-3/9 activation) and autophagic flux, while downregulating pro-survival Bcl-2 and upregulating Bax. It sensitizes cisplatin-resistant cancer cells by inhibiting P-glycoprotein efflux pump activity and suppressing PI3K/Akt survival signaling. In neuroinflammatory contexts, pomiferin attenuates microglial activation by blocking NF-κB nuclear translocation and reducing downstream cytokine production including TNF-α and IL-6.
All current evidence for pomiferin is preclinical, derived exclusively from in vitro cell culture experiments and in vivo mouse models with no completed human clinical trials. In cisplatin-resistant mouse tumor models, pomiferin co-administration measurably reduced tumor volume and restored drug sensitivity, though specific quantified effect sizes vary by study. Cell studies have demonstrated IC50 values in the low-to-mid micromolar range against several cancer cell lines, and anti-neuroinflammatory effects have been replicated in LPS-stimulated microglial cell models. The evidence base is considered preliminary and hypothesis-generating; extrapolation to human therapeutic use requires rigorous clinical validation.
No human safety data, established tolerable upper limits, or pharmacokinetic profiles exist for pomiferin, as it has not progressed to clinical trials. Because pomiferin inhibits P-glycoprotein, it carries a theoretical risk of elevating plasma concentrations of P-gp substrate drugs such as digoxin, certain chemotherapeutics, and immunosuppressants, potentially causing toxicity. Pregnant and breastfeeding individuals should avoid pomiferin entirely given the complete absence of reproductive safety data and its demonstrated potent cellular activity. Individuals on cisplatin or other platinum-based chemotherapy should consult an oncologist before considering any pomiferin-containing product, as synergistic effects, while potentially beneficial, are uncontrolled outside clinical settings.
